Cannabis Flashcards
What are the medical indications of Marijuana (5)
decrease N/V in chemotherapy
alleviates chronic pain (questions on safety and effectiveness)
Neurological Problems (subjective relief for MS, epilepsy and Huntingdon’s)
increase appetite in HIV patients
PTSD
What did the Henquet et Al 2005 paper prove?
a link between cannabis and schizophrenia
Describe the synthesis and metabolism of THC molecule (3)
made from cannabidiol into THC
THC is then converted into II-hydroxy THC which is a more active form that is highly lipophilic
or its converted into cannabiol which is the inactive metabolite
What are the natural agonists and partial agonists to CB receptors? (3)
cannabidiol and THC are natural agonists
AEA - anandimide is a partial agonist
2-AG - 2-arachidanoyl glycerol - full agonist
How is AEA synthesised? (2)
PLD binds to NAPE to form a complex
high Ca+ stimulates AEA synthesis
How is 2-AG synthesised? (2)
precursor is hydrolysed
DAGL and DAGL B hydrolyse
What is the stimuli for CB agonist production? (2)
increased concentation of phospholipid precursors
activation of GPCR, PLC and increased Ca+
Where are agonists produced? (4)
neurons, astrocytes and microglia
cardiac myocytes and blood vessels
vascular wall
gut
Why are endocannabinoids not neurotransmitters? (1)
they are not pre-synthesised and stored in vesicles
Describe the degradation processes of both AEA and 2-AG including the enzymes, pathways and studies supporting them. (8)
AEA becomes arachidonic acid and ethanulamine by FAAH in the COX pathway Kathuria 2002
2-AG becomes arachidonic acid and glycerol by MGL in the COX pathway Maccarone 2008
What is the function of CB1 agonists and antagonists in the hippocampus (2)
CB1 decreases spontaneous IPSP of GABAergic interneurons (causes inhibition)
antagonists block depolarisation-induced suppression of inhibition (DSI)
What are the therapeutic potentials of endocannabinoids based on their brain locations (7)
Basal Ganglia and cerebellum - motor function
hippocampus - learning and memory
cerebral cortex - high cognitive function
hypothalamus - thermal regulation, neuroendocrine regulation, appetite, depression and anxiety
amygdala - emotionality
spinal cord - peripheral sensation and pain
brain stem - N&V
Describe the evolution of CB receptors among species (7)
Plants have no CB or CBr
eCB homologues present
C. Elegans have no CB
eCB’s and FAAH
Insects have no CB, FAAH or NAPE-PLD
but they have 2-AG and DAGL
Vertebrates have CB1, CB2, NAPE-PLD, DAGL-B and those stated above
Describe the effect of CB1 on neurotransmission (4)
CBs are activated via DSI.
DSI occurs in hippocampal pyramidal cells, when cells are depolarised they suppress GABA-mediated inhibition
DSI is blocked by CB1 antagonist rimonobant
location of CB1 receptors and distribution of DAG-lipase and MAG-lipase fit idea that 2-AG could be a retrograde messenger in DSI
What are the differences between AEA, DEA and PEA? (1)
DEA and PEA act to inhibit CB1 and CB2 but are alike AEA in structure
