Passive Avoidance Behavior In Rats Research Articles

Serotoninergic mechanisms of the effects of neurotensin on passive avoidance behavior in rats

The aim of the present work was to identify the features of the actions of neurotensin on administration into the substantia nigra or dorsal cervical nucleus on the reproduction of passive avoidance reactions in rats. The results showed that the action of neurotensin administered into the substantia nigra was accompanied by sharp reductions in passive avoidance reactions, while administration into the dorsal cervical nucleus, conversely, led to increases in these reactions and slowing of their extinction. The effects of microinjections of the serotonin 5-HT(1A) receptor agonist 8-hydroxydipropylaminotetraline (8-OH-DPAT) into these brain structures were analogous to the effects of neurotensin. The different behavioral effects of administration of neurotensin corresponded to identifiable changes in the levels of serotonin and its metabolite 5-hydroxyindoleacetic acid in the caudate nuclei of the brain. These data led to the conclusion that the effects of neurotensin on passive avoidance behavior are associated with the regulation of the emotional state of the animals via actions on the functions of brain serotoninergic structures.

Effect of paradoxical sleep deprivation and stress on passive avoidance behavior

Previous studies have shown that several types of stress can induce memory impairment. However, the memory effects of paradoxical sleep deprivation (PSD), a stressor in itself, are unclear. We therefore compared passive avoidance behavior of rats undergoing PSD and PSD stress yoked-control (PSC) using the “reversed flowerpot method.” When rats were kept isolated on a PSC platform for 24 h immediately after criterion training, retention trials showed impaired aversive memory storage. When delayed for 24 h after criterion training, PSC stress did not disrupt retention performance. In rats subjected to PSD, either immediately or 24 h after criterion training, there was no disruption of aversive memory consolidation. These results suggest that, during stress, paradoxical sleep plays a role in erasing aversive memory traces, in line with the theory that we “dream in order to forget.”

Changes in the Concentration of NCAM in the Blood Serum after Amnesia of Passive Avoidance Behavior in Rats

Changes in the Concentration of NCAM in the Blood Serum after Amnesia of Passive Avoidance Behavior in Rats

Effects of combined block of α1-adrenoceptors and NMDA receptors on spatial and passive avoidance behavior in rats

The present study was designed to investigate the interactions between α 1-adrenoceptors and NMDA receptors in modulating spatial navigation and passive avoidance behavior in rats. Pretraining treatment with prazosin, an α 1-adrenoceptor antagonist, at 2 mg/kg i.p., impaired acquisition performance in a water maze navigation test and had no effect on passive avoidance behavior. Posttraining and pretest injections of prazosin had no effect on water maze or passive avoidance behavior. Pretraining treatment with ((±))-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), a competitive NMDA receptor antagonist, dose dependently (3 and 10 mg/kg) impaired passive avoidance and water maze behavior. Posttraining treatment with CPP had no effect on water maze and passive avoidance behavior. A pretraining combination of subthreshold doses of CPP (1 mg/kg) and prazosin (1 mg/kg) impaired water maze behavior. A combination of subthreshold doses of CPP (3 mg/kg) and prazosin (1 mg/kg) injected posttraining or pretest had no marked effect on water maze or passive avoidance performance. A control experiment showed that CPP 3 mg/kg or CPP 1 mg/kg and prazosin 1 mg/kg injected pretraining had no effect on cue navigation to a clearly visible platform, but CPP 10 mg/kg markedly impaired performance. The present results indicate that α 1-adrenoceptors and NMDA receptors may synergistically regulate acquisition of spatial navigation performance. Therefore, it would be interesting to study the effects of combined stimulation of α 1-adrenoceptors and NMDA receptors on age-related memory defects.

P-655 - Effect of newly synthesized analogue of [pGlu4,Cyt6]AVP(4-9) on passive avoidance behavior in rats.

P-655 - Effect of newly synthesized analogue of [pGlu4,Cyt6]AVP(4-9) on passive avoidance behavior in rats.

Effects of betahistine on locomotor activity and passive avoidance behavior in rats

Brain histaminergic and cholinergic systems are involved in the neuromodulation of cognitive functions and altered in some neuropsychiatric disorders such as Alzheimer's disease. In this study we have investigated the effects of betahistine dihydrochloride (BH) on locomotor activity (LA) and passive avoidance behavior (PAB) in control and scopolamine(SC)-treated male rats. In an open-field paradigm, BH increased LA at high doses and inhibited SC-induced hyperactivity at moderate ones, without effect on motor habituation. In an electronic maze paradigm, in which animals had to learn to avoid a 1.5 mA electric shock, BH reduced the number of trials required by SC-treated animals to learn to stay in a neutral platform during two consecutive trials. These results seem to indicate that BH influences basal and SC-induced locomotor activity, and attenuates the learning impairment caused by SC.

Effects of intracerebroventricular administration of calcitonin gene-related peptide on passive avoidance behaviour in rats

The effects of different doses of calcitonin gene-related peptide (CGRP) on passive avoidance behaviour were studied in male rats following its intracerebroventricular (i.c.v) administration. Treatment with doses of 200 ng, 300 ng, 500 ng or 1 μg was performed prior to learning, immediately and 6 h after the learning session and 30 min before the 24 h retention test. CGRP enhanced the avoidance latency in a dose-dependent manner at each time studied, with the exception of 6 h after the learning session. It is concluded that CGRP might be able to lengthen the passive avoidance latency by facilitating learning and memory formation.

The effects of receptor blockers on brain natriuretic peptide-32-induced action on passive avoidance behavior in rats

The effects of several doses of porcine brain natriuretic peptide-32 (pBNP-32) administered into the lateral brain ventricle were tested as regards the consolidation of passive avoidance learning in rats. The peptide was found to increase the passive avoidance latency in a dose-dependent manner. In order to clarify which transmitter systems might be involved in the action of pBNP-32, the experimental animals were pretreated with different receptor blockers in selected doses which did not influence the behavioral paradigm. Four of the receptor blockers (haloperidol, atropine, phenoxybenzamine and propranolol) effectively blocked the action of the peptide on the consolidation of passive avoidance learning. The other three (naloxone, bicuculline and methysergide) were ineffective. The results suggest that dopaminergic, cholinergic and α- and β-adrenergic mediations might be involved in the effects of pBNP-32 on the consolidation of passive avoidance learning in rats.

Effect of calcitonin gene-related peptide on passive avoidance behavior in rats. Role of transmitters.

Effect of calcitonin gene-related peptide on passive avoidance behavior in rats. Role of transmitters.

Differential effects of ACTH 4–10, DG-AVP, and DG-OXT on heart rate and passive avoidance behavior in rats

A computerized telemetry system was used to monitor heart rate (HR), core temperature (CT), and gross locomotor activity in rats treated with saline or neuropeptides during a passive avoidance behavior task. Rats were exposed to single mild footshock (0.15 mA, for 3 s). Retention tests were conducted at 24 and 48 h after the learning trial. One h prior to the 24-h retention test, each rat received one of the following treatments (SC): saline (SAL), desglycinamide [Arg 8]-vasopressin (DG-AVP), ACTH 4–10, or desglycinamide-oxytocin (DG-OXT), at a dose of 3 μg/rat for DG-AVP and DG-OXT, and 50 μg/rat for ACTH 4–10. Rats treated with SAL showed a modest increase in avoidance latency accompanied by bradycardia at both retention tests. Rats receiving DG-AVP retained the highest avoidance latency among the experimental groups at both the 24- and 48-h retention test. These rats showed a decrease in HR of the same magnitude as the SAL-treated animals at both retention tests. Rats treated with ACTH 4–10 showed an increase in avoidance latency during the 24-h but not during the 48-h retention test. In addition, following ACTH 4–10 treatment, a tachycardiac response was found during the 24-h retention test. DG-OXT induced both behavioral and cardiac responses opposite to those found in rats given DG-AVP. CT gradually increased while the rats remained on the platform, irrespective of the treatment. Changes in HR and CT were not influenced by somatomotor activity, as no difference in gross locomotor activity was found among the groups. As found previously, DG-AVP had a long-term and ACTH 4–10 a short-term effect on passive avoidance behavior. The finding that these peptides have opposite effects on HR, argues for different mechanisms of action—memory, respectively arousal—mediating these responses at both behavioral and autonomic levels. The finding that DG-OXT exerts actions opposite to those of DG-AVP further confirms its proposed role of an endogenous amnesic compound. Thus, it is concluded that neuropeptides differentially affect autonomic responses and behavior in rats.

The effects of receptor blockers on atrial natriuretic peptide-induced action on passive avoidance behavior in rats

In previous experiments, it was shown that rat atrial natriuretic peptide (rANP 1−28) is able to increase the passive avoidance latency in a dose-dependent manner in the learning and consolidation phase (3). In order to clarify whether ANP has a direct action on this behavioral paradigm, or whether the action is mediated by neurotransmitters, rats were pretreated with different receptor blockers. The selected doses of the different receptor blockers could themselves not influence the behavioral paradigms. Haloperidol or atropine blocked the action of ANP on the consolidation of the passive avoidance response. Phenoxybenzamine, propranolol, methysergide, bicuculline and naloxone were ineffective. The data suggest that dopaminergic and cholinergic mediations are involved in the action of ANP on the passive avoidance response.

Detection of the serotonin-modulated protein fraction and its role in organization of passive avoidance behavior in rats

Detection of the serotonin-modulated protein fraction and its role in organization of passive avoidance behavior in rats

Effect of calcitonin gene-related peptide on passive avoidance behaviour in rats. Role of transmitters

Effect of calcitonin gene-related peptide on passive avoidance behaviour in rats. Role of transmitters

Interactive effects of neurohypophyseal neuropeptides with receptor antagonists on passive avoidance behavior: mediation by a cerebral neurohypophyseal hormone receptor?

The neurohypophyseal neuropeptides (Arg8)-vasopressin (AVP) and [pGlu4,Cyt6]AVP-(4-8) (where pGlu is pyroglutamic acid and Cyt is cystine) facilitate the retention of one-trial-learning passive avoidance behavior in rats when administered into the cerebral ventricle immediately after the learning trial. The fragment [pGlu4,Cyt6]AVP-(4-8) was considerably more effective than AVP. Oxytocin (OXT) and [pGlu4,Cyt6]OXT-(4-8) have the opposite effect and attenuate passive avoidance behavior also when administered into the cerebral ventricle after the learning trial. Again the fragment was more active than the parent molecule. The ancient arginine-containing neurohypophyseal hormone vasotocin in "high" doses (10ng) had a vasopressin-like effect and in "low" doses (0.1 ng) had an OXT-like effect on passive avoidance behavior. Because both vasopressinergic (V1) and oxytocinergic receptors have been demonstrated in the central nervous system, we asked whether specific antagonists of the V1, V2, and OXT receptor could antagonize the effects of these neuropeptides on passive avoidance behavior. The three antagonists were approximately equally active in blocking the effect of vasopressin, whereas the fragment [pGlu4]AVP-(4-8) and the high dose of vasotocin were more readily blocked by the OXT antagonist. The attenuating effect of OXT, the fragment [pGlu4,Cyt6]OXT-(4-8), and the low dose of vasotocin was markedly reduced by the OXT antagonist. This effect could also be reduced by pretreatment with the V1 antagonist but not with the V2 antagonist. These results suggest the existence of a separate neurohypophyseal hormone receptor complex in the brain affecting memory processes that differs from the peripheral V1, V2, and OXT receptor.

The effects of atrial natriuretic peptide on passive avoidance behaviour in rats

The effects of rat atrial natriuretic peptide (ANP 1–28) on passive avoidance behaviour were tested following its administration into the lateral brain ventricle in rats. Different doses of ANP 1–28 were administered immediately after the learning trial of passive avoidance behaviour and the effects on the consolidation of learning were tested 24 h later. ANP 1–28, in doses in the range 50–2000 ng/rat, caused a dose-dependent increase in passive avoidance latency. Selected doses (100, 200 and 500 ng/animal) were given 30 min before the learning trial. These doses lengthened the passive avoidance latency in a dose-dependent manner. When the peptide was given 30 min before the retention trial, there was no significant alteration in passive avoidance response. The data suggest that ANP 1–28 is able to facilitate the learning and consolidation of fear-motivated passive avoidance behaviour.

Effect of dihydroergotoxine and cholinomimetics on passive avoidance behaviour in rats with disruption of cortical cholinergic innervation

Effect of dihydroergotoxine and cholinomimetics on passive avoidance behaviour in rats with disruption of cortical cholinergic innervation

Changes in heart rate and body temperature during passive avoidance behavior in rats

Heart rate, core temperature and gross locomotor activity during passive avoidance behavior in rats were recorded by a telemetry system connected to a computer data acquisition program. Passive avoidance latency and approach to the dark compartment were evaluated. Rats were assigned to five different groups, i.e., the shock groups that received different intensities of footshock (0.15, 0.25 and 1.0 mA, respectively, for 3 sec), a no footshock control group and a group that had no access to the dark compartment (i.e., no dark compartment control group). Retention tests were carried out 24 and 120 hr after the learning trial. Rats exposed to footshock showed a decrease in heart rate during the first 10 sec of the observation period in both retention tests. An average bradycardia was found in the lowest shock intensity group (0.15 mA) at both the 24- and 120-hr retention test whereas the other two groups (0.25 and 1.0 mA) showed a gradual increase in heart rate. This increase was more pronounced the longer the rats stayed on the platform. Similarly, a gradual rise in core temperature was observed in these rats as well as in the no dark compartment control group. The number of approaches to the dark compartment was significantly depressed in the group exposed to 1.0 mA footshock intensity. Gross locomotor activity was reduced in animals that exhibited maximum avoidance latency. Exposure of rats to the above-described behavioral paradigms induced autonomic activation resulting in changes in heart rate and temperature. These changes were not caused by gross locomotor activity and may thus be related to the various behavioral states. Differential activation of the sympathetic and parasympathetic components of the automatic nervous system in rats under different behavioral conditions are discussed.

Effect of fipexide on passive avoidance behaviour in rats

The effect of fipexide, administered at different intervals after the learning trial of a single step-through type passive avoidance situation was studied. The administration of fipexide immediately after the learning trial resulted in a long-lasting facilitation of passive avoidance behaviour. On the contrary, the administration of this compound 1 h prior to the retention test failed to influence passive avoidance behaviour. The results suggest that fipexide facilitates memory consolidation but does not influence retrieval processes.

Exponential data-analysis of passive-avoidance behavior in rats and mice

Data obtained with the passive-avoidance task are usually presented as the median values of the latencies to respond. In an earlier publication we described a better way of presenting such data based on the observation that the complement of the cumulative distribution of step-through latencies can be closely fitted by a simple exponential function. Thus the “step-through rate constant” (STRC) is concise and accurate quantitative description of population behavior in this test. In this paper we present two examples of the application of this procedure. In the first, variation in the interval between training and testing in rats changes the STRCs of the different groups. In the second (based on data published by Flood et al.) administration of cycloheximide is seen to partition the experimental population of mice into two subgroups with different STRCs.

Can vasopressin alone act as an unconditioned stimulus to produce passive avoidance behaviour in rats in a typical memory experiment?

The claim that vasopressin improves memory has been largely based on results obtained from shock avoidance experiments. In the majority of these studies, “memory” was defined operationally as the hesitation of a rat to enter the darkened compartment of a box in which it had once received an electric foot-shock. A single post-trial injection of arginine vasopressin (AVP) enhances such passive avoidance behaviour. In view of the recent demonstration that AVP has aversive effects, it was argued that vasopressin alone (without giving the rats foot-shock, prior to the peptide) might be a sufficient inhibitory stimulus to produce passive avoidance behaviour in a typlcal memory experiment. This hypothesis was tested in the present study. The results of these experiments indicate that a behaviourally active dose of AVP (10 μg/kg; s.c.) was a sufficient stimulus to produce passive avoidance behaviour in the rats. A small dose of AVP (1.25 μg/kg; s.c.) was without effect. However, AVP (10 μg/kg) was only effective with repeated administration (Experiment 1). This result is in contrast with the post-trial effect of the peptide on inhibitory avoidance behaviour, which is obtained with just one injection in the normal single trial step-through experiment. However, it was found that if the rats were injected with AVP (10 μg/kg) and placed in the dark compartment of the apparatus for 20 min, thereby ensuring that the animals made the explicit connection between the aversive effects of the peptide and the dark environment, they displayed avoidance behaviour after a single trial (Experiment 2). Thus, while it is unlikely that AVP (10 μg/kg) alone acts as the unconditioned inhibitory stimulus in a typlcal memory experiment, it is suggested that pairing the electric foot-shock with post-trial injection of AVP will tend to enhance the overall aversiveness of the paradigm, and hence facilitate passive avoidance behaviour.