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PubMed1992

Duration of retrograde amnesia induced by tetrodotoxin inactivation of the parabrachial nuclei is inversely related to the intensity of footshock in rat's passive avoidance response.

Previous work has demonstrated that in rats post-trial bilateral functional blockade of the parabrachial nuclei by local injection of tetrodotoxin (10 ng in 1 microliter) partially disrupts retention of an overtrained passive avoidance response. The time-course of functional blockade disrupting effects on passive avoidance response has been studied by altering both the acquisition-tetrodotoxin injection interval and footshock intensity as independent variables. When week footshocks (0.8 mA) were delivered, functional ablation of the parabrachial nuclei was still effective when induced up to 8 days after acquisition training. On the other hand, when rats were shocked with the stronger stimuli (1.2 mA), 2 days after acquisition functional ablation was no longer effective. The results are discussed in terms of unconditioned stimulus (US) intensity and engram consolidation.

Amnesia, Retrograde↗
PubMed2001

Interpretations of retrograde amnesia: old problems redux.

Recent evidence indicates that an old memory reactivated by cueing becomes labile and vulnerable to an amnesic treatment. Although the 'reconsolidation' concept derived from these findings challenges the traditional consolidation theory, here we argue that the new concept suffers from some of the same limitations as the earlier model. We propose an alternative retrieval-based theory that accommodates the recent data, as well as other puzzling related observations.

Amnesia, Retrograde↗
PubMed1999

Novelty causes time-dependent retrograde amnesia for one-trial avoidance in rats through NMDA receptor- and CaMKII-dependent mechanisms in the hippocampus.

Exposure to a novel environment (an open field) for 2 min, 1 h after one-trial inhibitory avoidance training, hindered memory of the avoidance task measured 24 h later. The effect was seen regardless of the intensity of the avoidance training footshock. The effect was not seen if the exposure to novelty was carried out 5 min before, or 6 h after, the avoidance training, or if the animals did not perceive the open field as new and react accordingly. The amnesic effect of the novelty presented 1 h after avoidance training was blocked by the intrahippocampal infusion of D-2-amino-5-phosphono-pentanoic acid (AP5, 25 nmoles per side) or 1-(N, O-bis-[5-isoquinolinylsulphonyl]-N-methyl-L-tyrosyl)-4- phenylpiperazine (KN62, 100 micromoles per side) but not by that of C32H25N3O6 (KT5720, 90 micromoles per side) given 5 min before the novelty. In the open field there was habituation, measured by the decrease in exploration between the first and second minute. AP5 and KN62 impaired this habituation, but not KT5720. Exploration of the open field was similar in the groups exposed to the avoidance task 5 min later, or 1 h or 6 h before. Therefore, there was no reciprocity between the effect of the two tasks: novelty was amnesic for the one-trial avoidance task, but the opposite was not true. The amnesic effect of novelty appears to rely on N-methyl-D-aspartate (NMDA) receptor- and calcium/calmodulin-dependent protein kinase II (CaMKII)-dependent, but not on PKA-dependent, aspects of its habituation learning.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2003

An emotion-induced retrograde amnesia in humans is amygdala- and beta-adrenergic-dependent.

The influence of emotion on human memory is associated with two contradictory effects in the form of either emotion-induced enhancements or decrements in memory. In a series of experiments involving single word presentation, we show that enhanced memory for emotional words is strongly coupled to decrements in memory for items preceding the emotional stimulus, an effect that is more pronounced in women. These memory effects would appear to depend on a common neurobiological substrate, in that enhancements and decrements are reversed by propranolol, a beta-adrenergic antagonist, and abolished by selective bilateral amygdala damage. Thus, our findings suggest that amygdala-dependent beta-adrenergic modulation of episodic encoding has costs as well as benefits.

Adult↗