ArticleChanges in rat brain cannabinoid binding sites after acute or chronic exposure to their endogenous agonist, anandamide, or to δ9-tetrahydrocannabinol
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Synaptic changes induced by cannabinoid drugs and cannabis use disorder
2022, Neurobiology of DiseaseEarly-life stress exacerbates the effects of WIN55,212-2 and modulates the cannabinoid receptor type 1 expression
2021, NeuropharmacologyCitation Excerpt :Nevertheless, in the present study, the total number of CB1 immunorreactive cells in granular layer of cerebellum remained unaltered. Although we did not find changes in the number of CB1-positive Purkinje cells, we could not discard changes in the affinity of their binding sites (Romero et al., 1995). Contrasting with the results obtained before the antagonist injection, SR141716A injected animals show no differences in the number of CB1-positive Purkinje cells, which could indicate a possible compensatory mechanism that increases the number of CB1-positive cells in the cerebellum.
Endogenous and synthetic cannabinoids induce the downregulation of cannabinoid CB1 receptor in retina
2019, Experimental Eye ResearchCitation Excerpt :Previous reports had suggested that subchronic/chronic administration of AEA produced differential adaptive changes in brain areas. In an earlier study in brain, it was shown that acute and chronic exposure to AEA led to differential effects in Bmax and Kd of [3H]CP-55,940 binding in different brain areas, none of which was the attenuation of receptor density (Romero et al., 1995). Rubino et al. (2000) reported that chronic administration of AEA reduced agonist stimulated [35S]-GTPγS in brain areas, yet downregulation of the receptor was not observed.
Long lasting effects of chronic WIN55,212-2 treatment on mesostriatal dopaminergic and cannabinoid systems in the rat brain
2018, NeuropharmacologyCitation Excerpt :In contrast, the acute WIN55,212-2 administration did not elicit any changes in CB1R binding sites in the aforementioned brain areas, proposing the existence of distinct regulatory mechanisms controlling CB1R adaptation after chronic and acute agonist treatment. Our results agree with previous studies demonstrating widespread desensitization of CB1R-mediated G-protein activation and down-regulation of CB1R binding after long-term, but not acute, administration of Δ9-THC, WIN55,212-2 or CP55,940 (Romero et al., 1995, 1997; Sim-Selley, 2003; Sim-Selley et al., 2006). Moreover, in the striatum and midbrain of regular marijuana users, CB1R binding capacity was reduced compared with non-users in postmortem human brains (Villares, 2007).
Reduced Brain Cannabinoid Receptor Availability in Schizophrenia
2016, Biological PsychiatryCitation Excerpt :However, the authors reported an increase in CB1R only in the cerebellum, a finding that would be consistent with the findings of the current study. Nicotine does not appear to have a direct effect on CB1R but exposure to nicotine may alter eCB levels (58,59), and elevated eCBs, in turn, can alter CB1R binding capacity by enhancing affinity (acutely) and increasing receptor density (chronically) (60). Thus, it is conceivable that chronic tobacco smoking is associated with increased CB1R availability, as was observed in our study.
Cannabinoids and schizophrenia
2015, Cannabinoids in Neurologic and Mental Disease