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Studying and Exam Taking / Re: Adderall-Law school finals/studying
« on: August 08, 2006, 01:40:23 AM »
Adderall is not as potent as Cocaine. In fact, their mechanisms of action differ.
Amphetamines
Amphetamines are drugs used to combat fatigue. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. As the animation to the right shows, once inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.
Amphetamines also seem to act by several other mechanisms. For example, they seem to reduce the reuptake of dopamine and, in high concentrations, to inhibit monoamine oxydase A (MAO-A).
Amphetamines may also excite dopaminergic neurons via glutamate neurons. Amphetamines would thus remove an inhibiting effect due to metabotropic glutamate receptors. By thus releasing this natural brake, amphetamines would make the dopaminergic neurons more readily excitable.
http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_amphetamine.html#drogues
Cocaine
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.
http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_cocaine.html#drogues
Amphetamines
Amphetamines are drugs used to combat fatigue. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. As the animation to the right shows, once inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.
Amphetamines also seem to act by several other mechanisms. For example, they seem to reduce the reuptake of dopamine and, in high concentrations, to inhibit monoamine oxydase A (MAO-A).
Amphetamines may also excite dopaminergic neurons via glutamate neurons. Amphetamines would thus remove an inhibiting effect due to metabotropic glutamate receptors. By thus releasing this natural brake, amphetamines would make the dopaminergic neurons more readily excitable.
http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_amphetamine.html#drogues
Cocaine
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.
http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_cocaine.html#drogues
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