Open field exposure "prevents" amnesia caused by blockade of either NMDA glutamate receptors or cholinergic muscarinic receptors in the juvenile and adult rat

SNITCOFSKY, MARINA; COLETTIS, NATALIA; KORNISIUK, EDGAR; CERCATO, MAGALÍ; BAEZ, VERÓNICA; AGUIRRE, ALEJANDRA; JERUSALINSKY, DIANA

Huerta Grande, Córdoba

Congreso; XXVIII Congreso Anual SAN; 2013

Sociedad Argentina de Investigación en Neurociencia

P { margin-bottom: 0.21cm; direction: ltr; color: rgb(0, 0, 0); widows: 2; orphans: 2; }P.western { font-family: "Times New Roman",serif; font-size: 12pt; }P.cjk { font-family: "Times New Roman",serif; font-size: 12pt; }P.ctl { font-family: "Times New Roman",serif; font-size: 12pt; } Muscarinic receptors (MAChR) or NMDA receptors (NMDAR) antagonism produced amnesia of an inhibitory avoidance (IA) to a mild footshock in the rat. We studied a previous open field (OF) exposure effect on adult and juvenile rats´ performance in IA, when either MAChR or NMDAR were blocked. Adult rats were to 1 or 2 OF sessions and trained in IA; the muscarinic antagonist scopolamine was immediately injected intrahippocampus (IH) and the IA long term memory (LTM) was assessed 24 h later: They expressed an IA LTM, while those not exposed to the OF were amnesic. Both adult and juvenile rats previously exposed to the OF showed an IA LTM, even though they received an intraperitoneal (IP) injection of scopolamine before IA training. It was reported an increase in hippocampal ACh release during and after OF exploration and reexposure. This increase could contribute to "prepare the substrate" (metaplasticity?) for synaptic plasticity, which would result in IA LTM. The blockade of hippocampal NMDAR channel with MK-801 during IA consolidation, though not during its acquisition in adult rats, caused amnesia, which was prevented by 2 OF sessions before IA training. Instead, IP MK-801 before IA training was amnesic in juvenile rats and this amnesia was also prevented by previous OF exposure. Based on these results and on recent findings of our lab (see Baez et al, SAN, 2013), we hypothesize that the OF substantially modifies NMDARs, facilitating synaptic plasticity and memory formation.