0
NMDA receptors are located in the brain, specifically on the surface of neurons. They play a crucial role in controlling synaptic plasticity and memory formation. Additionally, NMDA receptors are involved in regulating synaptic transmission and are important for learning and memory processes.
2 answers
Opioid Tolerance has been shown to be regulated by NMDA receptors. When somebody takes an opioid glutamate is released in the brain and binds to the NMDA receptors causing an increase in opioid tolerance. There have been several studies that show that taking and opioid with a NMDA antagonist (a drug that blocks NMDA receptors, effectively "turning them off") prevents the development of opioid tolerance. An accessible NMDA antagonist is DXM or Dextromethorphan which is found in many different cold medicine preparations. Be careful if taking a multiple ingredient cold medicine as many contain acetaminophin and other ingredients that can be dangerous if taken in high doses. Hope this helps, I included a link to a study if your interested.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2045628
1 answer
The main role of the NMDA receptor in the body is in ensuring neural plasticity. Further research is on-going to further refine understanding of this receptor, and this conclusion may change in future as more studies may find further roles for this receptor.
1 answer
The NMDA channel allows calcium and sodium ions to enter the nerve cell in response to glutamate binding. These ions play key roles in neuronal excitability and synaptic plasticity.
2 answers
Yes. This is mediated by ciprofloxacin's antagonism of the GABA(a) receptor, leading to NMDA receptor over-excitation and tinnitus.
1 answer
Ionotropic receptors are ligand-gated or transmitter gated ion channels. The binding of a neurotransmitter or other ligand to a particular site on a domain of a protein in the receptor causes a conformational change in the protein subunits. This allows a certain ion to pass through, poteitally potassium, sodium or chloride. There are two types of ionotropic receptors, non-NMDA and NMDA. Both are ligand gated receptors, however the NMDA is also voltage gated.
2 answers
Camille Buchholz Carroll has written:
'The role of the striatal NMDA receptor complex in the mediation of Parkinsonism'
1 answer
Angel Dust is the street term for Phencyclidine (PCP). PCP is a powerful dissociative anesthetic and hallucinogen which antagonizes NMDA receptors.
1 answer
PHENCYCLIDINE (PCP) blocks the activity of NMDA receptor for glutomate (amino acids in your body) it causes neurotoxic and hallucinogenic reactions.
1 answer
Ketamine is in a group of medications known as N-methyl d-aspartate (NMDA) receptor antagonists, and is legally used as an anesthetic for humans and animals.
1 answer
Ketamine is an antagonist at the N-methyl-D-aspartate (NMDA) receptor in the brain. It blocks the action of glutamate, an excitatory neurotransmitter, leading to its dissociative and anesthetic effects.
1 answer
They affect GABA, NMDA, opiod, adrenergic, histamine and acetylcholine receptors in your brain. Depressants can effect other parts of your brain aswell, these are just the parts of it that actually cause the depressant effects of the drugs. Alcohol for example effects the GABA, NMDA, acetylcholine and serotonin receptors but it's effect on the serotonin receptor doesn't cause any depressant effect but rather adds to the euphoric effects of alcohol.
2 answers
Jeffrey R. Gingrich has written:
'Unique domain anchoring of Src to synaptic NMDA receptors via the mitochondrial protein NADH dehydrogenase subunit 2'
1 answer
There are pain receptors in the brain. In fact if the brain didn't get and give the message to you that you were in pain it wouldn't register. The reason why we feel pain is to alert us that something is wrong and needs to be tended to.
A nociceptor is a sensory receptor that responds to potentially damaging stimuli by sending nerve signals to the spinal cord and brain. This causes the perception of pain.
There are also proteins in your brain called NMDA receptors which allow your neurons to communicate with each other. The neurons talk to each other which in turn reaches the NMDA receptors. The NMDA listens to the neurons and if sufficiently excited ions are expelled from a channel of receptors. Calcium ions then flow through the channel into the listening neuron at the synapse (pathway between the neurons) causing the pathway to be strengthened and giving you a loud signal (hot stove = pain!).
1 answer
Cholinesterase inhibitors and NMDA receptor antagonist for mainly cognition, neuroleptics for aggression and agitation, and antidepressant. Behavioral therapy is effective for programmatic behaviors such as wandering, hoarding, hiding objects, or repetitive questioning.
1 answer
Yes it reduces the chance of action potenctial to happen.
The NMDA receptor is normally block be a Mg molecule. To unblock it the neuron must "fire" (generate action potencial).
1 answer
PCP primarily acts as an antagonist of NMDA, which is a glutamate receptor. It also affects dopamine, norepinephrine, serotonin, acetylcholine, and GABA.
2 answers
Arylcyclohexylamines are a class of psychoactive substances that include drugs like ketamine, PCP, and DXM. These compounds are known for their dissociative effects, altering perception and creating a sense of detachment from the environment. They act mainly on the NMDA receptor in the brain.
1 answer
The main role of the NMDA receptor in the body is in ensuring neural plasticity. Further research is on-going to further refine understanding of this receptor, and this conclusion may change in future as more studies may find further roles for this receptor.
1 answer
Dxm is a NMDA receptor antagonist, classifing it a disossiative drug. DXM causes Olney's Lesions in lab animals but there has never been a recorded case in humans. Whether this is a case of it not happening or just not being found yet it unknown.
1 answer
Long-term potentiation (LTP) primarily depends on the neurotransmitter glutamate, specifically its activation of NMDA receptors to initiate the signaling cascade that underlies the strengthening of synaptic connections. Dopamine and other neurotransmitters also play modulatory roles in LTP.
2 answers
Depending on the hallucinogen, it may be either an agonist or an antagonist at certain receptors. Classic psychedelics such as LSD and psilocybin are 5-HT2A receptor agonists, whereas dissociatives (PCP, DXM, ketamine, etc.) are NMDA receptor antagonists. Deliriants, such as atropine and scopolamine, are muscarinic antagonists.
2 answers
Nitrous oxide works by inhibiting the activity of certain enzymes (such as NMDA receptors) in the brain, resulting in a decrease in pain perception and inducing a sense of euphoria. It also has a sedative effect and can cause partial loss of consciousness when used at high concentrations.
2 answers
It is used as a dissociative anaesthetic in surgery.
By this, it doesn't actually stop pain, so much as it "shifts" consciousness, allowing for a sort of disconnected state.
The same is said of out-of-body experiences, which are controlled by the same neurochemical mechanism.
It is able to do this by blocking (antagonizing) NMDA (N-methyl-D-aspartate) receptors used in glutaminergic neurotransmission.
1 answer
It is used as a dissociative anaesthetic in surgery.
By this, it doesn't actually stop pain, so much as it "shifts" consciousness, allowing for a sort of disconnected state.
The same is said of out-of-body experiences, which are controlled by the same neurochemical mechanism.
It is able to do this by blocking (antagonizing) NMDA (N-methyl-D-aspartate) receptors used in glutaminergic neurotransmission.
1 answer
Acetylcholinesterase inhibitors help to prevent the breakdown of acetylcholine, a neurotransmitter which functions suboptimally in dementia of the Alzheimer's type (Aricept and others). Also, NMDA receptor antagonists help to promote excitatory neurotransmitter function (Namenda).
2 answers
Nootropics or "smart drugs" improve the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors which are implicated in memory processes. Furthermore, they have an effect on NMDA glutamate receptors which are involved with learning and memory processes. Nootropics influence neuronal and vascular functions and increase cognitive function, while at the same time providing a natural source of energy to keep you alert and motivated.
1 answer
There has been a lot of research into the use of non-competitive NMDA antagonists to control tolerance to a variety of substances. Amphetamine tolerance is one of them, but the more promising area was in opioid tolerance, actually. There are basically two types of recreational stimulants (and stimulants being used for ADD), they are dopamine reuptake inhibitors (DARI) and dopamine releasers (DRE). These are ligands that bind to two different transporter proteins, DAT for DARIs and VMAT2 for DREs. Amphetamine is a releaser primarily (it's not a DAT ligand or has low affinity, but it does slow reuptake through a secondary mechanism). Amphetamine tolerance seems to be more responsive to NMDA type drugs, which memantine is. Memantine, however can have some nasty side effects. Ketamine, Dextromethorphan and Magnesium are all also NMDA antagonists that are effective in controlling tolerance. Dextromethorphan can be found in many OTC medicines, but use Dextromethorphan-ONLY containing products like the Robatussin Gel Caps (read the label carefully!). Standard dosage for this purpose is usually about 90 to 150mg. You may be a little sleepy so use it only at night. Ketamine is available on the blackmarket, and is extremely safe when taken without other drugs (besides your amphetamine) and you go to sleep or at least try to. Magnesium is available in health food stores, but I really can't suggest a dose, I'm not very familiar.
1 answer
Zoletil is a sedative drug that works by blocking receptors in the brain to depress the central nervous system. This results in decreased activity in the brain, leading to relaxation, sedation, and reduced awareness. It is often used in veterinary medicine for anesthesia and sedation in animals.
2 answers
The primary mechanism by which alcohol affects brain function is via its interaction with a class of inhibitory receptors, called 'GABA receptors' (GABA stands for Gamma-AminoBuytric Acid, which is a type of inhibitory neurotransmitter). Normally when GABA binds to its receptor, the neuron's activity is reduced. Since alcohol enhances the way GABA works at this receptor, the net effect at the level of a single cell is an increase in inhibition.
In addition, ethanol (alcohol) antagonizes (blocks) NMDA receptors. NMDA is N-methyl-D-aspartate and is a receptor type that both NMDA and glutamate bind with, allowing for short-term memory to be consolidated as long-term memory. As such, excessive alcohol consumption can induce a "blackout" state, whereby a person has no memory of events while intoxicated.
In general, alcohol reduces activity in the neocortex (responsible for higher-level thinking) and the cerebellum (responsible for coordination, posture, and fine movement). Higher concentrations of alcohol affect more of these areas in greater degrees. And, with extreme intoxication, it will affect the lower brain areas responsible for consciousness, and can even lead to a coma or death.
it slows down your brain. you don't think as fast. some connections are even disabled which means your not thinking about certain things as much if at all. this allows you to feel more relaxed. too much alcohol slows down your brains so much that it impairs your vision and memory and how you process information. this is why drunk driving is dangerous. your brain cannot process or calculate driving as well as when your not drunk.
3 answers
Magnesium can potentially enhance the effects of hydromorphone and increase the risk of side effects like drowsiness, dizziness, and difficulty concentrating. It is important to speak with a healthcare provider before combining these medications to ensure safe and appropriate use.
2 answers
Serine is found in several configurations: L-serine, beta-Hydroxyalanine, (S)-Serine, 56-45-1, L-ser, (S)-2-Amino-3-hydroxypropanoic acid and D-ser.
It is a non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE.
HO2CCH(NH2)CH2OH.
(2S)-2-amino-3-hydroxypropanoic acid
D-Serine, synthesized in the brain by serine racemase from L-serine (its enantiomer), serves as a neuromodulator by coactivating NMDA receptors, making them able to open if they then also bind glutamate. D-serine is a potent agonist at the glycine site of the NMDA-type glutamate receptor.
D-serine was only thought to exist in bacteria until relatively recently; it was the second D amino acid discovered to naturally exist in humans, present as a signaling molecule in the brain, soon after the discovery of D-aspartate.
D-Serine is being studied in rodents as a potential treatment for schizophrenia and L-serine is in FDA-approved human clinical trials as a possible treatment for ALS
1 answer
No lamictal doesn't cause sexual side effects. It's probably your underlying condition of bipolar disorder or depression itself. It doesn't affect serotonin like the SSRI antidepressants which cause sexual disfunction instead it works through and independent mode of action acting as an antagonist at the NMDA receptor.
3 answers
Ketamine and Cocaine are both powerful drugs with medical and recreational uses. On the street both drugs are usually seen as a white crystalline powder and both can be snorted. Despite these similarities in appearance and method of ingestion the two drugs are very different in both effect and in they way they act on the brain. Ketamine is a dissociative anesthetic pharmaceutical used legally to cause sedation and anesthesia (to knock people out before surgery). It is used illegally as a hallucinogen. Ketamine is not a typical anesthetic, it can cause more than sedation. At sub-anesthetic doses it causes hallucinations and sometimes out of body experiences (a "K-Hole") which can be euphoric for some and frightening for others or even the same person at different times. Ketamine is an NMDA receptor antagonist (it binds to NMDA receptors in the brain). Ketamine is in the same family of drugs as Dextromethorphan (DXM, Robitussin) and Phencyclidine (PCP, Angel Dust).
Cocaine is a powerful stimulant drug found in the leaves of the Coca plant. It is extracted from these leaves and purified many times, however it is often mixed with other drugs such as Lidocaine or Procaine (these numb the skin like Cocaine but cause no stimulation) in order for dealers to make larger profits. Cocaine is a Tropane alkaloid and is purely a stimulant with local anesthetic effects, it provides the user with lots of energy and will numb any skin it touches. Cocaine increases levels of Dopamine (the "reward/pleasure chemical"), Serotonin and Norepinephrine (Noradrenaline) in several brain regions. Cocaine releases more Norepinephrine than Dopamine and more Dopamine than Serotonin. Cocaine, unlike Ketamine causes no hallucinations unless it is used habitually, and those hallucinations are from psychosis. Cocaine increases heart rate and blood pressure, it can cause short lasting euphoria or anxiety, increase talkativeness, ego inflation and increased sexuality.
1 answer
Prior to the National Minimum Drinking Age Act of 1984, individual U.S. states determined at what age people were allowed to drink. The NMDA legislation required all states to raise their minimum purchase and public possession of alcohol age to 21; however, the Act did not specifically set a legal age for drinking.
Minors (those under the age of 21) are permitted to drink under special circumstances, such as when accompanied by a parent or spouse over the age of 21, or when prescribed for medical purposes by a licensed physician.
3 answers
Music therapy has been shown to be effective in treating the depression, agitation, wandering, feelings of isolation, and memory loss associated with Alzheimer's. Other treatments include nutritional supplements, antidepressants, cholinesterase inhibitors, and NMDA receptor antagonists. Psychosocial interventions are of limited value, but can help incontinence issues, and antipsychotics are sometimes given to help deal with aggression or psychosis that sometimes accompany Alzheimer's. Cognitive retraining can have some value. A feeding tube may be given when the condition progresses to where they cannot properly or safely swallow. There are also workarounds such as labeling objects to remind the patients of their proper use.
There are also experimental therapies on the horizon such as an Alzheimer's vaccine and compounds to help prevent or reduce the amyloid plaques in the brain. They are even experimenting with antivirals since herpes simplex is sometimes found in the amyloid lesions. Methylene blue is also being studied, and in vitro studies suggest that it can help Alzheimer's and Parkinson's Disease.
1 answer
It depends on which substance is taken, different drugs have different modes of action and different target areas in the brain. Stimulants for example, work on the neurotransmitter Dopamine, either through releasing more Dopamine into the synapses (the small gaps between the ends of each "string" of nerve fiber) or the re-uptake of Dopamine thus increasing the effects of the Dopamine already present in the synapses.
Most other drugs work in similar ways but by targeting other neurotransmitters. The drugs have a molecular structure that is very similar but slightly different to that of the neurotransmitter it targets, and because of this it fits on for example the Dopamine receptors (receptors are "keyholes" in which only a specific type of "key" fits to activate it, namely the neurotransmitter it is designed for) in the nerves thus mimicking Dopamine in it's effects. The same goes for most other types of drugs, such as Opioids which target the mu and kappa opioid receptors, most Hallucinogens which target the 5HT serotonin receptors, most Dissociatives which target the NMDA receptors and most Depressants such as Alcohol and tranquilizers which target the GABA-A receptors and it's sub-receptors.
1 answer
Acetylcholine is the primary neurotransmitter that is used throughout the cortex and the hippocampus to modulate attention and to consolidate short-term memory into long-term memory.
Dopamine and norepinephrine are used in the limbic system and the prefrontal cortex to drive the basal brain functions associated with the reward (mesolimbic) circuit. They give us the perception of relative pleasure vs relative pain, and steer our executive functions toward certain activities. As such, they are important in maintaining focus. This is why stimulant medications (such as Adderall and Ritalin) work well...they increase levels of dopamine in the brain.
Glutamic acid (glutamate) is also critical in learning and memory. It binds to AMPA and NMDA receptors to encode long-term memory.
In addition to this, there are other regulatory substances, such as integrins, BDNF (brain-derived neurotrophic factor), and NGF (nerve growth factor) that allow for neural plasticity, shaping and steering the migration of neurons so that they can make interconnections that form the basis of memory. BDNF also has an impact on mood as well, and is said to be one of the underlying bases behind depression.
1 answer
A smart drug, also known as a nootropic, is a substance that aims to enhance cognitive function, memory, creativity, or motivation. These substances can include prescription medications, over-the-counter supplements, or natural compounds, but their effects and safety can vary widely. It's important to consult with a healthcare professional before using any smart drug to ensure it is safe and appropriate for you.
2 answers
It depends on which substance is taken, different drugs have different modes of action and different target areas in the brain. Stimulants for example, work on the neurotransmitter Dopamine, either through releasing more Dopamine into the synapses (the small gaps between the ends of each "string" of nerve fiber) or the re-uptake of Dopamine thus increasing the effects of the Dopamine already present in the synapses.
Most other drugs work in similar ways but by targeting other neurotransmitters. The drugs have a molecular structure that is very similar but slightly different to that of the neurotransmitter it targets, and because of this it fits on for example the Dopamine receptors (receptors are "keyholes" in which only a specific type of "key" fits to activate it, namely the neurotransmitter it is designed for) in the nerves thus mimicking Dopamine in it's effects. The same goes for most other types of drugs, such as Opioids which target the mu and kappa opioid receptors, most Hallucinogens which target the 5HT serotonin receptors, most Dissociatives which target the NMDA receptors and most Depressants such as Alcohol and tranquilizers which target the GABA-A receptors and it's sub-receptors.
1 answer
Currently (as of fall 2008), there are 4 drugs specifically approved for the treatment of Alzheimer's disease. Three of these drugs belong to a class called acetylcholinesterase inhibitors. They inhibit the activity of acetylcholinesterase, which is an enzyme that breaks down acetylcholine, a neurotransmitter that, in the brain, is important to learning and memory. In Alzheimer's Disease, neurons in the brain make acetylcholine die, so these drugs help to boost the remaining levels of acetylcholine. These 3 drugs are: Aricept, Razadyne, and Exelon. They all work in the same way, but may differ somewhat in terms of tolerability and dosing. Razadyne and Exelon are indicated for use in patients with mild to moderate AD. Aricept is approved for use in patients with mild, moderate, and severe disease. There is 1 other type of drug - Namenda - which acts in a different way. This drug is a NMDA receptor agonist. This drug activates NMDA receptors, causing excitation of neurons; it is not known exactly why this drug helps patients with AD. Perhaps it helps whatever neurons remain in the brain to better communicate with one another. This drug is approved for use only in patients with moderate to severe disease. It is often used in combination with one of the acetylcholinesterase inhibitors. The nice thing about this drug is that it seems very well tolerated, with few side effects. One important thing to understand about all of these drugs - they do not cure or stop the disease. Instead, they all delay or slow symptom progression. In other words, they buy patients and their families precious time. For instance, let's say that someone who has Alzheimer's Disease chooses not take one of these medications. Within 1 year, this person may show losses in his or her ability to do everyday things, like how to fry an egg for breakfast, or remember the names of all his or her grandchildren. By contrast, someone taking one of these meds may take 2 years to show the same losses. So, while it may be disappointing that even with medication the disease progresses, it's important to keep in mind the value of maintaining basic functions over time. For many patients, it can mean the difference between nursing home placement versus living with a family member or in assisted care.
1 answer
- acetylcholine - stimulates motility (smooth muscle), induces long-term potentiation (stores long term memory) in the hippocampus, induces muscle contraction (skeletal muscle); main parasympathetic nervous system neurotransmitter (relaxation NT); broken down by acetylcholinesterase (can build up via acetylcholinesterase inhibitors - such as piracetam, aniracetam...and, in extreme cases, nerve gases, such as sarin, toman, VX, etc.)
- GABA - inhibitory neurotransmitter that reduces muscle tension and anxiety; function enhanced by ethanol, benzodiazepines, etc.
- glycine - inhibitory peptide NT; reduces muscle tension; is responsible for sleep paralysis; blocked by strychnine
- dopamine - monoamine, catecholamine NT; stimulates mesolimbic reward circuit; used to guide goal-oriented behavior; inhibits and regulates motor control (movement); aid memory recall; is deficient in attention deficit disorders; triggered by most stimulants, cocaine, methylphenidate, etc.
- norepinephrine - monoamine, catecholamine NT; induces fight-or-flight (sympathetic nervous system); increases aggression; aids memory storage; overactive in PTSD; triggered by most stimulants
- epinephrine - similar to norepineprhine in structure and effects...mostly peripheral effects
- anandamide - associated with cannabinoid-like activity in hippocampus; relaxation NT
- serotonin - monoamine, indoleamine NT; counters norepinephrine to reduce aggressive tendencies; counters depression; enhances mood; induces bonding and group cooperation behaviors (civility); triggers somnolence (sleepiness); target of most antidepressants
- glutamine - excitatory peptide NT; NMDA and AMPA receptors; strongly linked to memory storage; is overactive in cases of oxygen deprivation, and induces brain cell death; blocked by NMDA antagonists (such as ketamine and phencyclidine)
- histamine - formed from histidine; used in mast cells to stimulate inflammation and allergic response (H1 receptors)...blocked by antihistamines; H2 receptors in stomach induce gastric secretion for digestion (blocked by H2 antagonists, such as Prilosec, Zantac, etc.); induces vasodilation and brochoconstriction
- oxytocin - induces uterine contraction, lactation, and induces bonding behavior, particularly in women
- enkephalins and endorphins - typically peptide-based substances that act like opiates to block pain at specific enkephalin and endorphin receptors through the brain and body
-
1 answer
Heroin (diacetyl-morphine) by itself has very little effect on receptors in the brain. It's main physiological effects are attributed to the conversion of heroin by the body to its metabolites morphine and/or 6-monoacetylmorphine (depending upon the route of administration of heroin). But for all intents and purposes, this is a just a pharmacological technicality, as most drugs (such as codeine) are not very active in their own right and depend upon metabolism by the liver or other organs to produce the specific effects of the drug.
Heroin is an opioidergic drug and thus affects endogenous opioid receptors, acting as an agonist (meaning it plugs into and activates these receptors). It has the highest affinity for the μ-opioid (or "mu-opioid") sub receptor. This specific opioid-receptor is mainly responsible for providing all the classical narcotic effects of most opiate/opioid painkillers, including: pain relief, relaxation of smooth muscle (in the gut), euphoria, and central nervous system depression (which causes reduction in anxiety and hypertension).
Like most other opiates, heroin also binds to two other opioid receptors as an agonist. First, it has moderate affinity for the δ- (or "delta-") opioid receptor. The physiological effects of δ opioid receptor agonists is not as fully understood as the other types; but it is thought to play a role in dependence and tolerance; while also providing similar effects to μ-opioid receptors agonists, primarily pain relief and central nervous system depression.
Finally, heroin has some-but very low-affinity for the κ-opioid (or "kappa-opioid") receptor. The effects of κ-opioidergic drugs are extremely different than μ- & δ- opioid agonists. Effects include hallucinations, dissociation, delirium, and anesthesia. Most of the effects associated with the μ-opioid receptor do not occur with kappa agonists, including: euphoria, CNS depression, and relaxation of the smooth-muscle in the gut. Opposite to heroin, a substance that strongly binds to κ-opioid receptors, with very little affinity for μ- & δ- receptors, is salvinorin a, the active chemical in Salvia. In the 1970s, κ-opioid agonist drugs were investigated as atypical anesthetics, but were quickly abandoned due to their severely adverse, unpleasant, and hallucinogenic effects. However, heroin's affinity for this opioid receptor is minimal, even at high doses, compared to other opiates such as meperidine, which have far less abuse potential because of kappa-opioid agonist activity at higher doses.
Additionally:
All drugs that act as μ-opioid agonists, including endogenous endorphins, similarly indirectly impact dopamine and serotonin and induce antidepressant effects. Furthermore, heroin like nearly every other opiate, induces a histamine reaction (it is not known if this is due to an indirect or direct effect at the H1, or histamine, receptors). This can create some-allergic reactions like itchiness. Although other typical allergic-effects like watering-eyes are usually counteracted by μ-opioid agonist effects, which induce dryness in mucus membranes (such as in the mouth and eyes).
Note:
Unlike other opiates & opioids, heroin has not yet been shown to have any known affinity for other non-opioidergic systems in the brain, such as acting as an antagonist (i.e., a "blocking" agent) at NMDA receptors as seen with methadone (NMDA antagonists reduce glutamate levels and decrease anxiety and in higher doses can cause anesthesia, Ketamine is a potent NMDA antagonist). Heroin also has not been demonstrated to act at nociceptin receptors, like the synthetic-opiate buprenorphine. Nociceptin is a opioid-class receptor, but has opposite physiological effects, acting as an anti-analgesic; however, its overall impact upon opiate pharmacology is not fully understood.
3 answers
PCP is a very powerful high, and from personal experiences the high can be very different according too how much you have smoked. The first few hits make you feel very light headed followed by a very sensational feeling, some enjoy it others bug out. If you continue hitting it you will slowly become more what I like to call zombie like. You're still in control of your thoughts, but you're body feels crazy and much deeper thoughts are bombarding you're brain then usual. You feel like a deep thinker, Like you could carry the world. You feel like you could do anything like climb the biggest tree. I've never done anything stupid because while on this drug I could always tell reality from what was the drug messing with me. Usually when I smoke PCP with my friends its in the form of a dipped cigarette and at least one other person but usually three. ( never smoke one to you're face if you have never smoked before). We smoke until we get the feeling where we are freaking out, but a good kind of freaking out, We love to run around and do silly things and love to listen to techno type music and especially pink Floyd.
2 answers
they make you hallucinate, perceive the world differently, fell numb, dissy, excited, calm relaxed. it varies from person to person. i suggest http://www.druginfo.adf.org.au/druginfo/drugs/drug_statistics/#victoria
7 answers
As of the year 2012, nobody in the scientific community has really been able to answer this question with research. Although the brain itself does not possess sensory innervation, the outer covering of the brain, called the meninges, does. These meninges can sense pain through the meningeal branches of the trigeminal nerve. This is the reason why people can sense pain when they have meningitis and this is probably the reason why people can feel the electrical sensations that most on the internet have described as "brain zaps," "brain shivers," or "battery head."
Brain zaps are usually associated with taking or withdrawing from certain anti-depressants, such as SSRIs, but they can also be caused by taking or withdrawing from other drugs, such as benzodiazapines. Some may go as far as even claiming that they can have psychogenic origins, such as with anxiety or panic attacks.
It appears to be a form of post-acute withdrawal syndrome and some might argue that it falls under the purview of SSRI discontinuation syndrome. Whatever it is, one thing is certain: it is extremely uncomfortable, it is extremely irritating, and it must be scientifically investigated.
Theoretically, these symptoms could last anywhere from months, years, to a lifetime. These symptoms could be permanent, there is little known about how to best treat them, and it is not known whether or not these have any unforeseen long-term health consequences, such as predisposing an individual to early dementia. Nevertheless, anecdotal evidence exists on the internet regarding the use of GABA agonists and NMDA antagonists to treat this disease, such as acaprosate, memantine, magnesium, ketamine, dextromethorphan, and phencyclidine.
Genetics, GABA receptor downregulation, and NMDA upregulation must play a large role in the pathogenesis of these symptoms. It seems to be a phenomenon of cerebral neuroexcitability sensed via the meningeal branches of the trigeminal nerve.
It is entirely possible that coconsumption of GABA agonists while taking SSRIs may precipitate this symptom in the genetically susceptible. For example, studies have shown that the chronic administration of GABA agonists can cause hyperexcitability (Begleiter 1977) and binge drinking and depression are associated with serontonin receptor mutations (Herman et al 2003). Many people take benzodiazapines and/or drink alcohol while on SSRIs, so it is possible that they are causing permanent downregulation of the GABA receptors allowing for a hyperexcitable cerebral cortex--i.e. "battery head."
What seems to be the most disconcerting about this symptom, however, is the fact that Alzheimer's disease is associated with a hyperexcitable cerebral cortical cortex as well. Thus, in will interesting to see how many legal complaints will be filed against pharmaceutical companies if it turns out that there is an association between taking SSRIs and dementia in the near future.
Begleiter, H., & Porjesz, B. (1977). Persistence of brain hyperexcitability following chronic alcohol exposure in rats. Advances in experimental medicine and biology, 85B, 209-222.
Herman AI et.al. (2003). Serotonin Transporter Promoter Polymorphism and Differences in Alcohol Consumption Behavior in a College Student Population. Alcohol and Alcoholism 38: 446-449.
Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease.
Matthew R. Hynd, Heather L. Scott, Peter R. Dodd
Neurochem Int. 2004 October; 45(5): 583-595. doi: 10.1016/j.neuint.2004.03.007
3 answers
lysergic acid diethylamide (LSD) and Dimethyltryptamine (DMT)
although the vast majority of possible psychoactive and psychedelic drugs are yet undiscovered by man.
edit: DMT is wrong info, 5-MeO-DMT is the answer your looking for, and is not the same as DMT at all.
- Norwegian-acidfiend
7 answers
Mostly, NO. Heroin is psychoactive (which merely means it is neurologically active)--but it is not a hallucinogen nor a stimulant. It is a semi-synthetic opiate (meaning it specifically acts on mu-opioid receptors in the brain). This action in the brain causes central nervous system depression. This means it induces opposite effects than stimulative drugs, to name a few alternative centrally acting symptoms: somnolence/sleepiness, anxiolysis (reduction of anxiety), decrease response to external stimuli, ataxia (reduction of muscle coordination), lowered blood-pressure, decrease in heart rate, reduction of heart-rate (or BPM-rate), and hypotension. All of these symptoms mentioned are nearly completely opposite of that of stimulate effects on the body & brain.
Conversely, traditional hallucinogens (such as LSD, magic-mushrooms, and peyote) and stimulants do not impact endogenous opioid receptors whatsoever. Stimulants largely increase dopamine levels; and to a lesser degree, they non-selectively increase serotonin and norepinephrine levels--this results in a stimulant effect. Traditional hallucinogens (i.e., psychedelics) of both the tryptamine (DMT, LSD, psilocybin/"magic mushrooms") and phenethylamine (MDMA/ecstasy, 2c-b, mescaline/peyote) classes usually act selectively on serotonin receptors, specifically at 5-HT2 sub-receptors, this being the receptor most responsible for psychedelic effects associated with these drugs (although they also act at the serotoninergic receptors: 5-HT1a, 5-HT2a, & 5-HT2c. And also having some affinity for some dopamine-sub receptors; the action at these specific sub-receptors differs between psychedelics, and this is usually what contributes to the differentiation between hallucinogenic effects between similar psychedelics- such as the differences between peyote & LSD).
Non-traditional hallucinogens also do not act on the same receptors as heroin and thus do not produce similar psychoactive effects. Deliriants (like Datura) owe their effects to their anticholinergic effects- which cause delusional type effects, rather than less realistic hallucinations attributed to traditional hallucinogens like LSD. And dissociatives such as PCP, dextromethorphan (DXM), and ketamine--which are commonly considered "hallucinogens"--act as NMDA antagonists and agonists at PCP-receptor sites; which, again, create psychoactive effects quite different than pure-OPIOIDergic drugs. Although some opiates like methadone do act as NMDA antagonists, this effect is negligible even at very high doses and no "hallucinogenic" psychoactive effects are realized.
3 answers
Chemical signals in the form of neurotransmitters are used during neuron to neuron communication. Neurons release neurotransmitters into the synapse, where they bind to receptors on the next neuron, causing either excitation or inhibition of the receiving neuron.
2 answers
Nootropic drugs are a fascinating area of study for those interested in enhancing cognitive function and brain health. One specific benefit that some nootropics offer is the improvement of brain blood circulation. Enhanced blood flow to the brain can lead to better oxygen and nutrient delivery, which supports overall brain function and health.
Several nootropics are known for their ability to improve cerebral blood circulation:
Ginkgo Biloba: This natural supplement is often praised for its ability to enhance blood flow to the brain, which can improve memory and cognitive function.
Vinpocetine: Derived from the periwinkle plant, vinpocetine is believed to increase blood flow to the brain, supporting cognitive abilities and protecting against neural damage.
Piracetam: A well-known member of the racetam family, piracetam may enhance brain blood flow and improve various aspects of cognitive function, including memory and learning.
For more detailed information on nootropics and their benefits, including how they can improve brain blood circulation, you can visit this comprehensive guide.
3 answers
