The Brain
How Opiates Affect The Brain
There are three large pro-compounds: proenkephalin, prodynorphin, and pro-opiomelanocortin. Endorphins can further decompose to small fragments, oligomers, which are still active.
Oligomers pass the blood-brain barrier more readily. Enzymatic degradation of small-chain endorphins is accomplished by dipeptidyl carboxypeptidase, enkephalinases, angiotensinases, and other enzymes. This limits their lifetime in the unbound state.
Opiate receptors presynaptically inhibit transmission of excitatory pathways. These pathways include acetylcholine, the catecholamines, serotonin, and substance P.
Substance P is a neuropeptide active in neurons which mediate our sense of pain; its antagonists are currently under investigation as clinically useful mood-brighteners.
Endorphins are also involved in glucose regulation. Opiate receptors are functionally designated as mu, delta, kappa, etc. These categories can be further sub-classified by function or structure.
Opioidergic neurons are particularly concentrated in the ventral tegmental area. The VTA is an important nerve tract in the limbic system.
It passes messages to clusters of nerve cells in the nucleus accumbens and the frontal cortex.
This forms the brain's primary reward pathway, the mesolimbic dopamine system. Its neurons are called dopaminergic because dopamine is manufactured, transported down the length of the neuron, and packaged for release into the synapses.
GABA normally plays a braking role on the dopaminergic cells. Opiates and endogenous opioid neurotransmitters activate the presynaptic opioid receptors on GABA neurons.
This inhibits the release of GABA in the ventral tegmental area. Inhibiting GABA allows the dopaminergic neurons to fire more vigorously.
The release of extra dopamine in the nucleus accumbens is intensely pleasurable. The dopamine transporter responsible for its reuptake is blocked by cocaine. So cocaine allows more dopamine to accumulate in the synapses. Amphetamines act directly on the nerve endings and release extra dopamine too.
Chronic cocaine use causes a decrease in the production of enkephalin, one of the brain's natural opioids.
This in turn causes a compensatory increase in the number of mu-receptors. The number of unoccupied mu-receptors may be associated with the craving and abstinence syndrome.
The mu receptors are crucial to the rewarding and addictive properties of opioids. Mu-receptors are found mainly in the brainstem and the medial thalamus.
They have two sub-types: mu-1 and mu-2. Stimulation of the mu-1 receptors is primarily responsible for an extraordinary sense of euphoria, serenity and analgesia. Stimulation of the mu-2 receptors helps modulate respiratory depression. For obvious reasons, this is potentially dangerous.
Unfortunately, there is still a lack of clinically available opioids specific to the mu-1 receptors. Their advent will be an tremendous boon to mental and physical health.
From heroin.org
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