Effects of dehydroepiandrosterone on passive avoidance in ovariectomized female rats of different age

The aim of the present work was to study the influence of long-term treatment with dehydroepiandrosterone (DHEA) in doses of 0.1 and 0.7 mg/kg, i.p. on the passive avoidance performance in the ovariectomized female rats of 5- and 18-month old. The results obtained indicated that DHEA administration during 7 days in dose of 0.1 mg/kg normalized the passive avoidance performance in the ovariectomized rats of 5-month old while DHEA administration during 7 days in dose of 0.7 mg/kg restored passive avoidance performance in the ovariectomized rats of 18-month old.     

Effects of neurotensin on active and passive avoidance performance in rats with lesions of serotoninergic neurons

After a lesion of serotoninergic neurons performed by administration of 5.7-dihydroxytriptamine into the dorsal raphe nucleus, effects of neurotensin microinjections into the substantia nigra on rat behavior were investigated. Serotoninergic lesions resulted in enhanced fear of rats manifested as an increase in the number of intersignal avoidance reactions and intensification of escape reactions. Neurotensin microinjections into the substantia nigra diminished the neurotoxin action thus increasing the adaptive character of defensive behavior of rats with deficit of functions of serotonin neurons.     

Hippocampal MMP-3 elevation is associated with passive avoidance conditioning

Alterations in synaptic efficiency that underlie learning and memory consolidation appear to require an accompanying reconfiguration of the extracellular matrix (ECM). This restructuring of the ECM is carried out, in part, by a family of enzymes called, the matrix metalloproteinases, which includes matrix metalloproteinase-3 (MMP-3: stromelysin-1). The present study determined that a transient elevation in hippocampal MMP-3 expression occurred in rats following associative learning in the passive avoidance (PA) task. No change in MMP-3 was observed when rats were exposed either to the behavioral apparatus or the training stimulus alone. Furthermore, when an MMP-3 inhibitor was administered prior to PA training, dose-dependent learning deficits were observed, suggesting a causal relationship between learning-induced hippocampal MMP-3 elevation and associative memory formation. These findings suggest that increased hippocampal MMP-3 expression is an event that may play an important role in synaptic plasticity and memory consolidation.     

The effect of training conditions on passive avoidance performance in rats

Male outbred rats were trained for step-through avoidance in different experimental conditions: 1) in a two-compartment chamber with a small dark compartment and a chamber with illuminated suspended platform; 2) with or without acquaintance with experimental chamber 24 hours prior to learning; 3) with or without a possibility of the chamber exploration 3 min immediately before training procedure; 4) with inescapable or escapable pain reinforcement (5 electric footshocks, 0.45 mA, 1 s, with 2-s between-shock intervals); 5) with 2 or 5 inescapable footshocks of the same rate, duration, and intensity. The acquired performance was tested 24 h after training. It was shown that the procedure of exploration of the experimental chamber 24 prior to training improved the reproduction and the same procedure conducted immediately before training impaired the reproduction of the acquired behavior. Different training conditions improved the reproduction of the acquired behavior in the chamber with a suspended platform to a greater extent than in the two-compartment chamber. The decrease in the number of pain stimuli from 5 to 2 or the possibility to escape the punishment during training did not significantly change the reproduction.     

Effects of beta-casomorphin-5 on passive avoidance response in mice

The effects of intracerebroventricular (i.c.v.) injection of bovine beta-casomorphin-5 (beta-CM-5: Tyr-Pro-Phe-Pro-Gly), a micro-opioid agonist derived from milk beta-casein, on step-down type passive avoidance tasks were investigated in mice. Intracerebroventricular administration of a high dose (10 microg) of beta-CM-5 produced a significant decrease in step-down latency. beta-Funaltrexamine (5 microg, i.c.v.) almost completely reversed the beta-CM-5-induced shortening of step-down latency, although neither naltrindole (5 ng, i.c.v.) nor nor-binaltorphimine (5 microg, i.c.v.) had any significant influence on the effect of beta-CM-5. Meanwhile, a low dose (0.5 microg, i.c.v.) of beta-CM-5 inhibited scopolamine (1 mg/kg)-induced impairment of passive avoidance response. These results indicated that a high dose of beta-CM-5 induces amnesia, whereas a low dose ameliorates scopolamine-induced amnesia.     

Cholecystokinin octapeptide, proglumide, and passive avoidance in rats

Rats were conditioned to avoid a darkened chamber using electric footshock (0.25 mA for 2 sec). Cholecystokinin octapeptide (CCK-8), a CCK-8 antagonist proglumide, or 0.9% NaCl solution was injected immediately following the footshock to study the effect upon passive avoidance behavior. The passive avoidance behavior was observed one day following the conditioning footshock and treatment. CCK-8 produced a reduction of the passive avoidance latency of rats at doses ranging from 30 micrograms/kg to 500 micrograms/kg. Proglumide (5 mg/kg) was able to block the CCK-8 effect on rat passive avoidance conditioning. Proglumide by itself at a dose of 2 mg/kg decreased the latency to enter the darkened chamber. Endogenous CCK-8 activity may be involved in passive avoidance conditioning in rats.     

The retroactive action of paradoxical sleep deprivation and immobilization stress on the mechanisms of memory and passive avoidance in rats

Influence was studied of 48-hours deprivation of paradoxical sleep (DPS) and immobilization stress on conditioned reaction of fear and security--components of passive avoidance conditioned reflex (CRPA), with simultaneous studying of vertical, horizontal activity, grooming reactions and defecations in an illuminated chamber. The obtained results allow to conclude that DPS inhibits reproduction of memory traces of fear reaction but intensifies the process of learning and activity of memory traces of security reaction. Depending on condition of CRPA elaboration, DPS may disturb or, on the contrary, prolong preservation of passive avoidance. It has been found that the immobilization stress does not influence CRPA preservation and does not weaken the reaction of fear but increases the horizontal activity. It is suggested that the observed changes in behaviour and trace processes are connected with disturbance of sensory informational homeostasis of the nervous system at DPS.     

Impaired passive avoidance acquisition in Wistar rats after restraint/cold stress and/or stresscopin administration

Stresscopin (SCP) and related peptides are new members of the corticotropin-releasing factor (CRF) peptide family that are selective ligands for CRF type 2 receptor; these ligands are essential for maintaining homeostasis after stress. SCP (i.p. injections) was tested on the passive avoidance learning task in stressed Wistar rats; it impaired the formation of memory trace. The retention performance deficit induced by SCP was comparable with the deficit induced by the stressor of restraint/cold. More profound impairment of avoidance response occurred following combined application of SCP and stressor. More specific actions of SCP can be expected from its studies with targeted intracerebral applications.     

Pregnene-type steroids and impairment of passive avoidance behavior in rats.

Several pregnene-type steroids, such as progesterone, 19-norprogesterone, dydrogesterone, hydroxydione, corticosterone, deoxycorticosterone, cortisone, and hydrocortisone, were tested on passive avoidance behavior. All steroids except dydrogesterone resulted in an impairment of passive avoidance behavior as shown by decreased avoidance latencies, whereas cortisone appears to have only a weak effect in this respect.     

Effects of oxytocin and vasopressin on retrieval of passive avoidance response in melatonin-treated and/or pinealectomized male rats

The role of the pineal gland and its hormone-melatonin-as to the impact of vasopressin (VP) and/or oxytocin (OT) on the regulation of behavior was studied, the passive avoidance task being chosen as an experimental model. The results showed that VP facilitated the avoidance latency during the first retention trial; after pinealectomy, however, VP was ineffective in this regard. Intraperitoneal application of OT was ineffective in modifying the passive avoidance latency when compared with respective saline-treated animals. Melatonin alone, when injected to shamoperated animals 30 min before behavioral experiment, did not affect the passive avoidance response in SA- or OT-treated rats, but blocked the VP-induced lengthening of the passive avoidance latency in the first retention trial. In pinealectomized and OT-treated animals the passive avoidance latency during the second retention trial was severely diminished by melatonin when compared to respective control. We conclude that: a) VP needs a regulated pineal function for developing short-term effects on the passive avoidance response and b) the effect of OT on the avoidance latency in pinealectomized rats develops after melatonin treatment as a long-term effect.     

Effects of cholecystokinin-related peptides on retention of passive avoidance behaviour

Effects of intraperitoneal administration of cholecystokinin (CCK)-related peptides were studied on retention of single-trial learning passive avoidance behaviour. The COOH-terminal octapeptide of CCK (CCK-1-8-SE), the unsulfated octapeptide (CCK-1-8-NS), as well as the COOH-terminal tetrapeptide of CCK (CCK-5-8), administered immediately after the learning trial, facilitated passive avoidance behaviour. The data indicate that these peptides may influence memory consolidation processes.     

Optimizing action of synthetic peptide Selank on active avoidance conditioning test in rats

The action of a synthetic peptide Selank on learning and memory in active avoidance conditioning test was studied in rats with initially low learning ability and normal animals. The peptide was administered repeatedly 15 min prior the training session (4 days). The effect of Selank (300 micrograms/kg) was compared to that of Pyracetam (400 mg/kg). Selank was found to significantly improve learning in rats with low level ability even after a single administration on the first day of training session. The effect progressively increased with repeated Selank treatment: the total numbers of reactions and correct reactions increased, and the number of errors decreased (p < 0.05). In normal rats, the effect was maximal on the third day of treatment and training, i.e., after the completed initial consolidation. Some distinguishing features were revealed in the dynamics of activatory effects of Selank and Pyracetam. These data together with the evidence for ansiolytic effect of Selank show that this drug is promising for optimization of mnestic functions under conditions of high emotional stress.