PMC:3951193 / 72356-74807 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3951193","sourcedb":"PMC","sourceid":"3951193","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3951193","text":"Caffeine\nCo-administering caffeine and cannabis has a long history. Bell [272] claimed that oral administration of hashish with coffee increased the effects of cannabis, and at the same time diminished its duration. He proposed a pharmacokinetic mechanism—coffee promoted more rapid absorption of hashish.\nCaffeine and theophylline are antagonists of adenosine receptors. Adenosine receptors are tonically activated by adenosine, their endogenous ligand. Rodent studies indicate that A1-subtype adenosine receptors tonically inhibit CB1 activity [273]. Thus the antagonism of A1 receptors by caffeine and theophylline enhances eCB system function (e.g., activation of CB1 by 2-AG). Caffeine potentiated CB1-mediated activity stimulated by THC and WIN-55,212 in hippocampus slices [273]. Consistent with this, the simultaneous application of WIN-55,212 plus an A1 agonist produced less than additive stimulation of [35S]GTPγS binding in mouse cerebellar membranes [274].\nIn whole animals, however, caffeine's effects are biphasic and vary by dosage and acute versus chronic administration. In humans, the acute administration of caffeine decreases headache pain, but exposure to chronic high doses, ≥300 mg/day, may exacerbate chronic pain [275]. In rabbits, an acute dose of caffeine antagonized THC-induced changes in cortico-hippocampal electroencephalogram recordings [276]. In mice, chronic caffeine at high doses potentiated CB1-dependent stimulation by eCBs and HU210 at striatal GABAergic, but not glutamatergic, synapses [277]. A single dose or a subacute dose (one day of caffeine in water) rescued the sensitivity of GABAergic synapses to HU210 in mice exposed to chronic stress.\nChronic caffeine at moderate doses increased THC's effects on short-term memory in mice [278]. Surprisingly, CB1 density decreased in the caffeinated mice, measured by [3H]SR141716A binding. Cortical and hippocampal tissues also showed a decrease in WIN55,212-2-stimulated [35S]GTPγS binding, but this attenuation was not seen in THC-stimulated [35S]GTPγS binding. This highlights the fact that caffeine-induced changes observed in vitro do not necessarily reflect the effects of caffeine upon integrated brain circuitry in vivo. Lastly, acute antagonism of A1 with DPCPX did not modulate the effects of THC on short-term memory [278], which further supports our hypothesis that chronic and acute blockade of A1 receptors have different functional 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