Opioids, GABA, and Glutamate
Opioids and the Cholinergic System
There are a variety of different substances that interact with the cholinergic receptors, among them not only acetylcholine, but also muscarine and nicotine, plant alkaloids found in herbal medicines like Amanita muscaria and Nicotiana or Tabacum spp. (respectively). In the amygdala, activation of the kappa opioid receptors can increase anxiety levels and anxiety-like behaviors. These same receptors also are known to increase the rewarding effects of nicotine specifically, perhaps in part due to nicotine’s anti-anxiety properties, which may increase the probability of addiction in people who are more susceptible to this interaction.Click here to schedule a health coaching session with us.
Opioids also interact with the muscarinic receptors in the cholinergic system. One study found for example that opioid receptor agonistic drugs may potentiate the effects of anticholinergic muscarinic receptor antagonistic drugs. Opioid receptors also act to modulate the transmission of synaptic messages that are managed by muscarinic receptors, particularly in the hippocampus. Other research also suggests that agonistic activation of both the mu opioid receptors and the M2 muscarinic receptors of the parasympathetic nervous system (more specifically, on the sphenopalatine ganglion neurons) may provide more effective relief from migraines and facial pains like trigeminal neuralgia.Mu and kappa opioid receptor agonistic activities are particularly important in terms of cholinergic receptor activity (the delta receptors appear to have little to no relevance in regard to the cholinergic receptors). Agonistic activity of both the mu and kappa receptors can effectively inhibit the release of acetylcholine as a result of exposure to nicotine, serotonin, and tachykinin. Endogenous opioids in the body have also been found to modulate the autoinhibition of muscarinic receptors, particularly in cases where the autoinhibition system of these receptors is dysfunctional. Ultimately, in most cases, activation of the mu and kappa opioid receptors in the autonomic nervous system results in inhibition and modulation of the cholinergic receptors.
The Opioid-Endocannabinoid Connection
The opioid and endocannabinoid systems in the body have long been known to be intimately connected and to interact frequently with each other. The mu opioid receptors and the CB1 endocannabinoid receptors are especially closely linked, with these occurring in close proximity to each other in the same brain regions, often even on the same neurons. Activation of both of these receptors is necessary in order for 9-delta-THC and/or morphine to produce the motivational effects that stimulate eating as a kind of reward (“food reinforcement”).Click here to do a free trial of EMDR to Release Trauma.
The CB1 receptors are also involved in modulating some of the effects of the mu opioid receptors. Specifically, CB1 receptor activation is involved in regulating the reward and motor function effects of mu opioid receptor activation. It’s also important to note that both the CB1 receptors and the mu opioid receptors perform similar effects in terms of reducing adenylyl cyclase levels, as well as in causing a calcium current blockade and activation of potassium channels at a cellular level. These specific actions of both receptors are generally linked to inhibited neurotransmitter release.The endocannabinoid and opioid systems also both manage similar things in the body at a higher level. Endogenous opioids and endocannabinoids are both involved with temperature regulation, sedation, blood pressure, intestinal motility, and locomotor activity, and antinociception, for example. Activation of either system is also widely acknowledged to potentiate the effects of the other system.
