Drugs Of Abuse Flashcards
Which pathway is reward pathway to reinforce behaviour
Dopaminergic
Where are DA cell bodies found in dopaminergic reward pathway
VTA
Where does signalling go to from the VTA da body
Ventral striatum (dorsal striatum is to do with Parkinson’s)
Then to pre frontal cortex
What is the nucleus called on the ventral striatum where D2 receptors are for VTA dopamine release
Nucleus accumbens
Which things stimulate both the n accumebns and VTA
Glutamate EPSP which binds to nmda receptors causing AP
Which things are inhibitory for the VTA and also for n accumbens
Gaba ipsp
What do amphetamines do
Increase levels of monoamines (da, nadr, 5HT) in synapse
What does amphetamine structure look like
Other monoamines eg DA and nadr and 5HT
How do amphetamines enter which blocks reuptake
Via reuptake transporters (Dat, nat, 5htt )
How do amphetamines once in via reuptake transporters get inserted to vesicle
Via VMAT2
What does insertion to vesicles via VMAT 2 cause
Ph levels lower in vesicle to release monoamines eg nadr, da, 5HT
What allows for the transport of the NT from vesicle to the cleft when amphetamines enter via vmat2
Reuptake transporters reverse due to higher conc in cytosol than cleft
These therefore carry the Monoamines in cleft and blocks reuptake
What would happen if DAT was targeting via amphetamines
DA would increase in cleft
Causes psychosis and reward stimulation
What would happen is NAT was the highest affinity
Nadr would increase in cleft and cause alertness, anxiety
What actions would occur if 5HT was increased in synapse
Anoretic and empathogenic behaviours
Where does dopamine increase due to amphetamines in the reward pathway
More released from the VTA to then bind to D2 on n accumbens (ventral striatum)
How does cocaine work to increase DA in the synapse between VTA and n accumbens
Blocks the DAT reuptake transporters (as well as nat and 5htt)
Why does crack cocaine have quicker and larger effect
Lipophillic to enter brain and faster action
Which receptors on VTA does nicotine bind to to cause stimulation and therefore release of DA from VTA
Nicotinic acH receptors (cusses AP)
What substance causes psycho activity from cannabis
9 THC
Which gcpr does THC from cannabis bind to
Cb1 and cb2
Are cb1 presynpstic autorecepotrs
Yes
What binds to CB1 to cause stoped release of things like gaba
Cannabinoids
How can cannabinoids increase DA release from VTA
If they bind to CB1 on ipsp neurones which stops release of gaba
= disinhibit the VTA
Can cannabinoids also stop release or EPSP eg glutamate via cb1
Yes
Which receptors do opiates bind to causing rewarding effects (increase in DA from VTA and n accumbens)
Mu receptors
What happens when opiates bind to mu receptors
Prevents the release of gaba from IPSP
Disinhibits the VTA and n accumbens
= increase in DA
