Passive avoidance in rats and gerbils as a function of species-specific exploratory tendencies

Both muscarinic antagonists, such as scopolamine, and benzodiazepine receptor (BZR) agonists, such as diazepam, produce a reliable impairment in the performance of one trial passive avoidance. Such deficits are frequently interpreted as drug-induced amnesia. However, these deficits could also result from a learning impairment. The present experiments compared the effects of two BZR agonists, lorazepam (0, 0.125, 0.25, and 0.375 mg/kg, IP) and diazepam (0, 0.78, 1.56, and 3.13 mg/kg, IP) with the effects of two muscarinic antagonists, scopolamine (0, 0.6, 0.8 and 1.0 mg/kg, SC) and atropine (0, 15, 30 and 60 mg/kg, IP) on a multiple trial passive avoidance task. In this procedure, the rats were trained with a 5-min inter-trial interval until a learning criterion was achieved. Retention was assessed 24 h later. This enabled the effects of the drugs on the acquisition and the retention of a passive avoidance response to be dissociated. Both atropine and scopolamine produced a marked impairment in the acquisition of the passive avoidance response, but did not impair retention. In contrast, diazepam and lorazepam did not alter the acquisition of a passive avoidance response, but did produce a dose-dependent impairment of retention. These results therefore demonstrate a double dissociation between the effects of muscarinic antagonists and BZR agonists on the acquisition and retention of passive avoidance.

Reversible inactivation of the median raphe nucleus enhances consolidation and retrieval but not acquisition of passive avoidance learning in rats

Neonatal alcohol exposure reduces number of parvalbumin-positive interneurons in the medial prefrontal cortex and impairs passive avoidance acquisition in mice deficits not rescued from exercise

The effects of chronic ethanol consumption and withdrawal on passive avoidance task and serum cholinesterase level in rats

Three distinct nuclei of the chick forebrain--the intermediate medial hyperstriatum ventrale (IMHV), lobus parolfactorius (LPO), and paleostriatum augmentatum (PA)--show metabolic, morphological, and neurophysiological changes following training on a passive avoidance task, suggesting that these and other areas of the chick forebrain participate in memory formation for this task. Considerable evidence exists for lateralization of memory processes in the chick. Several experiments examined the effects of lesions in the IMHV on the ability of chicks to learn and retain the avoidance task. Pre-training bilateral lesions in the IMHV produced an impairment in avoidance responding tested three hours after training. Pre-training unilateral lesions in the left but not the right IMHV resulted in a similar impairment. However, bilateral IMHV ablations, given either 1 or 6 h post-training, did not impair retention. IMHV lesions did not impair retention of a simple escape learning task. These results are consistent with other studies that have examined the effects of bilateral IMHV lesions on acquisition of passive avoidance and extend these findings by demonstrating lateralization of acquisition involving the left IMHV. The results also suggest that, as early as one hour post-training, the IMHV is not necessary to retain the memory and indicate that other forebrain structures, possibly the LPO or PA, may maintain the memory trace following training. Hypotheses to account for these results and indications of future research are discussed.

Analysis of the avoidance learning deficit induced by the serotonin releasing compound p-chloroamphetamine

The hippocampus plays an important role in learning and memory, but the precise nature of that involvement remains uncertain. Transection of the perforant path, a primary input pathway to the hippocampus, has been shown to produce changes in reaction to novelty and acquisition of active avoidance; the nature and magnitude of these changes vary with lateral or medial perforant path damage. In a series of experiments on adult rats, the role of these pathways in spontaneous alternation, exploration, acquisition and extinction of conditioned responses, passive avoidance, and conditioned taste aversion was investigated. Lateral transection reduced exploration while medial transection facilitated acquisition of an active avoidance response; no effects were observed on any other measure. Results are discussed in terms of what perforant path damage might reveal regarding the interactions of the hippocampus with other brain regions.

Cysteinyl methyl ester of AVP(4–8), a potent agonist on the maintenance of passive avoidance in rats

Multiple retention deficit in passive avoidance in rats is eliminated by suprachiasmatic lesions

Active and passive avoidance learning in rats neonatally treated with intraventricular 6-hydroxydopamine

Effects of cadmium on memory processes in mice exposed to transient cerebral oligemia

Differential effects of electrical stimulation of amygdala, caudate-putamen or substantia nigra pars compacta on taste aversion and passive avoidance in rats

Rats of four age groups: young (30 days of age), adolescent (180 days of age), adult (365 days of age), and old (547 days of age) were trained on active and passive avoidance tasks. There was impaired acquisition and 30-day rentention of passive-avoidance learning in both young and old rats, compared to the intermediate age groups, and marked impairment of acquisition and retention of active-avoidance learning in the old rats. Learning impairment is thus associated with immaturity as well as senescence.

Three experiments examined the hypothesis that the effects of septal lesions and systemic injections of scopolamine on avoidance acquisition could be attributed to the effects of either of these treatments on adrenocorticotropic hormone (ACTH) secretion. Septal lesions and scopolamine facilitated 2-way conditioned avoidance response acquisition, and the lesions retarded passive avoidance acquisition. However, neither the injections of dexamethasone, a synthetic glucocorticoid which inhibited ACTH secretion as did septal lesions, nor injections of ACTH which mimicked the facilitatory effects of scopolamine on basal ACTH secretion, affected avoidance in these paradigms. Thus, the main hypothesis was not supported. The finding that scopolamine did not affect passive avoidance indicates that a cholinergic system may not be involved in mediating the suppressive effects of punishment.

Passive avoidance learning and retention, as well as locomotor and exploratory behaviors, were assessed in rats after intraventricular 192 immunoglobulin G-saporin injections on either Postnatal Day 1 (PND1) or PND7. PND1-lesioned rats were not significantly impaired on acquisition or retention of passive avoidance. PND7-lesioned rats acquired the task slower than controls, but retention was not affected. PND7-lesioned rats were less exploratory than controls and showed reduced wall rearing. Histological analysis of PND1- and PND7-lesioned rats revealed no neuronal degeneration in hippocampus or cortex. There was a marked reduction of choline acetyltransferase (ChAT) activity in the hippocampus, cortex, and septum in the PND7-lesioned rats and a slight but significant ChAT depletion in the cortex of PND1-lesioned rats. These data suggest that the cholinergic system is critical for the learning of passive avoidance and exploratory behaviors in the developing rat.