Were you a chemistry geek at school? Have you always gone for the complicated explanation? Then here is the advanced explanation for physical dependency on drugs, based on what many biologists call “pleasure pathways” in our brains which evolved to make sure we get into things like sex and food that keep our species going.
Endorphins and dopamine
Endorphin pathways have even been found in insects. Endorphins are natural hormones that reduce pain and make us feel good. They like to bind with ‘opiate receptors’ in our brain which then stimulate production of dopamine which keeps all those electrical signals going from one brain cell to the next.
Increased dopamine activity is often met by a decrease in the number of receptors sensitive to dopamine, as the brain, like the rest of our body, loves to keep things in balance (or homeostasis if you like the big words).
Tolerance
This down-regulation, or decreased number of receptors, tends to result in reduced electrical activity along post-synaptic nerve pathways, unless some behaviour or substance causes a continued high level of dopaminergic stimulation. The absence of a pleasurable sensation in conditions that were formally sufficient can cause a mild feeling of let-down after receptors have been down-regulated. The increased requirement for dopamine to maintain the same electrical activity is the basis of both physiological tolerance and withdrawal associated with addiction.
The result? Your body adapts to the drug with frequent use, so you don’t get the same effect anymore. Also, you feel like crap when you stop using.
The middle striatal reward pathway has been most strongly linked with addictive and reward behaviour. This pathway uses dopamine as a neurotransmitter and receives presynaptic input (from earlier in the circuit — it gets signals from these earlier in the circuit cells) from cells that respond to cannabinoids, nicotine (receptor subtype is nicotinic), and from cells that respond to endogenous opioid substances such as endorphins or enkephalins. Cells that are said to respond to a particular neurotransmitter contain, at the postsynaptic end (receiving area of the cell) receptors for that neurotransmitter. Many scientific boffins believe more neurotransmitters are involved with addiction than just dopamine; such as serotonin, norepinephrine, and the endocannabinoid anandamide.
Withdrawal
In cases of physical dependency on depressants of the central nervous system such as opioids, barbiturates, or alcohol, the absence of the substance can lead to symptoms of severe physical discomfort. Withdrawal from alcohol or sedatives such as barbiturates or benzodiazepines (valium-family) can result in seizures and even death. By contrast, withdrawal from opioids, which can be extremely uncomfortable, is rarely if ever life-threatening. In cases of dependence and withdrawal, the body has become so dependent on high concentrations of the particular chemical that it has stopped producing its own natural versions (endogenous ligands) and instead produces opposing chemicals. When the addictive substance is withdrawn, the effects of the opposing chemicals can become overwhelming. For example, chronic use of sedatives (alcohol, barbiturates, or benzodiazepines) results in higher chronic levels of stimulating neurotransmitters such as glutamate. Very high levels of glutamate kill nerve cells (called excitatory neurotoxicity).
Why opiates can be tough
Opioids like heroin and morphine present higher risks of dependency because they are chemically similar to endorphins, causing an up-regulation of dopaminergic receptors without stimulation of the endorphin systems. Cocaine and amphetamines also pose risks associated with physical attenuation, in both cases because they cause increases in the levels of the neurotransmitters dopamine and norepinephrine which acts indirectly to stimulate dopaminergic pathways in the brain. So where possible, try to balance your use with the risks of dependency!
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