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propofol,have also been demonstrated to act at extrasynaptic receptors and enhance tonicinhibition in hippocampus
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eGABA A Rs may also be the preferential high-affinity tar-get of the naturally occurring GABA precursor γ-hydroxybutyric acid (GHB), adepressant drug that is also used recreationally. However, this observation remainscontroversial since the α4β1δ subunit combination expressed in Xenopus oocytes inthis study are believed to exist only in very low numbers, if at all, in the mammalianbrain
Test on a4b2d receptors rather than a4b1d that they used
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The effects of THIP on extrasynapticGABA receptors are, in fact, thought to account for its ability to promote both slow-wave (non-REM) and REM sleep since in animals lacking δ subunits the hypnoticeffects of the drug are lost (Winsky-Sommerer et al. 2007)
This compound, a muscimol derivative, promotes both non-REM and REM sleep.
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Fig. 1.1
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this form of GABAergic cellular communi-cation is more similar to the type of volume transmission observed with monoamineneurotransmitters like serotonin, dopamine and histamine
I'm going to hang onto the wording of volume transmission.
It makes me think about an alternative hypothesis to the functions behind Cannabis causing HPPD, as the psychedelics typically responsible for that symptom are serotonergic.
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that very low (nM) concentrations of GABA,which typically occur in the cerebrospinal fluid (CSF) of the extracellular space,can persistently activate a population of non-synaptic GABA A receptors resultingin a ‘tonic’ increase in membrane conductance
GABA typically occurs in the CSF, and very small levels of GABA can activate extrasynaptic receptors.
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