Yes

Over-activity of dopaminergic nerves can be caused by factors such as excessive dopamine release, increased dopamine receptor sensitivity, or decreased dopamine reuptake. This can lead to conditions like schizophrenia, bipolar disorder, and Parkinson's disease.

No, parkinson's affects the dopaminergic neurons of the substantia nigra, which is part of the mid-brain.

Michael Bryan Goldberg has written:

'Dopaminergic effects on intraocular pressure and binding in the cileary processes'

No. It is a neurologic disease, originating in the dopaminergic pathways of the brain, including the substantia nigra, caudate and putamen, as well as other structures.

Bromocriptine (dopaminergic agonist drug) has longer duration of action than levodopa (dopamine precursor).

Yes, neurologists can provide evaluation and treatment recommendations for children with ADHD. They can assess the child's symptoms, recommend medication if needed, and work with other healthcare providers to create a comprehensive treatment plan.

The midbrain, in particular the substantia nigra, produces a specific type of cell called dopaminergic neurons. These neurons play a crucial role in the regulation of movement and are primarily affected in Parkinson's disease.

The parts of the brain thought to be involved in schizophrenia include the prefrontal cortex, hippocampus, and thalamus. Dysfunction in these areas can impact cognition, emotion regulation, and sensory processing, contributing to symptoms of schizophrenia such as disorganized thinking, hallucinations, and delusions.

As far as we know, dopamine is the main culprit in psychosis. Autospies have shown excess dopaminergic receptors in the brain's of people who suffered psychosis. Other neurotransmitters are also affected.

To date, no pharmacological treatments for aphasia have proven effective, although a number of drugs (dopaminergic, cholinergic, and neurotrophic) continue to be investigated, usually in conjunction with behavioral treatments for aphasia.

Instead of drugs, many aphasia patients benefit from intensive speech therapy.

BPA which stands for Bisphenol A is a compound used in making many plastics used today. It has been in question in regard to negative human heath effects since the 1930's. It has been linked to obesity, Neurological issues, breast cancer reproductive issues and Disruption of the dopaminergic system.

Benadryl is Primarily an antihistamine, although it possesses some anticholinergic and (maybe) some dopaminergic activity. So if a patient is on compazine or promethazine these drugs will block dopamine at the receptor, causing EPS. Diphenhydramine will then block acetylcholine and this will bring balance to the dopamine and acetylcholine system in the substantia nigra - reducing or eliminating the EPS.

Antiparkinson drugs attempt to restore the balance through one of several mechanisms, depending on drug type. The most effective drugs, called dopaminergic drugs, replace dopamine, or mimic its action in the brain.

Edward James Hamilton has written:

'Plasma HVA levels and contrived leisure experiences of female college students' -- subject(s): Dopamine, Dopaminergic mechanisms, Leisure, Neural stimulation, Neuropsychology, Pleasure, Psychological aspects, Psychological aspects of Leisure, Psychology, Self-perception, Women, Women college students

Parkinson Disease is a gradual neurodegenerative disorder caused by motor deficits which is due to dopaminergic neurons loss in the substantia nigra and the production of lewy bodies. In this case the facial muscles are affected including upper and lower extremities and this also leads to a condition name parkinsonism. In order to purchase the Parkinson Disease research sample online, contact Central BioHub.

In paralysis agitans, which is another term for Parkinson's disease, the group of brain cells that are primarily affected are the dopaminergic neurons in the substantia nigra region of the brain. These neurons are responsible for producing dopamine, a neurotransmitter that helps regulate movement and coordination.

Parkinson Disease is a gradual neurodegenerative disorder caused by motor deficits which is due to dopaminergic neurons loss in the substantia nigra and the production of lewy bodies. In this case the facial muscles are affected including upper and lower extremities and this also leads to a condition name parkinsonism. In order to purchase the Parkinson Disease research sample online, contact Central BioHub.

There are two classes of the drugs: dopaminergics and anticholinergics.

The dopaminergic drugs include the following:

A: Levodopa drugs: such as levodopa and madopar

B: Dopamine releasing agents (DRAs), such as amantadine and memantine

C: Dopamine agonists, such as piribedil and pramipexoleD: MAO-B inhibitors,such as selegiline

E: Catechol-O-methyl transferase(COMT) inhibitors: such as entacapone and tolcapone

Anticholinergics include trihexyphenidyl, benztropine mesylate etc.

The chemical you are referring to is likely methamphetamine. While it can be dangerous due to its potential for addiction and serious side effects, methamphetamine's ability to affect dopaminergic and glutamatergic systems may have potential therapeutic applications in treating Parkinson's disease, Tourette's syndrome, and Alzheimer's disease. Research is ongoing to explore its potential benefits in these conditions.

Dopamine acts on specific receptors in the kidneys, which leads to the dilation of blood vessels supplying the kidneys. This increased blood flow to the kidneys enhances their filtration rate and urine production. Dopamine also helps regulate the balance of salt and water in the body, which can further influence urine output.

Cocaine blocks the reuptake of dopamine and, to a lesser extent, norepinephrine and serotonin in the brain. This causes the accumulation of dopamine, leading to euphoria and excitation. The increased stimulation of dopaminergic neurons in the mesolimbic (reward) circuit leads to addiction.

Alcohol binds with GABA receptors producing inhibitory effects on neural activity. This produces cognitive impairment and reduced anxiety (disinhibition). Activation of GABA receptors also produces postsynaptic dopamine release, which stimulates the mesolimbic circuit in the brain, producing euphoria and addiction.

These include anti-nausea drugs such as Antivert, Atarax, Compazine and Phenergan. Calcium channel blockers that are often used to treat heart conditions should be avoided. In addition, most anti-depressants tend to exacerbate symptoms.

This because dopamine because it has postive inotropic effect , chronotropic effect on the heart ( activate B1 receptrors ). It overcome hyptension by activation of alpha receptor . it activates also the dopaminergic receptors in renal and splanchnic arterioles , thus increase blood flow to the kideny and other viscera . this protect the kideny in case of cardiogenic shock .Adrenaline did not provide this protection even may reduce blood supply to these vital organ. (Dr. A. S. Ali Assocaite prof of pharmacology. creative pharmasit gate )

Any antiemetic drug that can cause extrapyramidal symptoms (or whose mechanism relies on dopaminergic antagonism such as domperidone, metoclopramide etc) should be absolutely avoided in patients with PD. Certain H1 blocking antiemetics such as cyclizine can cause EPS hence always check wirh your Phramcist or Physician before taking any of these medicines. Anti emetics that can be safely given to PD patients include the setron family of 5HT-3 antagonists. Also, diphenhydramine (BENADRYLTM) an H1 antihistaminic is free from EPS therefore, it can also be used safely for nausea and vomiting in PD patients.

Methylenedioxymethamphetamine (MDMA) is also know as ecstacy. It should be noted that according to US law that it is illegal to use as it is considered a drug with high potential for addiction.

SSRI therapy primarily affects serotonin levels in the brain, not dopamine. While it may indirectly influence dopamine levels in certain regions of the brain, the impact is typically not as significant as its effects on serotonin.

Reinforcement is too vague of a word for a specific answer, but I will give it my best:

Eating, especially foods such as chocolate which contain small amounts of phenethylamine, induces a dopamenergic response in the brain. Your brain rewards you with dopamine when you eat, exercise, and engage in positive social interactions. This is an evolutionary trait that helped humans keep their bodies and minds healthy. This is also why sometimes you might eat or snack without being hungry. Your brain naturally seeks activities that induce this dopaminergic reward.

When speaking of dopaminergic reinforcement, you are indicating the possibility of addiction. It is obvious to see that some people can become addicted to eating. This is because they either get too small of a dopamine response from other activities - so they rely heavily on eating to attain this reward - or they get an excessive reward for eating so that other activities pale in comparison.

When speaking of a social or psychological reinforcement, you are indicating that some people find eating to be a form of social acceptance or a source of positive self-esteem. This can be linked to any past experience from childhood that taught the child that 'eating makes me a good person'.

For some children, sitting around the dinner table for a meal might be the only time the children interact with their parents, or it could be the only time that the family can get along. In turn, over years of reinforcing this lesson this child grows into an adult that finds eating to be a very positive social event or maybe the only way they can feel 'at home'. The hypotheticals are endless for psychological speculation on how a specific behavior can be reinforced. (See: Pavlov's Dogs)

Typically No, it will not, but some listed side effects of the medication include confusion, agitation, hallucinations (seeing things that are not there), dizziness, and tired feeling. Usually euphoria needs to be listed to get a recreational high from a drug.

Cephalexin is a penicillin-based antibiotic and should contain nothing to make you high. Following an accident I was prescribed to take cephalexin at 12-hour intervals for five days. During this time I drove and operated heavy machinery. Although I worried it might turn me yellow, I experienced none of the possible side effects.

Neuroleptics primarily impact the dopamine receptors in the brain, specifically the dopamine D2 receptors. They also affect other neurotransmitter systems, such as serotonin and norepinephrine, which contribute to their antipsychotic effects.

Long-term use of amphetamines can lead to weight loss, skin problems, dental issues, and a generally unhealthy appearance. Users may appear gaunt, with dilated pupils and skin picking behaviors, leading to a deterioration in physical appearance over time.

Many chemicals are released when the body experiences pleasure. Dopamine is one f them and is released in the brain when pleasure is experienced, and is increased when many recreational drugs are used - this is partly responsible for the strong euphoric effect and addictive potential. There are other neurotransmitters that also are responsible for pleasure and they would include serotonin, melatonin, oxytocin, endorphins and enkephalins.

Yes there are. Long-term use of Levodopa to treat Parkinson's disease may cause fluctuations in therapeutic effects in such a way that the symptoms might be worse. We call this motor fluctuations. Usually motor fluctuations appear after a few years of regular use of L-Dopa (this is why patients with a young-onset Parkinson's disease are usually given dopaminergic agonists first instead of L-Dopa/carbidopa; doctors want to prevent motor fluctuations to appear).

Symptoms of motor fluctuations may include severe dyskinesia when serum L-Dopa reaches its peak level; and gradual, foreseeable loss of therapeutic effects after a few hours. This results in patients with marked bradykinesia and resting tremor without medication, and choreo-athetosic dyskinesia when L-Dopa is given. When a patient reaches motor fluctuations, his or her disease becomes more difficult for physicians to control.

For more info, please consult your physician or pharmacist.

Cocaine affects the central nervous system by increasing dopamine levels, leading to heightened feelings of energy and euphoria. It can also impact the cardiovascular system by constricting blood vessels and increasing heart rate and blood pressure. Additionally, long-term cocaine use can cause damage to various organ systems, including the liver and kidneys.

Can peticide exposure cause Parkinson’s? Parkinson’s disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. The major pathologic feature of PD is the profound loss of pigmented neurons, mainly in the pars compacta of the substantia nigra (SN). Associated with this neuronal loss is the presence of large eosinophilic inclusions, called Lewy bodies, within the remaining pigmented neurons, made up of a series of proteins, including neurofilaments, α-synuclein fibrils, ubiquitin, parkin, and proteasomal elements. The first clinical signs of PD, however, become apparent only after the loss of about 70–80% of dopaminergic neurons (Schapira 1999), and although the diagnosis of PD is entirely clinical, histopathology on autopsy is the only way to definitively confirm a diagnosis. The mean age of onset of PD is typically between 60 and 65 years, and in Europe the prevalence of PD has been estimated to be 1.8% in persons ≥ 65 years of age (de Rijk et al. 2000), with an incidence of approximately 16–19 per 100,000 per year (Twelves et al. 2003). Although age is unequivocally associated with increasing PD risk, the underlying process of PD is distinct from the natural aging process (Goldman and Tanner 1998). PD prevalence is also similar among ethnic groups living in the same location (Morens et al. 1996), but may differ among ethnic groups living in different locations (Schoenberg et al. 1988) Genetic factors can influence the risk of PD, and higher rates of PD have been found in relatives of those with PD (Foltynie et al. 2002). However, twin studies have consistently shown low rates of concordance (5–8%) in monozygotic and dizygotic twins (Foltynie et al. 2002), suggesting that other factors play a part in the etiology of PD. A number of causative factors have been found to induce parkinsonism similar to that of idiopathic PD, including vascular insults to the brain, repeated head trauma, neuroleptic drugs, and manganese toxicity (Adler 1999). In particular, the toxicant 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) resulted in the development of acute parkinsonism, similar to the idiopathic disease in nearly all clinical, pathologic, and biochemical features, in a small group of drug addicts (Langston et al. 1983). It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. This rekindled an interest in the possible role of exogenous toxicants in the development of PD and parkinsonism generally, in particular, compounds that are toxicologically or structurally similar to MPTP, including pesticides such as rotenone and paraquat (Goldman and Tanner 1998). Numerous epidemiologic and toxicologic studies have examined pesticides as a risk factor for PD and parkinsonism and the possible mechanisms by which pesticides may act. Review undertaken on behalf of the U.K. Advisory Committee on Pesticides. In addition, we identified three autopsy studies that examined the levels of various pesticides and their metabolites in the brains of PD cases (Corrigan et al. 1998, 2000; Fleming et al. 1994). Exposure In most studies, a positive association was observed between exposure to herbicides and PD risk. In one study, exposure to herbicides was a significant independent risk factor after adjustment for insecticide and other exposures (Semchuk et al. 1992). Exposure to insecticides is also generally positively associated with PD (Figure 2). Fungicide exposure was not found to be a significant risk factor for PD, nor was exposure to rodenticides (Behari et al. 2001) or acaricides (Hertzman et al. 1994; In two studies, paraquat exposure was shown to be significantly associated with PD (Hertzman et al. 1990; Liou et al. 1997), especially with > 20 years of exposure (Liou et al. 1997). However, other studies have not found a significant association, although PD risk was still elevated (Firestone et al. 2005; Hertzman et al. 1994; Kamel et al. 2001). Other specific groups of pesticides have also shown positive associations with PD, including organochlorines (Figure 2). Three autopsy case–control studies found increased levels of dieldrin and lindane in the brains of deceased PD patients compared with other diseased brains (Corrigan et al. 1998, 2000; Fleming et al. 1994). Positive associations were also seen with exposure to organophosphates and carbamates pesticides (Firestone et al. 2005; Wechsler et al. 1991; The relationship between exposure duration and PD risk was investigated in six case– control studies. Four found a significant association between increasing pesticide exposure duration and PD risk (Chan et al. 1998; Gorell et al. 1998; Liou et al. 1997; Seidler et al. 1996) The remaining two studies showed nonsignificant positive associations with exposure duration (Jiménez-Jiménez et al. 1992; Zayed et al. 1990). These studies suggested that PD risk is increased when the duration of exposure to pesticides exceeds a particular threshold, because associations were often only significant for the longest exposure duration categories (e.g., > 10 or > 20 years) A positive association was also observed with high doses of pesticides compared with low doses (Nelson et al. 2000), although the risk with regular use was seen to be lower compared with occasionaluse (Kuopio et al. 1999). In addition, several studies observed a positive correlation with duration of exposure to, and high doses of, herbicides and insecticides (Nelson et al. 2000; Seidler et al. 1996). Significant increases in PD risk were also associated with a history of occupational use of pesticides between the ages of 26 and 35 years, herbicides between the ages of 26 and 35, 36 and 45, and 46 and 55 years, and insecticides between the ages of 46 and 55 years (Semchuk et al. 1992). In a few of these studies, multivariate analyses were performed to examine the relationship between the various risk factors. Koller et al. (1990) found that wellwater consumption was dependent on rural living, suggesting the risk factors were interrelated. In one study, well-water use was found to be positively and independently associated with PD (Zorzon et al. 2002) Several studies have also found farming to be an independent risk factor, in addition to pesticide exposure (Gorell et al. 1998; Zorzon et al. 2002) Other sources of cases included lists of patients receiving anti-PD drugs, residential care centers, community or support groups, or door-to-door surveys. Sources of controls included the general population, the spouses of cases, electoral rolls, subjects suggested by their cases, and friends and relatives of the cases. Use of hospitals could result in selection bias for both cases and controls if attendance was influenced by factors such as severity of PD (with particularly severe or mild conditions being admitted elsewhere or not attending), geographic location, and social class. The use of neighborhood controls or friends and relatives of cases can result in the exposure prevalence being similar in both cases and controls, resulting in overmatching, driving the risk estimate toward the null. defined a case on the basis of the presence of two or more of the cardinal signs of PD (tremor, rigidity, bradykinesia, and postural instability); some also used additional criteria, including responsiveness to L-dopa therapy and/or a progressive disorder. Other diagnostic criteria used included the Unified Parkinson’s Disease Rating Scale, the Hoehn and Yahr PD Staging Scale, and the UK PD Society Brain Bank Clinical Diagnosis Criteria (Fahn and Elton 1987; Hoehn and Yahr 1998; Hughes et al. 1992a Misdiagnosis is especially common during the early stages of the disease, even among movement disorder specialists (Litvan et al. 1996) The Movement Disorder Society Scientific Issues Committee suggested that this limitation could strongly affect the power of epidemiologic studies and clinical trials (Litvan et al. 2003) to detect a risk, by classifying individuals as cases when they should not be. A few studies found that pesticide exposure was not a significant risk factor after adjustment for confounding variables (Chan et al. 1998; Stern et al. 1991; Taylor et al. 1999; Werneck and Alvarenga 1999). In contrast, pesticide exposure was shown to be a significant risk factor after adjustment in several studies (Butterfield et al. 1993; Gorell et al. 1998; Hertzman et al. 1990; Hubble et al. 1993; Liou et al. 1997; Menegon et al. 1998; Seidler et al. 1996; Semchuk et al. 1992; Zorzon et al. 2002). These studies were not consistent in the variables used to adjust risk, and some did not include risk factors found to be associated with PD and related to pesticide exposure, such as rural living, well-water consumption, and farming as an occupation, which could result in residual confounding. Studies that have investigated these factors in relation to PD have found ORs to be generally of the same order and direction as those for pesticide exposure. Many studies have postulated that these factors and exposure to pesticides are closely linked and interrelated. However, there still remains uncertainty as to the exact nature of the relationship between farming, rural living, and pesticide exposure and their relationship to PD risk. Exposure assessment. Assessment of exposure to pesticides relied upon subjects recalling their lifetime exposures over some previous 20–30 years, leading potentially to differential recall bias. For individuals occupationally exposed to pesticides, the accuracy of their historical self-reported pesticide exposure was high for broad categories of pesticides and commonly used pesticides, but not for specific pesticides (Engel et al. 2001; Hoppin et al. 2002). However, the accuracy of recall for nonoccupational or residential exposure is questionable (Teitelbaum 2002) The questions used to assess pesticide exposure varied considerably between studies and in some reports were not given. A number of studies simply asked “Have you ever been exposed to pesticides?” the assessment of exposure in most studies does not take into account the timing of exposure compared with onset of symptoms, the dose of pesticide, the mechanism of exposure, or the chemical classes of the pesticides. Furthermore, the exposure category pesticides represents many hundreds of chemicals, and these may not be comparable between studies. It could be that exposure to only a few pesticide compounds results in an increased risk of developing PD At present, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure Given the complexity of the many factors and substances to which the populations described in the epidemiologic studies have been exposed, in this section we review experimental studies on relevant pesticides to gain an insight on whether single or groups of pesticides, or related substances, may contribute to the apparent increase in PD seen in these populations. Several factors to be considered when assessing the mechanistic evidence for a role for pesticides in PD development and to identify further candidate substances for consideration in experimental or epidemiologic studies: a) effects on the striatal dopaminergic system (these may include a decrease in dopamine levels and/or an increase in dopamine turnover as a shortterm compensatory mechanism, which would be identified by an increase in metabolites or the enzyme tyrosine hydroxylase); b) effects on the SN (most dopaminergic neurons are present in the basal ganglia, including the SN, and changes in the SN—although not necessarily specific—would be expected to occur with an agent involved in the development of PD); and c) mechanistic effects (for example, on oxidative stress, mitochondrial dysfunction/ complex I inhibition, and α-synuclein levels and aggregation. Rotenone Rotenone is a naturally occurring insecticide and is a well characterized, high-affinity specific inhibitor of complex I (NADH-dehydrogenase). It is extremely hydrophobic and crosses biologic membranes easily. Therefore, unlike MPTP, rotenone does not require a dopamine transporter (DAT) for access to the cytoplasm and therefore is likely to produce systemic inhibition of complex I (Betarbet et al. 2000). Continuous infusion of rats with rotenone reduces specific complex I binding by 75%, at a low free-rotenone concentration in the brain of about 20–30 nmol/L, accompanied by nigrostriatal dopaminergic lesions, suggesting that striatal nerve endings are affected earlier and more severely by rotenone than are nigral cell bodies (Betarbet et al. 2000). Rats with these lesions had cytoplasmic inclusions containing α-synuclein in the nigral neurons, which resembled the pale body precursors to Lewy bodies found in humans with PD. Rotenone-treated animals also developed motor and postural deficits characteristic of PD, the severity of which correlated with the extent of the pathologic lesions, even after cessation of the rotenone treatment. However, Betarbet et al. (2000) also reported that rotenone seems to have little toxicity when administered orally (Sherer TB, Greenamyre JT, unpublished data) Other experiments suggest that dopaminergic synapses in the SN pars compacta and in the nigrastriatal pathway are sensitive to the action of rotenone (Alam and Schmidt 2002). This is in contrast to the findings of Betarbet et al. (2000), who found that changes in the SN were later events. In behavioral tests, the treated animals showed a dose–dependent increase in catalepsy and decrease in locomotion. The authors surprisingly suggested that this (sub)chronic intraperitoneal dosing was comparable with chronic environmental exposure and was thus comparable with a real-life situation. In mice and rat neuron–glial cell cultures, a nontoxic or minimally toxic concentration of rotenone and the inflammatory agent lipopolysaccharide synergistically induced dopaminergic degeneration (Gao et al. 2003). Niehaus and Lange (2003) have suggested that inflammatory factors such as lipopolysaccharide might be an environmental factor in the development of PD. The presence of brain microglia has been implicated in rotenone neurotoxicity, and these cells release reactive oxygen species as well as inflammatory factors (Gao et al. 2002; Liu and Hong 2003). Paraquat. Paraquat is a nonselective contact herbicide with high pulmonary toxicity (Corasaniti et al. 1998). One of the major considerations in relation to the potential neurotoxicity of paraquat is the extent to which it can cross the blood–brain barrier (BBB). Paraquat is a charged molecule, which may not cross the BBB, and it is not metabolized to a species more likely to gain access to the brain (Sanchez-Ramos et al. 1987). Naylor et al. (1995) found that after subcutaneous administration to neonatal, adult, and aging rats, most of the paraquat associated with structures lying outside the BBB (pineal gland and linings of the cerebral ventricles) or without a BBB [anterior portions of olfactory bulb, hypothalamus, and area postrema (Naylor et al. 1995; Widdowson et al. 1996)]. Overall, paraquat did not appear to pose a major neurotoxicologic risk in brain areas with a functional BBB. However, in the only study identified in which paraquat was given orally, neonatal mice dosed on gestation days 10 and 11 showed hypoactivity and reductions in striatal dopamine and dopamine metabolite levels (Fredriksson et al. 1993); this contrasts with the increase in activity and dopaminergic systems associated with PD-like mechanisms. Other groups have reported that paraquat administered by intraperitoneal injection can cross an intact BBB (Corasaniti et al. 1998; Shimizu et al. 2001). Further experiments suggested the involvement of the neutral amino acid transporter in the carriage of paraquat into the brain, followed by transportation into striatal, possibly neuronal, cells, in a Na+-dependent manner (Shimizu et al. 2003). Inhibition of paraquat uptake into rat striatal tissues, including dopaminergic terminals, has also been shown to operate by a specific dopaminetransport inhibitor (Shimizu et al. 2001). Although not directly relevant to human exposure pathways, paraquat has been shown to be neurotoxic after direct injection into areas of the brain (Bagetta et al. 1992; Calò et al. 1990; Corasaniti et al. 1992, 1998; De Gori et al. 1988; Iannone et al. 1988, 1991). Depending on the brain region into which the paraquat was injected, it produced different behavioral patterns, increased locomotor activity, and caused convulsions; these effects were accompanied by neuronal cell death. In general, these studies suggest that paraquat neurotoxicity is not specific to the dopaminergic nigrostriatal system because effects were observed when paraquat was injected into regions of the brain where other neurotransmitter systems are located. Several studies have observed neurotoxicity after systemic administration of paraquat. An increase in dopaminergic neuronal death in the SN pars impacta was observed in treated rats, with no depletion in striatal dopamine but enhanced dopamine synthesis indicated by increased tyrosine hydroxylase activity (McCormack et al. 2002). The authors suggested that the apparent discrepancy between neurodegeneration and a lack of dopamine loss was probably a reflection of compensatory mechanisms by which neurons that survive damage were capable of restoring neurotransmitter tissue levels. When rats were treated intravenously with paraquat, the brains had lower complex I activity and higher levels of lipid peroxides (indicating free radical activity) and a lower level of dopamine in the striatum (Tawara et al. 1996). Mice treated with paraquat showed an up-regulation and aggregation of α-synuclein (Manning-Bog et al. 2002). However, the studies of Woolley et al. (1989) in mice and of Naylor et al. (1995) in rats The major pathologic feature of PD is the profound loss of pigmented neurons, mainly in the pars compacta of the substantia nigra (SN). Associated with this neuronal loss is the presence of large eosinophilic inclusions, called Lewy bodies, within the remaining pigmented neurons, made up of a series of proteins, including neurofilaments, α-synuclein fibrils, ubiquitin, parkin, and proteasomal elements. Combination of paraquat and maneb Maneb [manganese ethylenebisdithiocarbamate (manganese-EBDTC)] is a dithiocarbamate herbicide, and the areas of use of maneb and paraquat have a marked geographic overlap in the United States (Thiruchelvam et al. 2000a). Mice exposed to paraquat or maneb, either alone or in combination, showed a sustained decrease in motor activity only in the combined exposure groups, with increased striatal dopamine and dopamine metabolite levels immediately postinjection, decreasing after 7 days, and reduced levels of tyrosine hydroxylase and DAT in the dorsal striatum (Thiruchelvam et al. 2000a, 2000b). Combined exposure thus potentiated effects that appear to target the nigrostriatal dopaminergic systems. The authors suggested that mixtures of pesticides could play a role in the etiology of PD. In a series of studies on developmental exposure to the combined pesticides, mice had reduced motor activity and striatal dopamine levels (Thiruchelvam et al. 2002). Although the greatest loss of nigrostriatal dopaminergic cells was seen after combined treatment, there was significant loss with all treatments after rechallenge when adult, suggesting that a state of silent toxicity had been unmasked upon adult rechallenge. There was also evidence that prenatal exposure to maneb may lead to alterations of the nigrostriatal dopaminergic system and enhanced susceptibility to adult exposure to paraquat (Sherer et al. 2002). In a further study on mice of different ages using higher doses (Thiruchelvam et al. 2003), reduction in locomotor activity and motor coordination and reduction in dopamine metabolites and turnover were greatest in the oldest mice (18 months of age). The decrease in the number of nigrostriatal dopaminergic neurons was progressive, particularly in the oldest mice given paraquat and maneb in combination. The result demonstrates an enhanced sensitivity of the aging dopamine pathway particularly to paraquat and maneb. Dithiocarbamates. There is some evidence for the neurotoxicity of dithiocarbamates, including studies on the manganese-containing pesticide maneb, alone or in combination with paraquat. Although manganese has been shown to cause PD-like effects in workers at high occupational exposure, it affects the globus pallidus rather than the SN and is also resistant to the beneficial effects of L-dopa. However, neurotoxic effects have been observed in toxicologic studies with the nonmanganese- containing parent compound, EBDTC, from which maneb is derived (McGrew et al. 2000). Cyclodienes. Bloomquist and colleagues have carried out studies examining possible effects of the organochlorine cyclodiene pesticides, in particular, dieldrin and heptachlor, on possible biomarkers of PD. Heptachlor increased the maximal rate of striatal dopamine uptake, which was attributed to induction of the DAT and a compensatory response to elevated synaptic levels of dopamine (Bloomquist et al. 1999; Kirby et al. 2001; Miller et al. 1999). Kirby et al. (2001) suggested that heptachlor and perhaps other organochlorine pesticides exert selective effects on striatal dopaminergic neurons and may play a role in the etiology of PD. There is some evidence that dieldrin may interfere with electron transport and increase the generation of superoxide radicals (Stedeford et al. 2001). In proliferating PC12 cells exposed to dieldrin, there was evidence for increased oxidative stress. In mesencephalic cell cultures (Sanchez-Ramos et al. 1998) and PC12 cells (Kitazawa et al. 2001), there was a rapid release of dopamine and its metabolite, followed by apoptotic cell death. Although the convulsant and proconvulsant actions of endosulfan have been attributed to an antagonistic action on GABA, a dopaminergic involvement has been suggested for its induction of hypermotor activity and circling movement (Ansari et al. 1987; Paul and Balasubramaniam 1997). Administration of endosulfan during gestation and lactation in rats up to 2–3 weeks of age produced a significant decrease in the affinity and maximum numbers of striatal dopaminergic receptors without affecting other receptor profiles, suggesting that dopaminergic receptors are unusually sensitive to the action of endosulfan (Seth et al. 1986). Pyrethroids. During investigations into the possible involvement of the pyrethroid permethrin and the organophosphate chlorpyrifos on the etiology of PD and Gulf War illness, mice treated with permethrin showed increased dopamine uptake at low doses (e.g., 134% at 1.5 mg/kg), whereas at higher doses dopamine uptake was depressed [e.g., 50% at 25 mg/kg (Karen et al. 2001)]. Reduced mitochondrial function was observed in in vivo synaptosome preparations, and although striatal dopamine levels were not decreased, there was an increased dopamine turnover and decreased motor activity. Although frank parkinsonism was not observed, dopaminergic neurotransmission was affected by exposure to permethrin. Mice treated with deltamethrin showed a 70% increase in maximal dopamine uptake in ex vivo synaptosomes suggestive of an up-regulation in DAT expression (Kirby et al. 1999). Unlike MPTP, deltamethrin did not decrease dopamine, although there was some evidence of increased turnover. When the pyrethroid insecticide fenvalerate was given orally to rats, there was a pronounced, but not dose-related, inhibition of dopamine and its metabolites and decreased dopamine binding in several brain regions, including the corpus striatum (Husain et al. 1991). In another study, fenvalerate or cypermethrin given during gestation and lactation to pregnant and nursing dams (Malaviya et al. 1993) showed a significant increase in dopamine and muscarinic receptors of striatal membranes in the pups. Malaviya et al. (1993) suggested that the findings demonstrated disturbance of both the dopaminergic and cholinergic pathways. Other pesticides. Although there is evidence for neurotoxic effects of some other pesticides, all the mechanistic systems seen in PD are not consistently effected Interaction of pesticides with α-synuclein. The formation of Lewy bodies may be integral to the cause of the disease rather than being an accompanying effect. Studies in vitro have suggested that a number of pesticides (alone or in combination with certain metals) may induce a conformational change in α-synuclein and accelerate the formation of α-synuclein fibrils (Uversky et al. 2001, 2002). Pesticides known to induce this effect are hydrophobic and include rotenone, DDT, 2,4-dichlorophenoxyacetic acid, dieldrin, diethyldithiocarbamate, paraquat, maneb, trifluralin, parathion, and imidazoldinethione; those having no significant effect include iprodione, glyphosate, methomyl, thiuram, mevinphos, carbaryl, alachlor, thiobencarb, and also MPP+ Conclusions The epidemiologic studies suggest a relatively consistent association between exposure to pesticides and an increased risk of developing PD, despite differences in study design, case ascertainment and definition, control selection, and pesticide exposure assessment. Particular classes of pesticides found to be associated with PD include herbicides, particularly paraquat, and insecticides; evidence from case reports and case–control studies for an association with exposure to fungicides alone is equivocal. Duration of exposure has also been found to be a risk factor, with those exposed to pesticides for > 10 or 20 years being associated with a increased risk of developing PD. However, in addition to pesticides, several other risk factors are associated with an increased risk of developing PD, including rural living, well-water consumption, and farming. We found no studies that have been able to determine whether these risk factors are independent risk factors or correlated with pesticide exposure. The toxicologic evidence suggests that, with certain routes of administration, rotenone and paraquat may have neurotoxic actions that could potentially play a role in the development of PD. These include effects on dopaminergic systems in the SN, and α-synuclein aggregation. There is also some evidence that the mechanisms of neurotoxicity associated with exposure to pyrethroids are those that would be suggestive of a role in the development of PD and that dithiocarbamates may interact with other xenobiotic agents to increase neurotoxicity. Studies on various other pesticides suggest that, while they have neurotoxic actions, they do not act on systems in the brain of relevance to PD. However, many of these studies reviewed were designed to elicit acute toxicity in order to study the mechanisms of action. We identified no study that administered pesticides at levels comparable with those encountered by pesticides users, nor were the routes of administration those that would be experienced by pesticide users (i.e., oral, inhalation, or dermal). As a result, it is difficult to interpret the relevance of such studies to humans, although the difficulty in modeling a disease such as PD is acknowledged. Of potential toxicologic importance are the few studies that reported dopaminergic neurotoxicity after combined low-level exposure to multiple environmental neurotoxicants, including paraquat and maneb, the combined effects of pesticides and metals on α-synuclein, and rotenone and lipopolysaccharide (which may be present due to inflammation or infection). For example, although PD is a disease of aging, the studies of Thiruchelvam et al. (2003) on the developmental exposure to maneb and paraquat indicate that early exposure may lead to PD-like toxic effects upon adult rechallenge. Such studies suggest that exposure to multiple low-level environmental neurotoxicants, perhaps at an early age, may be an etiologic factor in the development of PD. Recent toxicologic studies have suggested that multiple genetic and environmental factors could be involved in the etiology of PD. Studies with transgenic mice suggest that the genetic background and expression of the α-synuclein gene may have a role to play in neurodegeneration of the SN (Thiruchelvam et al. 2004) and may also lead to increased vulnerability to the neurotoxic effects of the pesticides maneb and paraquat. There is evidence that developmental exposure to pesticides may have an increased neurodegenerative effect as well as making the SN more susceptible to subsequent adult exposure to pesticides, and that combined exposure to pesticides such as maneb and paraquat has a greater neurotoxic effect than either pesticide alone (Cory- Slechta et al. 2005). Other recent studies also suggest some interaction between the neurodegenerative effects of pesticides and inflammatory proteins produced by microglia in the SN (Gao et al. 2003, Liu and Hong 2003). These genetic and environmental factors could be considered in future epidemiologic studies of this multifactorial disease. Most of the epidemiologic studies that we reviewed used a case–control design with relatively small numbers of cases. Pesticide exposure history was, by necessity, collected retrospectively, generally using questionnaires. Information and recall bias are inherent limitations of this type of design. The exposure assessments were also limited in their collection of information on the types of pesticides, specific chemicals, and levels of exposure experienced. Of all the studies we reviewed, the two most reliable were large case–control studies that attempted to investigate exposure to different groups of pesticides (Semchuk et al. 1992; Seidler et al. 1996). Despite these considerations, it seems unlikely that the relatively consistent association between PD and reported exposure to pesticides observed in the epidemiology studies could be explained wholly by a combination of chance, bias and confounding, and selective reporting. The toxicologic literature indicates several areas that would benefit from further research, including the effect of exposure at different ages, early exposure and developmental changes, the role of inflammatory disease, and the potential for gene–environment interactions. Epidemiologic studies of an appropriate design and size, that collect detailed information on exposure to specific pesticides and other chemicals, including early life exposures, would be required to investigate these issues. Studies to date have not had sufficient power to disentangle the relative importance of intercorrelated risk factors and to evaluate each risk with any confidence. We are aware of several ongoing studies that are addressing some of these areas of concern. In conclusion, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists, but it is not sufficient to conclude that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined exposure to pesticides and other exogenous toxicants. In addition, the multifactorial etiology of PD hampers unequivocally establishing the role of any individual contributory causal factor. I believe so, but am not sure....

ANTIEMETICS are a large class of dugs whos' main function is to prevent or help fight nausea and vomiting. Examples: DRAMAMINE, ANZEMET, MARINOL, KYTRIL, BONINE, REGLAN, ZOFRAN, COMPAZINE, and a few more. <<>> The answer above is absolutely correct :), but I just wanted to add one more - which is probably the most prescribed - Phenergan (promethazine). Anti-emetics can be further classified for the type of n/v being treated. For example, Bonine (meclizine) and Dramamine (dimenhydrinate) contain anti-histamines and can be purchased over the counter. These types of drugs are best suited for motion sickness. Zofran (ondansetron) is a prescription drug generally used for chemotherapy related nausea and sometimes morning sickness.

Parkinson's disease is an illness that affects nerve cells in the brain, especially dopamine-producing neurons. When dopamine levels decrease, it causes abnormal brain activity, leading to impaired movement and other symptoms of Parkinson's disease.

Its causes are unknown but factors that can affect this disease are

• Genes: Researchers have found that some people with many family members affected by Parkinson's disease have mutations in the LRRK2 gene. The presence of these gene variations can increase a person's risk for Parkinson's disease but only slightly. Therefore, genetic testing cannot predict who will or will not develop Parkinson's disease.

• Environment: Being exposed to certain toxins or environmental factors, especially during a vulnerable time such as childhood, may cause the development of Parkinson's disease. However, this is considered to be a minor factor in this disease.

Since drugs are addicting it is not hard to become dependent on drugs. Drug dependence may lead to abuse as the addiction may lead to an overuse and complete reliance on drugs that may not be readily available to you. This may also lead to the fabrication of drugs using household materials or household cleansers which is in itself an abuse of potentially addictive substances. Abuse of prescription medicine or even non-prescription medicine can also be seen as abusive to drug use and is therefore drug abuse.

During physical exertion in extreme sports like whitewater kayaking or skydiving, the brain releases a surge of dopamine. The exact amount can vary depending on the individual and the intensity of the activity, but it is typically higher than during normal, everyday activities. Dopamine is a neurotransmitter associated with pleasure and reward, and its release contributes to the thrill and excitement experienced during extreme sports.

Norepinephrine is a neurotransmitter and hormone that plays a crucial role in the body's fight-or-flight response. It helps increase heart rate, constrict blood vessels, and increase blood sugar levels to prepare the body for action. Norepinephrine is also involved in regulating mood, attention, and focus.

Both my mother and step father work in psychiatry, they know of my exorbitant marijuana use and have advised me that it will result in your serotonin levels being completely effed for about 2 weeks after using. This will result in possible depression, anxiety etc.

If you are planning on doing this you should definitely take some precautions especially if its your first time smoking weed. Zoloft greatly increases the high. My first time smoking marijuana i was on Zoloft and it was honestly an extremely frightening experience. So make sure you are with people you completely trust as you may need someone to talk you down. Your heart will probably beat extremely fast to the point where you will think your having a heart attack this apparently happens to people not on Zoloft so its nothing to worry about unless it becomes too accelerated. it may be a good idea to read up on others experiences on erowid in the cannabis or sertraline combinations sections.

http://www.erowid.org/experiences/exp.cgi?A=Search&S1=88&S2=1&S3=-1&C1=-1&S4=-1&GenderSelect=-1&Context=-1&DoseMethodID=-1&Title=&AuthorSearch=&A1=-1&Lang=&Group=-1&Str=&Intensity=&I2=

These may seem frightening but remember that these are but a few experiences and its very subjective, more unstable people may find the experience of combining these two terrible while more stable people may find it bearable or even nice.

My personal experience with this combination has been shaky at best. I really love marijuana but in combination with Zoloft it can take a scary turn. you can have the greatest time of your life or the most unbearable experience that will stick with you. I've found it mostly depends on:

A) your mood going into the experience
B) your environment
C) the people you surround yourself with
D) Your own insecurities

If any of these are negative it can leave you feeling terrible. I would suggest, if you must do it, be in a dimly lit room doing something that you like (video games etc) listening to nice music and with at least one person you can really count on. You WILL become quite paranoid but I've found it helps if you just tell yourself you don't care. Most paranoia come from you thinking you are saying something weird or thinking that someone knows you are high. just try not to care about these and you will probably have an alright trip.

I've had people who know i take both tell me they tried it and they cant believe i do them together. So be cautious the experience may not be for you.

Just a warning marijuana while on Zoloft is bad for you, but completely stay away from drugs like ecstasy or drugs that work like ecstasy (cocaine etc) these will cause your serotonin receptors to burst and could seriously fry your brain.

Good luck!