title: The GABAA receptor-mediated recurrent inhibition in ventral compared with dorsal CA1 hippocampal region is weaker, decays faster and lasts less.
abstract: Hippocampal functions appear to be segregated along the dorso-ventral axis of the structure. Differences at the cellular and local neuronal network level may be involved in this functional segregation. In this study the characteristics of CA1 recurrent inhibition (RI) were measured and compared between dorsal (DH, n = 95) and ventral (VH, n = 60) hippocampal slices, using recordings of suprathreshold field potentials. RI strength was estimated as the percentile decrease of the population spike (PS) amplitude evoked with an orthodromic stimulus (at the Schaffer collaterals) when preceded by an antidromic stimulus (at the alveus). Varying the interpulse interval (IPI) between the two stimuli, we estimated RI duration. Alvear stimulation produced significant PS suppression in both VH and DH at every IPI tested, from 10 to 270 ms. Moreover, gradually more oblique DH (but not VH) slices displayed increasing RI, which at IPIs < or = 125 ms was reversibly abolished by the GABAA receptor antagonist picrotoxin (10 microM). The GABAA-mediated RI, measured under the blockade of GABAB receptors, was weaker, decayed faster and lasted less in VH compared to DH slices, regardless of the slice orientation. Specifically, in VH compared to DH, the PS suppression at 20 ms was 34.4 +/- 4.5% versus 69.9 +/- 6.5% (P < 0.001), the time constant of RI decay was 29 +/- 2.4 versus 87.5 +/- 13.6 ms (P < 0.01) and the duration was 50 versus 125 ms (P < 0.001). Thus, GABAA-mediated RI may control the CA1 excitatory output less effectively in VH compared to DH. The observed dorso-ventral differences in RI contribute to the longitudinal diversification of the structure and may underlie to some extent the region-specificity of hippocampal functions.
authors.affiliation: Department of Physiology, Medical School, University of Patras, 26 504 Patras, Greece.
authors.forename: Theodoros
authors.initials: T
authors.lastname: Petrides
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Georgopoulos
authors.forename: George
authors.initials: G
authors.lastname: Kostopoulos
authors.forename: Costas
authors.initials: C
authors.lastname: Papatheodoropoulos
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018756:GABA Antagonists / Q000494:pharmacology; D006624:Hippocampus / Q000033:anatomy & histology* / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009943:Organophosphorus Compounds / Q000494:pharmacology; D019580:Perforant Pathway / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
chemical_list: D018756:GABA Antagonists; D009943:Organophosphorus Compounds; D010852:Picrotoxin; D011963:Receptors, GABA-A; C066430:CGP 35348