Involviment of the hippocampus, amygdala, entorhinal cortex and posterior parietal cortex in memory consolidation

A total of 182 young adult male Wistar rats were bilaterally implanted with cannulae into the CA1 region of the dorsal hippocampus and into the amygdaloid nucleus, the entorhinal cortex, and the posterior parietal cortex. After recovery, the animals were trained in a stepdown inhibitory avoidance task. At various times after training (0, 30, 60 or 90 min) the animals received a 0.5-mul microinfusion of vehicle (saline) or O.5 mug of muscimol dissolved in the vehicle. A retention test was carried out 24 h after training. Retention test performance was hindered by muscimol administered into both the hippocampus and amygdala at 0 but not at 30 min posttraining. The drug was amnestic when given into the entorhinal cortex 30, 60 or 90 min after training, or into the parietal cortex 60 or 90 min after training, but not before. These findings suggest a sequential entry in operation, during the posttraining period, of the hippocampus and amygdala, the entorhinal cortex, and the posterior parietal cortex in memory processing.

Memory consolidation of a habituation task: role of n-methyl-D-aspartate, cholinergic muscarinic and gaba-a receptors in different brain regions

The immediate post-training microinjection of the N-methyl-D-aspartate receptor antagonist amino-5-phosphonopenmtaanoic acid (5 ug) or of scopolamine, the cholinergic muscarinic antagonist (2 ug), into the dorsal hippocampus of rats caused retrograde amnesia for habituation to a novel environment, as measured by the number of rearings and crossings performed in a test session. In contrast, picrotoxin (0.08 ug), the indirect GABA-A antagonist, caused retrograde memory facilitation. Receptor agonist administered into the hippocampus had effects opposite to those of the respective antagonists: glutamate (5 ug) and oxotremorine (2 ug) enhanced memory and muscimol (0.03 ug) was amnestic. Aminophosphonopentanoic acid, scopolamine and picrotoxin had no effect when injected into the amygdala mor medial septum. Our result contrasted with the recent report of an inhibitory avoidance task in which these drugs, at the doses used here, were effective when injected post-training into any of the three structures. These findings suggest that similar neurotransmitter mechanisms operate in different brain regions in order to regulate memory consolidation processes; however, there is a specialization of these brain regions in relation to different types or components of memory