title: The interactive role of CB(1) and GABA(B) receptors in hippocampal synaptic plasticity in rats.
abstract: Long-term potentiation (LTP) of synaptic transmission is a cellular process underlying learning and memory. Cannabinoids are known to be powerful modulators of this kind of synaptic plasticity. Changes in GABAergic inhibition have also been shown to affect synaptic plasticity in the hippocampus. GABA receptor type B (GABAB) and cannabinoid receptor type 1 (CB1) exhibit overlapping anatomical localization in some brain areas including the hippocampus. CB1 and GABAB are also localized to the same cells and share a common signaling pathway in some brain areas. In this study, we examined the hippocampal effects of co-administrating AM251 and CGP55845, which are CB1 and GABAB antagonists, respectively, on LTP induction in the dentate gyrus (DG) of rats. LTP in the hippocampal area was induced by high-frequency stimulation (HFS) of the perforant path. Our results showed that HFS coupled with administration of the CB1 antagonist increased both the population spike (PS) amplitude and field excitatory post-synaptic potential (fEPSP). Conversely, the GABAB antagonist decreased these parameters along with decreased LTP induction. We also demonstrated that the co-administration of CB1 and GABAB antagonists had different effects on the PS amplitude and fEPSP slope. It is likely that GABAB receptor antagonists modulate cannabinoid outputs that cause a decrease in synaptic plastisity, while in the simultaneous consumption of two antagonists, CB1 antagonists can alter the release of GABA which in turn results in enhancement of LTP induction. These findings suggest that there are functional interactions between the CB1 and GABAB receptor in the hippocampus.
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
authors.forename: Masoumeh
authors.initials: M
authors.lastname: Nazari
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. Electronic address: Komaki@umsha.ac.ir.
authors.forename: Alireza
authors.initials: A
authors.lastname: Komaki
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
authors.forename: Ruhollah
authors.initials: R
authors.lastname: Karamian
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
authors.forename: Siamak
authors.initials: S
authors.lastname: Shahidi
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
authors.forename: Abdolrahman
authors.initials: A
authors.lastname: Sarihi
authors.affiliation: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
authors.forename: Masoumeh
authors.initials: M
authors.lastname: Asadbegi
mesh_terms: D000818:Animals; D063387:Cannabinoid Receptor Antagonists / Q000494:pharmacology; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D058788:GABA-B Receptor Antagonists / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010721:Phosphinic Acids / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D017208:Rats, Wistar; D043884:Receptor, Cannabinoid, CB1 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018080:Receptors, GABA-B / Q000378:metabolism*
chemical_list: D063387:Cannabinoid Receptor Antagonists; C543264:Cnr1 protein, rat; D058788:GABA-B Receptor Antagonists; D010721:Phosphinic Acids; D010880:Piperidines; D011412:Propanolamines; D011720:Pyrazoles; D043884:Receptor, Cannabinoid, CB1; D018080:Receptors, GABA-B; C085075:CGP 55845A; C103505:AM 251
keywords: AM251; CGP55845; Cannabinoid; GABAergic; Hippocampus; Long-term potentiation