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Science Project: The Affects Of Drugs & Alcohol On The Brain

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How Drugs And Alcohol Ruin Your Brain
 
BeLoW
 
ArE SoMe ExAmPlEs Of DrUgS & aLcOhOl AnD tHe AfFeCtS.

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Alcohol & It's Affects On The Brain.
 
Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.
Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.
Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.
The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.
However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.
Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.

I Got My Information From World Book 2000

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Cocaine & It's Affect On The Brain
 
Cocaine acts by blocking the reuptake of certain neurotransmitters such as dopamine, norepinephrine, and serotonin. By binding to the transporters that normally remove the excess of these neurotransmitters from the synaptic gap, cocaine prevents them from being reabsorbed by the neurons that released them and thus increases their concentration in the synapses (see animation). As a result, the natural effect of dopamine on the post-synaptic neurons is amplified. The group of neurons thus modified produces the euphoria (from dopamine), feelings of confidence (from serotonin), and energy (from norepinephrine) typically experienced by people who take cocaine.
In addition, because the norepinephrine neurons in the locus coeruleus project their axons into all the main structures of the forebrain, the powerful overall effect of cocaine can be readily understood.
In chronic cocaine consumers, the brain comes to rely on this exogenous drug to maintain the high degree of pleasure associated with the artificially elevated dopamine levels in its reward circuits. The postsynaptic membrane can even adapt so much to these high dopamine levels that it actually manufactures new receptors. The resulting increased sensitivity produces depression and cravings if cocaine consumption ceases and dopamine levels return to normal.
Dependency on cocaine is thus closely related to its effect on the neurons of the reward circuit.             
 
Ecstasy
 
Ecstasy (MDMA) is a synthetic drug. It acts simultaneously as a stimulant and a hallucinogen because of its molecular structure, which is similar to that of both amphetamines and LSD. Like amphetamines and cocaine, ecstasy blocks the reuptake pumps for certain neurotransmitters, thus increasing their levels in the synaptic gap and their effect on the post-synaptic neurons’ receptors.
While ecstasy also potentiates the effects of norepinephrine and dopamine, it is distinguished from other psychostimulants by its strong affinity for serotonin transporters. The initial effect of ecstasy is thus an increased release of serotonin by the serotonergic neurons. The individual may then experience increased energy, euphoria, and the suppression of certain inhibitions in relating to other people.
A few hours later, there is a decrease in serotonin levels, amplified by the reduced activity of tryptophane hydroxylase, the enzyme responsible for synthesizing serotonin. This decrease can last much longer than the initial increase. Once again, an artificial increase in the level of a neurotransmitter exercises negative feedback on the enzyme that manufactures it. As a result, when intake of the drug ceases, the excess turns into a shortage.
Like all psychoactive drugs that produce a sensation of pleasure, ecstasy also increases the release of dopamine into the reward circuit. In addition, the extra serotonin produced by ecstasy leads indirectly to excitement of the dopaminergic neurons by the serotonergic neurons that connect to them.
The toxicity of ecstasy for humans has not been clearly established, but animal studies have shown that chronic high doses of MDMA lead to selective destruction of the terminal buttons of the serotonergic neurons.
 
These are just some of the drugs and their frightning affects on the BRAIN! :)

Jordon's Project