Cannabis Flashcards
What are the psychotropic effects of cannabis?
General change in perception, euphoria, increased appetite, relaxation, enhanced recollection, increased awareness of sensation.
At higher doses it can cause hallucinations and ataxia
What are the somatic effects of cannabis?
Increased heart rate, dry mouth, reddening of the eyes, reduction in intraocular pressure, muscle relaxation, more persistent alpha waves (EEG)
What are the risks associated with cannabis use?
Potential to trigger psychosis, increased risk of developing schizophrenia, anxiety, paranoia, lung problems, increased blood pressure and social risks such as prison
How does activation of CB1 receptors produced the psychotropic effects of cannabis?
THC travels through the body and attaches to CB1 receptors in the hypothalamus (which increases appetite), the amygdala (which leads to anxiety) and the brain stem (nausea)
What are the synaptic effects of cannabinoid receptors?
CB1 agonists reduce action potential dependent release via inhibition of calcium channels as they reduce evoked IPSPs but not their frequency or amplitude.
How do you know if an effect is presynaptic or postsynaptic?
Reduced amplitude > postsynaptic effect
Reduced frequency > presynaptic effect
No effect > presynaptic action potential dependent effect
What does DSI result in?
Depolarisation of the postsynaptic cell results in a transient reduction in GABAergic transmission - it is observed in cerebrellar purkinje cells, medium spins neurons and hippocampal pyramidal cells.
What are the four pieces of evidence that mean DSI is mediated by a retrograde messenger?
1) Increase in postsynaptic calcium concentration is necessary for induction of DSI - blockers of calcium ion entry and postsynaptic calcium ion chelating ages both prevent DSI and artificially raising calcium ion concentration induces DSI (THE POSTSYNAPTIC TRIGGER)
2) The frequency of spontaneous inhibitory synaptic events is reduced therefore fewer vesicles are released presynaptically.
3) Postsynaptic sensitivity to exogenously applied GABA is not affected by depolarisation.
4) It is not blocked by classical neurotransmitter antagonists
5) DSI is not synapse or cell specific
What is evidence that DSI is mediated by endocannabinoids?
1) Synthesis and release of endocannabinoids are dependent on calcium ions
2) CB1 antagonists depress GABAergic transmission
3) DSI is blocked by CB1 antagonists
4) DSI is mimicked by blocking endocannabinoid uptake
5) DSI is absent in the CB1 knockout mouse
Endocannabinoids are released in response to…
postsynaptic depolarisation resulting in suppression of GABA release.
