Short-term marijuana use is known to increase dopamine levels in the brain indirectly. This is because cannabinoids, such as THC, act on the body's endocannabinoid system (ECS), which temporarily suppresses GABA inhibitors. GABA neurons are neurons that inhibit dopamine production; when suppressed, dopamine production increases. Studies have shown that consuming THC also causes a short-term increase in dopamine levels in the brain, which activates the brain's reward system.
Cannabinoid type 1 (CB) receptors associated with motivational, emotional and affective processing are usually abundant in these areas, so upregulation of CBD1 receptors can positively affect THC-induced brain damage. Instead of stimulating dopamine directly, THC is able to indirectly increase dopamine release by reducing GABA release. Acute THC causes increased dopamine release and neuronal activity, while its long-term use is associated with weakening of the dopamine system. Future research should examine the drug's long-term and developmental dopaminergic effects.
Cognitive and psychomotor effects in men after smoking a combination of tobacco and cannabis containing up to 69 mg of delta-9-tetrahydrocannabinol (THC) suggest that cannabinoids increase neuronal dopamine activation by decreasing GABAergic inhibition of dopamine neuronal activity. In vitro synaptosomal studies have also suggested that cannabinoids might increase dopamine concentrations in the nucleus accumbens, in part, by binding to the dopamine transporter and, therefore, decrease uptake at presynaptic terminals. Other studies show that THC is more effective than CBD in terms of having a positive impact on dopamine in the short term. Increases in dopamine from the nucleus accumbens are theorized to mediate the major positive reinforcement and reward properties of all known drugs of abuse.
In addition, legalizing the commercial sale and promotion of high-THC cannabis for recreational use can lead to significant increases in THC intoxication and dependence, and addiction to euphoria. The amount of cannabis consumed (dose of THC) seems to be an important factor when it comes to developing anhedonia and depression. If you're a marijuana user, you may find that the plant increases your dopamine level in the short term. It should be noted, however, that genetic factors partially determine the magnitude of cannabinoid-induced increases in accumbal dopamine concentration. The evidence suggests that short-term marijuana use can increase dopamine levels in the brain indirectly by acting on the body's endocannabinoid system (ECS). This temporarily suppresses GABA inhibitors which leads to an increase in dopamine production.
Studies have also shown that consuming THC causes a short-term increase in dopamine levels which activates the brain's reward system. Furthermore, legalizing high-THC cannabis for recreational use can lead to significant increases in THC intoxication and dependence. The amount of cannabis consumed (dose of THC) seems to be an important factor when it comes to developing anhedonia and depression. It should be noted, however, that genetic factors partially determine the magnitude of cannabinoid-induced increases in accumbal dopamine concentration.
In conclusion, acute THC causes increased dopamine release and neuronal activity while its long-term use is associated with weakening of the dopamine system. Future research should examine the drug's long-term and developmental dopaminergic effects.
