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02-02-2007, 03:03 AM
Opiates (heroin, morphine, etc.)
The human body naturally produces its own opiate-like substances and uses them as neurotransmitters. These substances include endorphins, enkephalins, and dynorphin, often collectively known as endogenous opioids. Endogenous opioids modulate our reactions to painful stimuli. They also regulate vital functions such as hunger and thirst and are involved in mood control, immune response, and other processes.
The reason that opiates such as heroin (http://www.heroin.org)and morphine affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids. There are three kinds of receptors widely distributed throughout the brain: mu, delta, and kappa receptors.
These receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors.
This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons of the ventral tegmental area come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released (see animation). Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.
Chronic consumption of opiates inhibits the production of cAMP, but this inhibition is offset in the long run by other cAMP production mechanisms. When no opiates are available, this increased cAMP production capacity comes to the fore and results in neural hyperactivity and the sensation of craving the drug.
The human body naturally produces its own opiate-like substances and uses them as neurotransmitters. These substances include endorphins, enkephalins, and dynorphin, often collectively known as endogenous opioids. Endogenous opioids modulate our reactions to painful stimuli. They also regulate vital functions such as hunger and thirst and are involved in mood control, immune response, and other processes.
The reason that opiates such as heroin (http://www.heroin.org)and morphine affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids. There are three kinds of receptors widely distributed throughout the brain: mu, delta, and kappa receptors.
These receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors.
This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons of the ventral tegmental area come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released (see animation). Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.
Chronic consumption of opiates inhibits the production of cAMP, but this inhibition is offset in the long run by other cAMP production mechanisms. When no opiates are available, this increased cAMP production capacity comes to the fore and results in neural hyperactivity and the sensation of craving the drug.