tkadm30 Posted January 18, 2017 Share Posted January 18, 2017 (edited) The effects of cannabinoids on neural communication (synaptic plasticity) are poorly understood. Does cannabinoids (THC) fine-tune or disrupt neural oscillations in the gamma range? I find the hypothesis that THC may disrupt neural oscillations pretty much obsolete as there no evidences of disruption of synchrony by exogenous THC administration. Edited January 18, 2017 by tkadm30 Link to comment Share on other sites More sharing options...
CharonY Posted January 18, 2017 Share Posted January 18, 2017 How do you define "fine tune"? What specific adjustment would improve physiological responses and at which point would you consider it a disruption? Most publications discussing disruptions of gamma band oscillations by THC are fairly recent do you have a key publication that directly refutes that? We can start with this one here: Cortes-Briones et al Neuropsychopharmacology 2015 40(9). With the free version here. Link to comment Share on other sites More sharing options...
tkadm30 Posted January 18, 2017 Author Share Posted January 18, 2017 How do you define "fine tune"? What specific adjustment would improve physiological responses and at which point would you consider it a disruption? Most publications discussing disruptions of gamma band oscillations by THC are fairly recent do you have a key publication that directly refutes that? We can start with this one here: Cortes-Briones et al Neuropsychopharmacology 2015 40(9). With the free version here. I'm thinking of dopaminergic "fine-tuning" as a dopamine-mediated enhancement of synchrony in the gamma range. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697121/ Link to comment Share on other sites More sharing options...
tkadm30 Posted January 19, 2017 Author Share Posted January 19, 2017 Can THC, as a CB1 partial agonist, modulate dopamine cross-talk and synchrony in the gamma range? Link to comment Share on other sites More sharing options...
tkadm30 Posted January 24, 2017 Author Share Posted January 24, 2017 (edited) Dopamine/CB1 receptor cross-talk = fine-tuning of dopamine D2 receptors = enhances cAMP activity "Concurrent stimulation of cannabinoid CB1 and dopamine D2 receptors enhances heterodimer formation: a mechanism for receptor cross-talk?" http://molpharm.aspetjournals.org/content/67/5/1697.short cAMP is a promoter of calcium-dependent synaptic exocytosis. Edited January 24, 2017 by tkadm30 Link to comment Share on other sites More sharing options...
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