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A nerve poison that blocked neurotransmitter receptors on the dendrites would?
prevent transmission across the synaptic cleft
What will happen if lack of acetylcolinesterase in the synaptic cleft?
Neurotransmitters would continue to bind and rebind with the postsynaptic receptors, which would continue induction of a signal in the postsynaptic neurons, which would repropagate the initial signal. The case in drugs that block reuptake transporters (such as in serotonin reuptake inhibitor and norepinephrine reuptake inhibitor antidepressants, and dopamine reuptake inhibition found with cocaine and methylphenidate). This is also seen in cases where drugs block the breakdown of neurotransmitters at the synapse: - monoamine oxidase inhibitors (MAOIs) - Nardil, Parnate, selegiline - which prevent the breakdown of serotonin, norepinephrine, and dopamine - acetylcholinesterase inhibitors (AChE inhibitors) - organophosphase pesticides, nerve gas, racetams
How can I Dial a Blocked Telephone number from my Blocked Telephone number?
You can't.
What type of nuclear radiation can be blocked by a block of lead Beta particles or alpha particles?
Both Beta and alpha particles can be blocked by a block of lead. Alpha particles can even be blocked by a sheet of paper, and beta particles can be blocked by a thin aluminium plate.
What is partially blocked by ozone in the stratosphere?
The UV rays are partially blocked by ozone. It is present in stratosphere.
What parts of brain do the neurolyptics effect?
The theory behind why individuals develop 'psychotic' symptoms is based upon the idea that there are elevated levels of dopamine in the brain. Dopamine is a neurotransmitter, a molecule that passes messages between neurons. For example, when a nerve impulse arrives at a dopaminergic neuron (also known as a pre-synaptic neuron), dopamine is released from the cell and diffuses through a space between two neurons, called the synaptic cleft. Dopamine then binds to specific dopamine receptors on a different neuron (post-synaptic neuron) producing a specific signal, impulse or effect. Dopamine is then released from its receptors and 're-absorbed' into the pre-synaptic neuron, or degraded by enzymes in the synaptic cleft. The neuroleptics block dopamine receptors thereby inhibiting the ability of dopamine to attach to these receptors and generate signals. However, unlike the typical neuroleptics, the atypicals merely transiently block the receptors therefore allowing some dopamine to bind to the receptors and generate signals. The atypical neuroleptics are also able to block serotonin receptors located on dopaminergic neurons. When serotonin binds to these receptors it inhibits dopamine release. However as these receptors are blocked by atypical neuroleptics, the dopamine secretion is increased. The transient rather than permanent blocking of dopamine receptors and the blocking of serotonin receptors and subsequent increases in dopamine, it is for these reasons that the atypicals are thought to produce fewer adverse effects than the typical neuroleptics. However, the atypical drugs differ in their 'stickyess' when binding to dopamine receptors and also in the ratio of which dopamine ad serotonin receptors are affected. This may result in some atypicals producing higher levels of specific adverse effects than others. The atypicals may also bind to other receptor types, producing further adverse effects (see side effects of atypicals section).
What happens when acetylcholine receptors are blocked?
There are several compounds and drugs that may block acetylcholine receptors. They are collectively known as cholinergic antagonists.
A nerve poison that blocked neurotransmitter receptors on the dendrites would?
prevent transmission across the synaptic cleft
Why is it difficult to smell something with blocked nose?
Because the mucus blocking your nose is preventing the smell receptors doing their 'job' properly.
How drugs affect the nervous system?
Depressant Drugs: Alcohol, Benzodiazepines, Barbiturates and other central nervous system depressant drugs act primarily on a neurotransmitter substance known as GABA (Gamma Aminobutyric Acid). GABA is an inhibitory neurotransmitter that makes other neurons less likely to activate. The depressant drugs are GABA agonists, acting to help GABA reduce neuronal activation more efficiently than it usually would. Alcohol also inhibits (acts as an antagonist against) another excitatory neurotransmitter (Glutamate), making it harder for Glutamate to get the nervous system excited. Stimulant Drugs Amphetamines have their primary effects on the neurotransmitter Dopamine. Amphetamines both induce the terminal button of Dopamine-producing neurons to let more Dopamine out than normal, and also keep that Dopamine out in the synapse longer than it normally would be allowed to stay. Amphetamine also acts agonistically on receptors for a different neurotransmitter, Norepinephrine, by competing with Norepinephrine for post-synaptic receptors and turning those post-synaptic receptors on. Cocaine has its major effect by blocking the re-uptake of the neurotransmitters Dopamine and Serotonin. Opioid Drugs: Opioid drugs bind to special endorphin receptors in the brain (the 'mu', 'kappa', 'sigma' 'delta' and 'gamma' receptors) that have to do with pain. When these receptors are occupied and activated, the perception of pain lessens. Drug treatments for opioid addictions sometimes include the administration of Naltrexone, which is an opioid antagonist. Naltrexone competes with the opioids for their receptor sites, but is not itself capable of activating those receptor sites. An opioid addict on Naltrexone is thus rendered more or less incapable of getting high from their opioid drug of choice; they may take an opioid, but it will be blocked from the opioid receptors by the Naltrexone, and will not have its effect. Cannabinoids: Marijuana has a complex set of effects. It acts on the neurotransmitters Serotonin, Dopamine and Acetylcholine. It also binds to a receptor for a recently discovered neurotransmitter known as Anadamide. Hallucinogens: LSD is known to antagonize Serotonin by blocking its release.
What would happen to people exposed to a chemical warfare agent that blocked acetylcholine from binding to muscle receptors?
Muscle contractions would be prevented, causing paralysis.
What is the definition of the word opiods?
An opioid is a naturally occurring compound that will bind to opioid receptors within your body. When an opioid receptor is blocked by an opioid a person is likely to feel less pain.
Can you take Tylenol 3 with codeine while on methadone if you are in extreme pain from toothaches and headaches?
Yes but it probably wont work since your receptors are blocked with methadone
Why does high level of atropine cause vasodilation?
this from katznug pharma( almost all vessels containendothelial muscarinic receptors that mediate vasodilationThese receptors are readily blocked by antimuscarinic drugs.At toxic doses, and in some individuals at normal doses, antimuscarinic agents cause cutaneousvasodilation, especially in the upper portion of the body. The mechanism is unknown)
How do stimulants increase nervous activity?
Depressant Drugs: Alcohol, Benzodiazepines, Barbiturates and other central nervous system depressant drugs act primarily on a neurotransmitter substance known as GABA (Gamma Aminobutyric Acid). GABA is an inhibitory neurotransmitter that makes other neurons less likely to activate. The depressant drugs are GABA agonists, acting to help GABA reduce neuronal activation more efficiently than it usually would. Alcohol also inhibits (acts as an antagonist against) another excitatory neurotransmitter (Glutamate), making it harder for Glutamate to get the nervous system excited. Stimulant Drugs Amphetamines have their primary effects on the neurotransmitter Dopamine. Amphetamines both induce the terminal button of Dopamine-producing neurons to let more Dopamine out than normal, and also keep that Dopamine out in the synapse longer than it normally would be allowed to stay. Amphetamine also acts agonistically on receptors for a different neurotransmitter, Norepinephrine, by competing with Norepinephrine for post-synaptic receptors and turning those post-synaptic receptors on. Cocaine has its major effect by blocking the re-uptake of the neurotransmitters Dopamine and Serotonin. Opioid Drugs: Opioid drugs bind to special endorphin receptors in the brain (the 'mu', 'kappa', 'sigma' 'delta' and 'gamma' receptors) that have to do with pain. When these receptors are occupied and activated, the perception of pain lessens. Drug treatments for opioid addictions sometimes include the administration of Naltrexone, which is an opioid antagonist. Naltrexone competes with the opioids for their receptor sites, but is not itself capable of activating those receptor sites. An opioid addict on Naltrexone is thus rendered more or less incapable of getting high from their opioid drug of choice; they may take an opioid, but it will be blocked from the opioid receptors by the Naltrexone, and will not have its effect. Cannabinoids: Marijuana has a complex set of effects. It acts on the neurotransmitters Serotonin, Dopamine and Acetylcholine. It also binds to a receptor for a recently discovered neurotransmitter known as Anadamide. Hallucinogens: LSD is known to antagonize Serotonin by blocking its release.
Why is Webkinz blocked?
If it is blocked at home your parents blocked it, but if it is blocked at school the blocked it because it was a game.
How long does it take to digest caffeine?
When you take in caffeine, these receptors get blocked, your heart rate speeds up, and you get a jolt of heightened alertness - which might be what you want so you can keep going, but meanwhile your brain is looking to sleep, not caffeine, for restoration.
