Pharmacological differences between memory consolidation of habituation to an open field and inhibitory avoidance learning.

M.R.M Vianna,I Izquierdo,L.A Izquierdo,J.H Medina,C Rodrigues,M.M De Souza,M.K Sant'Anna,D.M Barros

doi:10.1590/s0100-879x2001000200011

Abstract

Rats implanted bilaterally with cannulae in the CA1 region of the dorsal hippocampus or the entorhinal cortex were submitted to either a one-trial inhibitory avoidance task, or to 5 min of habituation to an open field. Immediately after training, they received intrahippocampal or intraentorhinal 0.5-microl infusions of saline, of a vehicle (2% dimethylsulfoxide in saline), of the glutamatergic N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphono pentanoic acid (AP5), of the protein kinase A inhibitor Rp-cAMPs (0.5 microg/side), of the calcium-calmodulin protein kinase II inhibitor KN-62, of the dopaminergic D1 antagonist SCH23390, or of the mitogen-activated protein kinase kinase inhibitor PD098059. Animals were tested in each task 24 h after training. Intrahippocampal KN-62 was amnestic for habituation; none of the other treatments had any effect on the retention of this task. In contrast, all of them strongly affected memory of the avoidance task. Intrahippocampal Rp-cAMPs, KN-62 and AP5, and intraentorhinal Rp-cAMPs, KN-62, PD098059 and SCH23390 caused retrograde amnesia. In view of the known actions of the treatments used, the present findings point to important biochemical differences in memory consolidation processes of the two tasks.

Highlights

Habituation to a novel environment is believed to be one of the most elementary forms of learning, in which the decreased exploration as a function of repeated exposure to the same environment is taken as an index of memory [1,2]
Long-term memory consolidation of inhibitory avoidance begins by activation of N-methyl-D-aspartate (NMDA), D,L-a-amino-3-hydroxy-5-methyl-4-isoxalone propionate (AMPA) and metabotropic glutamate receptors [3,6,14], followed by activation of calcium-calmodulin dependent protein kinase II (CaMKII) [5,15,16,17], protein kinase C (PKC) [6] and mitogen-activated protein kinase kinase (MAPKK)
In the present investigation we studied the effect of the post-training intrahippocampal or intraentorhinal administration of several drugs known to act upon the core mechanisms of consolidation of inhibitory avoidance, both on that task, and on the retention of a 5-min session of habituation to an open field

Summary

Introduction

Habituation to a novel environment is believed to be one of the most elementary forms of learning, in which the decreased exploration as a function of repeated exposure to the same environment is taken as an index of memory [1,2] This is normally studied in two or more brief sessions of exposure to an open field or similar environment [1,2,3,4,5]. Mediately after acquisition [7] and lasts several hours [6,7,8,9] It coexists with, but is not dependent upon, short-term memory processes, which operate through biochemical systems of their own [10,11,12]. Long-term memory consolidation of inhibitory avoidance begins by activation of N-methyl-D-aspartate (NMDA), D,L-a-amino-3-hydroxy-5-methyl-4-isoxalone propionate (AMPA) and metabotropic glutamate receptors [3,6,14], followed by activation of calcium-calmodulin dependent protein kinase II (CaMKII) [5,15,16,17], protein kinase C (PKC) [6] and mitogen-activated protein kinase kinase (MAPKK)

Methods

Results

Conclusion