dec 28, 2004 - Cannabis


The principle receptor for cannabinoids, CB1R, is strongly expressed in the DLPFC (Eggan et al, 2007) and in the neocortex, CB1Rs are localized to the axon terminals of the GABA-containing basket neurons that contain CCK (CCKBC) and the axon terminals of pyramidal neurons (Karson et al, 2009; Eggan et al, 2010; Katona et al, 2006). However, there is a much higher density of CB1R's in the axon terminals of CCK basket cells than of pyramidal cells (Katona et al, 1999; Katona et al, 2001; Hajos et al, 2000). The inhibitory axon terminals from CCKBC neurons make direct synaptic contact with both pyramidal neurons and parvalbumin basket cell neurons (PVBC) (Karson et al, 2009; Eggan et al, 2010) and CCK activates PV cells directly via cholecystokinin B (CCK2) receptors (Foldy et al, 2007). Activation of CB1Rs as a result of cannabis use suppresses GABA release from CCK neuron axon terminals onto pyramidal neurons (Klausberger et al, 2005), and CCK basket neurons also regulate pyramidal neuron activity (Karon et al, 2009; Foldy et al, 2007; Karon et al, 2008). A such, exogenous cannabinoids in the form of cannabis broadly suppress CCK neuron-mediated inhibition of pyramidal neurons and parvalbumin neurons and lack the tightly regulated, spatiotemporal selectivity that endocannabinoids have. These findings suggest a plausible biological mechanism through which exposure to cannabis, which results in nonphysiological activation of CB1Rs, could modify the maturation of PVBCs and shift the balance of perisomatic inhibition to a pathologic state, leading to disruptions in γ oscillations and working memory (Curley and Lewis, 2012).

Similar to the CB1 receptor [184], the α7nAChR are presynaptic receptors and modulate the release of GABA, dopamine, noradrenaline and serotonin neurotransmitters, however in contrast to CB1 it enhances their release [185]. Hence, the α7nAChR share a number of functions with the CB1R including learning, memory or nicotine addiction [182].

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dec 28, 2004
~ 13 years ago