Pharmacologic Action of Meth

Stimulant drugs such as the amphetamines and methamphetamines alter the release and/or re-uptake of neurotransmitters. They affect the "Pleasure Reward Pathway"(PRP) by altering the level of dopamine present in the synapse. Methamphetamine is chemically similar to dopamine and norepinephrine and readily crosses the blood/brain barrier. It produces its effects by causing dopamine and norepinephrine to be released into the synapse in several areas of the brain. Methamphetamine enters nerve terminals by passing directly through nerve cell membranes. It is also carried into the nerve terminals by transporter molecules (See step 8) that normally carry dopamine or norepinephrine from the synapse back into the nerve terminal. Once in the nerve terminal, meth is taken up by the vesicles that contain dopamine and norepinephrine causing the release (See step 5 - exocytosis) of these neurotransmitters.

Additionally, meth blocks the breakdown of excess dopamine and norepinephrine. It does so by blunting the effects of Monoamine oxidase (MAO), which is an enzyme capable of cleaving monoamines such as dopamine, norepinephrine and serotonin. The result is an excess of neurotransmitters in the synapse that are free to act on the postsynaptic terminal potentially causing abberant action potentials among affected neurons.

The high concentration of dopamine within the PRP elicits feelings of pleasure and euphoria. Excess norepinephrine may be responsible for the hightened alertness and anti-fatigue effects of methamphetamine.

Interactive Synapse

(Explore the numbered components in the diagram with your cursor)

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