Evelin Lisete Schaeffer

Sequential Role of Hippocampus and Amygdala, Entorhinal Cortex and Parietal Cortex in Formation and Retrieval of Memory for Inhibitory Avoidance in Rats

The hippocampus and amygdala, the entorhinal cortex and the parietal cortex participate, in that sequence, both in the formation and in the expression of memory for a step‐down inhibitory avoidance task in rats. Bilateral infusion of AP5 or muscimol caused retrograde amnesia when given O min after training into both hippocampus and amygdala, when given or 180 min after training into the entorhinal cortex, or when given 180 min after training into the parietal cortex. Therefore, memory formation requires the sequential and integrated activity of all these areas mediated by glutamate NMDA receptors in each case. Pre‐test administration of CNQX 1 day after training into hippocampus and amygdala, 1 or 31 days after training in entorhinal cortex, or 1, 31 or 60 days after training in the parietal cortex temporarily blocked retention test performance. Therefore, 1 day after training, all these brain structures are necessary for retrieval; 1 month later, the hippocampus and amygdala are no longer necessary for retrieval but the entorhinal and parietal cortex still are; and 60 days after training only the parietal cortex is needed. In all cases the mechanisms of retrieval require intact glutamate AMPA receptors.

Different brain areas are involved in memory expression at different times from training.

Rats were trained in a step-down inhibitory avoidance task and tested for retention 1, 31, or 60 days later. Three to 7 days prior to testing, they were bilaterally implanted with cannulae in the CA1 region of the dorsal hippocampus and in the amygdaloid nucleus (H + A), in the entorhinal cortex (EC), and in the posterior parietal cortex (PPC). Ten minutes prior to testing, the animals received, through the cannulae, 0.5-microliter microinfusions of vehicle (20% dimethylsulfoxide in saline) or of 0.5 microgram of CNQX dissolved in the vehicle. A second test session was carried out 90 min after the first. CNQX blocked retention test performance when given into H + A 1 day after training but not later; when given into EC 1 or 31 days after training, but not later; and when given into PPC 1, 31, or 60 days after training. In all cases performance returned to normal levels in the second test session. The data suggest that H and A are involved in memory expression for only a few days after acquisition; that EC is involved in memory expression for up to 31, but less than 60, days after acquisition; and that PPC is involved in memory expression for up to at least 2 months after acquisition.

Sequential involvement of NMDA receptor-dependent processes in hippocampus, amygdala, entorhinal cortex and parietal cortex in memory processing

Rats bilaterally implanted with cannulae in the CA1 region of the dorsal hippocampus and/or in the amygdaloid nucleus, in the entorhinal cortex, and in the posterior parietal cortex, were trained in a step-down inhibitory avoidance task. At various times after training (immediately, 30, 60 or 90 min) they received, through the cannulae, 0.5 μl microinfusions of saline or of 5.0 μg of APS dissolved in saline. A retention test was carried out 24 h after training. Retention test performance was hindered by AP5 given into hippocampus, amygdala, or both hippocampus and amygdala immediately but not 30 min post-training. 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 at earlier times. The findings suggest a sequential entry in operation, in the post-training period, of NMDA-receptor mediated mechanisms involved in memory processing; first in hippocampus and amygdala, 30 min later in entorhinal cortex, and 30 min later in posterior parietal cortex.