This is not an easy question to answer, but the truth is that cannabis models other drugs of abuse, and conditioned stimuli predicting drug availability, when it comes to increasing mesolimbic dopamine transmission.
In addition, a decrease in mesolimbic dopamine function is observable during drug withdrawal – including during cannabis-withdrawl syndrome.
What this means is that cannabis elicits a similar neurochemical response to other drugs of abuse that could shape drug-seeking or reward-seeking behaviour, as well as persistent relapsing behaviours.
So, despite the misconception that cannabis is unique from other drugs of abuse, the reality is that it exerts identical effects on the mesolimbic dopamine system.
The Mesolimbic Dopamine System
If it isn’t already clear, the mesolimbic dopamine system plays a major role in drug-seeking behaviour, and persistent relapsing behaviours due to withdrawal symptoms.
The mesolimbic pathway, or reward pathway, is a series of projection neutrons in the brain that release and synthesize the neurotransmitter dopamine.
The mesolimbic pathway releases dopamine to the ventral striatum, a cluster of neutrons in the subcortical basal ganglia of the forebrain.
What is Incentive Salience?
Together, nucleus accumbens and the olfactory tubercle form the ventral striatum. When dopamine is release from the mesolimbic pathway in the midbrain into the nucleus accumbens in the forebrain, it activates a cognitive process known as incentive salience.
This cognitive process confers a desire or want attribute, and entails some motivational component to a rewarding stimulus.
In other words, it is the attractive and motivating property of a stimulus (like a drug) that causes appetitive behaviour, approach behaviour, or consummatory behaviour.
The fact that cannabis patterns other drugs of abuse, albeit to a lesser degree, means that there is a risk of cannabis addiction.
Cannabis-withdrawl is characterized by a set of symptoms ranging from anxiety, nervousness, decreased appetite and weight loss, to restlessness, sleep difficulties including strange dreams, chills, depressed mood, stomach pain, physical discomfort, shakiness, and sweating.
It is important to note however, that the severity of withdrawal in lab tests differed depending on how the symptoms were induced. In cases where test subjects were abruptly forced to abstain from using experimenter-administered cannabinoids, the symptoms were mild and difficult to detect.
However, when withdrawal was induced with a CB1R antagonist known as Rimonabant, robust and immediately observable withdrawal symptoms occurred.
This leaves little room for debate as to whether or not cannabis addiction exists.
What remains to be answered;
- what are the risks of cannabis addiction, are they as severe as other drugs of abuse?
- how does disrupting endocannabinoid signalling show potential for treating addiction?