3.3.7 Recreational drugs
Effects of Common Recreational Drugs on Neurotransmission and the Link to Mental Health Symptoms
Recreational drugs interfere with neurons in order to send, process, and receive signals with the help of neurotransmitters. Opioids (including morphine and heroin) and marijuana are able to activate the neurons because these chemical substances can mimic the natural neurotransmitters present. These chemical substances will attach to the neuron and activates them (Cowen, 1999).
Opioids:
Opioids are a class of drugs that bind to specific receptors in the brain and modulate neurotransmitter function, particularly the neurotransmitter systems involved in pain perception and reward. Opioids act by increasing the release of neurotransmitters, such as dopamine, which produce feelings of pleasure and euphoria.
While opioids can provide effective pain relief and produce pleasurable effects, they can also lead to changes in the brain’s reward system, resulting in tolerance, dependence, and withdrawal symptoms. Chronic opioid use has been linked to a number of mental health symptoms, including anxiety, depression, and insomnia. In addition, opioid use has been associated with an increased risk of developing mood and psychotic disorders, such as bipolar disorder and schizophrenia. This may be due to the long-term effects of opioids on the brain’s reward system, as well as its effects on neurotransmitter systems and brain structure and function.
Opioids have two activated sites, one is on the presynaptic nerve terminal and the other one is on the postsynaptic neuron. Opioids’ postsynaptic actions are inhibitory and opioids’ presynaptic action inhibits the release of neurotransmitters. This is hypothesised to be a cause for the major disturbance in the nervous system. Individuals using opioids for a long period of time can induce changes in their white matter tracts and become the reason for insomnia, sexual dysfunction, chronic constipation, kidney diseases and menstrual cycle disturbance.
The periaqueductal grey (PAG) area of the midbrain is rich in opioid receptors and endogenous opioids and is a primary target for analgesia. The analgesic impact of opioids on the PAG is thought to function by reducing the inhibitory effects of the neurotransmitter gamma-aminobutyric acid (GABA) on neurons in a descending antinociceptive pathway. Opioids reduce the likelihood of presynaptic neurotransmitter release, which inhibits GABA-mediated (GABAergic) synaptic transmission in the PAG and other brain areas, although the processes involved are unknown (Vaughan, 1997).
Cocaine:
Cocaine is a highly addictive stimulant drug that affects the neurotransmitter systems in the brain, particularly the dopamine, norepinephrine, and serotonin systems. Cocaine blocks the reuptake of these neurotransmitters, leading to an accumulation of neurotransmitters in the synaptic cleft and an increased transmission of signals between neurons.
This increase in neurotransmitter signalling produces feelings of euphoria and increased energy, as well as increased heart rate, elevated blood pressure, and decreased appetite. However, repeated use of cocaine can lead to changes in the brain’s reward system, which can result in tolerance, dependence, and withdrawal symptoms. Long-term use of cocaine has been linked to a number of mental health symptoms, including anxiety, depression, and paranoia. These symptoms may be due to changes in the brain’s reward system, as well as changes in the function of neurotransmitter systems, such as the dopamine system.
Opioids increase the stimulation of dopamine, whereas cocaine affects existing dopamine by blocking the reuptake thus increasing the longer pleasurable effects. Both of these drugs influence and reinforce the brain to repeatedly use the drugs. Long-term usage might cause a decrease in the ability to decision-making and an individual’s response toward stress. Euphoria is a long-term symptom that leads an individual toward increased arousal and alertness, increased level of paranoia, depression, insomnia and tremors etc. It also increases the risk of heart attack, stomach inflammation, and ulcers.
Cannabis:
Cannabis contains compounds known as cannabinoids, which bind to specific receptors in the brain and modulate neurotransmitter function. The primary psychoactive component of cannabis, delta-9-tetrahydrocannabinol (THC), acts on the endocannabinoid system and affects neurotransmitter systems including the dopamine, glutamate, and GABA systems.
The effects of THC on neurotransmitter systems can result in changes in mood, perception, and cognition. For example, THC can increase dopamine release in the brain, which can produce feelings of euphoria and increased appetite. THC can also reduce glutamate release, which may contribute to its effects on memory and learning.
While cannabis use can produce short-term effects that are pleasurable for some users, it can also produce negative effects, particularly in individuals who are vulnerable to mental health symptoms. Cannabis use has been associated with the development or exacerbation of mental health symptoms such as anxiety, depression, and paranoia.
In addition, heavy and long-term use of cannabis has been linked to an increased risk of developing psychotic disorders, such as schizophrenia. This is thought to be due to the effects of THC on the dopamine system, as well as its effects on brain structure and function.
It is important to note that the relationship between cannabis use and mental health is complex and influenced by a number of factors, including individual differences in genetic susceptibility, the dose and frequency of use, and the presence of co-occurring medical or psychiatric conditions.
Overall, while cannabis can produce pleasurable effects in some individuals, it can also have negative effects on mental health, particularly in individuals who are vulnerable to mental health symptoms. As a result, it is important for individuals to be aware of the potential risks associated with cannabis use and to consult with a healthcare professional if they have concerns about their use.
References:
(1) Cowen, M.S. and Lawrence, A.J., 1999. The role of opioid-dopamine interactions in the induction and maintenance of ethanol consumption. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 23(7), pp.1171-1212.
(2) Vaughan, C.W., Ingram, S.L., Connor, M.A. and Christie, M.J. (1997). How opioids inhibit GABA-mediated neurotransmission. Nature, 390(6660), pp.611–614. doi:10.1038/37610.