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

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-µl 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 µg/side), of the calcium-calmodulin protein kinase II inhibitor KN-62, of the dopaminergic D 1 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.

Persistent Disruption of a Traumatic Memory by Postretrieval Inactivation of Glucocorticoid Receptors in the Amygdala

“…Indeed, several reports have shown that the memory loss observed after amnesic treatments applied following memory reactivation can either revert spontaneously (Lewis 1976;Judge and Quartermain 1982;Lattal and Abel 2004;Prado-Alcala et al 2006) or be restored by the administration of a reminder (Miller and Kraus 1977;Vianna et al 2001,Anokhin et al 2002Salinska et al 2004). Therefore, we tested whether the RU 38486-induced memory disruption was i) persistent over time and ii) resistant to the effect of reminders.…”

“…In contrast, previous studies have shown that a variety of reminders are effective in reinstating memories following amnesic treatments that targeted consolidation, reconsolidation or extinction of a conditioned response. (Lewis 1976;Miller and Kraus 1977;Mactutus and Riccio 1978;Mactutus et al 1980;Vianna et al 2001;Anokhin et al 2002;Millin et al 2001). However, it is possible that in the consolidation and reconsolidation experiments, the amnesic treatment may not have been sufficiently effective, and therefore may have caused a temporal shift rather than a disruption of the memory.…”

The Role of Muscarinic and Nicotinic Cholinergic Neurotransmission in Aversive Conditioning: Comparing Pavlovian Fear Conditioning and Inhibitory Avoidance

“…Pre-and posttraining lesions of the dorsal CA1 field or ventral CA3 field reduce consolidation of inhibitory avoidance learning (Martinez et al 2002). Similarly, posttraining infusions of the protein kinase A inhibitor Rp-cAMPs, the calcium-calmodulin kinase II inhibitor KN-62, and the NMDA receptor antagonist AP5 all reduce consolidation of inhibitory avoidance learning (Vianna et al 2001). Additionally, posttraining infusion studies indicate that the hippocampus is involved in consolidating contextual but not aversive aspects of inhibitory avoidance training.…”

Neuropharmacological activity of Eupatorium buniifolium aqueous extract in mice

“…The disruptive effects of DZ on learning and memory seem to be dependent on an interaction of this drug with benzodiazepine receptors (Nabeshima et al, 1990). Memory for inhibitory avoidance is processed by the hippocampus, entorhinal cortex and other brain regions (Vianna et al, 2001), which could be targets for EB.…”