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The dose-related effects of intravenous THC on auditory steady-state gamma coherence (40 Hz) at electrode Cz. FROM: Cortes-Briones, J.A., Skosnik, P.D., Mathalon, D., Cahill, J.D., Pittman, B., Williams, A., Sewell, R.A., Ranganathan, M., Roach, B.A., Ford, J., D’Souza, D.C. (2015). ∆9-THC Disrupts Gamma (γ)–Band Neural Oscillations in Humans. Neuropsychopharmacology. 40(9), 2124-34
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Illustration of the known locations of CB1Rs in the cerebellar cortex. CB1Rs primarily occupy glutamatergic granule cell axons (i.e. parallel fibers), and GABAergic stellate and basket cell axon terminals. Purkinje cells synthesize, release, and metabolize endocannabinoids, but do not express CB1Rs. FROM: Skosnik, P. D. (2011). Cannabinoids and the Cerebellum: A Potential Role in the Development of Psychosis, Marijuana and Madness, 2nd Edition, Cambridge University Press.
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Grand-averaged time X frequency plots demonstrating mean trial power (MTP) for midline electrodes during the perception of coherent motion for healthy controls and cannabis users. FROM: Skosnik, P. D., Krishnan, G. P., D’Souza, D. C., Hetrick, W. P., and O’Donnell, B. F. (2014). Disrupted Gamma-Band Neural Oscillations During Coherent Motion Perception in Heavy Cannabis Users. Neuropsychopharmacology. 39(13), 3087-99.
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The effect of endogenous and exogenous cannabinoids on synaptic transmission in the DLPFC. GABA release induces on-demand postsynaptic synthesis of endocannabinoids, which act in a retrograde manner to inhibit presynaptic GABA release by binding to CB1Rs. CB1Rs then inhibit the release of GABA by decreasing Ca2+ influx into the presynaptic neuron via the inhibition of adenylate cyclase and N-type Ca2+ channels. After the application of CB1R agonists such as THC, CB1Rs may become overactive, disrupting DSI and longer forms of synaptic plasticity such as LTP and LTD. This could affect neurocognitive processes such as WM. Abbreviations: dorsolateral prefrontal cortex (DLPFC); gamma aminobutyric acid (GABA); glutamate (GLU); central cannabinoid receptor 1 (CB1R); ∆-9-tetrahydrocannabinol (THC); depolarization induced suppression of inhibition (DSI); long-term potentiation (LTP); long term-depression (LTD); dopamine (DA). FROM: Skosnik, P. D., Ranganathan, M., and D’Souza, D. C. (2012). Cannabinoids, Working Memory and Schizophrenia. Biological Psychiatry. 71(8), 662-3.