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Lecture 6

PSYT 301 Lecture Notes - Lecture 6: Gaba Receptor, Alcohol Withdrawal Syndrome, General Anaesthetic

Course Code
PSYT 301
Kathryn Gill

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Lecture 6: Etiology of alcohol/drug dependence; focus on genetic factors, twin, adoption and
linkage studies
Read: Rewel et al., 2012, Arias et al. 2014
Neural substrate between human and monkeys, similar reward pathways lead to
similar drinking patterns
What are the intrinsic pathways towards the effects of alcohol?
Action of alcohol
Sedation: GABA and NMDA
change in the subunit structure to a more alcohol resistant structure may help
build tolerance
hyperexcitability occurs in withdrawal
Alcohol has a GABA a agonist action (increased channel opening in terms of duration
and frequency leading to greater Cl- influx, inhibits neurons (hyperpolarization)
GABAa receptors are composed of isoforms
different GABAa receptors are different in the different parts of the brain and
different sensitivities to alcohol that are dependent on subunit configuration
the large numbers of subunits may account for variable sensitivity to
benzodiazepine, barbiturates, ethanol, general anaesthetic
alcohol sits in a protein and alters its function (allosteric) -- not a classical
binding site
most synaptic GABAa receptors are composed of 2 alpha, 2 beta and one y
no all subunits are equally sensitive to alcohol
prefrontal cortex is first affected region, midbrain/cortical next, brainstem last
(respiratory function) as blood alcohol level rises, inhibition is dose time
very strong dose and time dependent effect of neuronal firing, alcohol is only
a depressant, suppressing GABA function
PET: 2 ivs, one tracer, IV, looks at the ligand that was injected over time
metabolic waste (glucose) is seen in the brain, varying levels
brain activity recovery in alcoholics after getting sober
low levels of glucose in the brain in detox: lethargic, withdrawal,
photosensitivity, ultrasensitive, can’t retain information, no reading
long acting benzos are used in detox to suppress withdrawal, benzos are then
withdrawn over time in a medical setting
ethanol primarily depresses neuronal firing - via an agonist activity at GABAa
receptors (increased inhibition), and an antagonistic action at NMDA receptors
presence of GAD enzyme determines if a neuron is GABAergic or glutaminergic
GABA release must happen for the GABA receptor to open
is blocking subunits or changing their structure in the GABA receptor a viable way to
treat alcoholism?
might not have neuronal effects but it is still in the body -- liver effects and
other effects still present
non-specific fix, might try to overcome the blockade by consuming more
GABAa antagonists have been shown to reduce bar-pressing for oral alcohol in rats
(SR95531, picrotoxin, bicuculline)
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