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PubMed1976

The effect of diethyldithiocarbamate on passive avoidance learning by chicks (Gallus domesticus).

Diethyldithiocarbamate (DDC), a competitive inhibitor of dopamine-B-hydroxylase, produced a dosage-related depletion of neural NE and impairment of passive avoidance learning in young chicks. Retention was not impaired, however, as shown by normal relearning of the task a day later, when the drug was no longer active. Perhaps, neural NE depletion impairs ability to inhibit responding and, thus, impairs passive or inhibitory avoidance learning indirectly. Alternatively, NE depletion may slow down learning by interfering with consolidation, but if the task is well learned, it is remembered.

Animals↗

PubMed1992

Effects of dopamine receptor agonists on passive avoidance learning in mice: interaction of dopamine D1 and D2 receptors.

The present study examined the effects of dopamine D1 and D2 receptor agonists on the acquisition stage of passive avoidance learning and on locomotor activity in mice. The D2 agonist, RU 24213 (1-10 mg/kg s.c.), and the non-selective agonist, apomorphine (0.3-3 mg/kg s.c.), but not the D1 agonist, SKF 38393 (1-10 mg/kg s.c.), impaired learning and activated locomotion. RU 24213 (1 mg/kg s.c.) was more effective in impairing learning than in activating locomotion. The concurrent administration of SKF 38393 (10 mg/kg i.p.) and RU 24213 (1 and 3 mg/kg s.c.) produced a synergistic effect in both behavioral situations. The D1 antagonist, SCH 23390 (0.025 mg/kg i.p.), slightly inhibited the effects of apomorphine and of the combination of SKF 38393 and RU 24213 on learning but not on locomotion. The D2 antagonist, (-)-sulpiride (40 mg/kg i.p.), completely blocked these effects in both situations. These results suggest that dopamine receptor agonists impair passive avoidance learning through the D2 receptor, and that D1 and D2 receptors act synergistically in this impairment, as they do in their effects on locomotion. The involvement of D1 and D2 receptors is qualitatively similar in each of these behaviors, although some small differences may exist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1987

Development of amygdaloid cholinergic mediation of passive avoidance learning in the rat. II. Nicotinic mechanisms.

Young rats 10-30 days of age received bilateral injections of antinicotinic and/or nicotinic agents into the lateral (L), the basolateral (BL), or the cortical (CO) amygdaloid nucleus, and were trained to learn a cool-draft stimulus passive-avoidance task, 17 min later. Mecamylamine produced age- and dose-dependent acquisition deficits; these deficits appeared on day 11, increased similarly after injections into any of the three nuclei until day 16, and decreased thereafter, more rapidly after administration into CO nucleus than after injections into L and BL nuclei. In the latter nucleus, the deficits had nearly disappeared on day 30. Nicotine injected alone induced slight facilitatory effects, significant at 20 days but not reliable at earlier stages. However, nicotine could hinder the antagonistic effects of mecamylamine, when given in combination, as early as the 11th day of age on. The results suggest the existence of nicotinic synaptic elements in the basal lateral part of the rat amygdala; however, these seem to play an important role in passive avoidance learning only during the early stages of ontogenesis.

Acetylcholine↗

PubMed1992

Comparative effects of carbamazepine, phenytoin, diazepam and clonazepam on inhibitory avoidance learning in mice.

Four antiepileptic drugs were investigated in an inhibitory avoidance task in mice. Following IP administration 30 min prior to training, carbamazepine (32 mg/kg), phenytoin (30-60 mg/kg), diazepam (2-8 mg/kg) and clonazepam (0.125-0.5 mg/kg) impaired retention. When administered 30 min prior to the retention test none of the drugs under investigation affected retention. The drugs did not affect latencies in the hot plate test. This indicates that in the case of pretraining drug administration effects on retention cannot attributed to elevated pain thresholds. Carbamazepine and phenytoin impaired avoidance learning at doses above those which prevent electroshock induced tonic hindlimb convulsions. Diazepam and clonazepam were effective at lower than anticonvulsant doses. The results of the study are relevant to the evaluation of CNS side effects of anti-epileptic drugs in mice.

Animals↗

PubMed1976

The effect of lithium chloride on one-trial passive avoidance learning in rats.

1 Expression of a one-trial passive avoidance learning response in rats was examined following injections of lithium chloride or sodium chloride before and after initial training and before the first day of testing. Five tests were given at daily intervals, 24 h after training being the time of the first test. 2. Lithium given before the first day of testing impaired response expression on the first and all subsequent days of testing; the rate of extinction was unaffected. 3. Given both before and immediately after initial training, lithium impaired response expression on the first day of testing but slowed down the subsequent rate of extinction, leading eventually to improved performance on the fifth day, as compared with placebo-treated control subjects. 4. The results are interpreted in the light of the hypothesis that lithium impaired the central processing of sensory information.

Animals↗

PubMed1985

Mediation of passive avoidance learning by nicotinic hippocampo-entorhinal components in young rats.

Young rats, 11, 16, and 20 days of age, received bilateral injections of three antinicotinic agents into the posteroventral hippocampo-subiculo-entorhinal area, and were trained to learn a cool-draft-stimulus, passive-avoidance task shortly after (17 min). Gallamine triethiodide had no action at low doses and provoked convulsions at higher concentrations. Pempidine tartrate produced age- and dose-dependent impairments of the passive avoidance, and was much more effective in younger groups (11 and 16 days) than at 20 days. alpha-bungarotoxin also induced dose-dependent deficits. These results, together with the mecamylamine-induced deficits already reported, suggest that nicotinic cholinergic synapses located in the posteroventral part of the hippocampal complex play a role in passive-avoidance learning in the young rat as soon as this type of conditioning is possible, but become relatively less important at older ages, when muscarinic mechanisms also become involved.

Age Factors↗

PubMed1986

Behavioral activity and active avoidance learning and retention in rats neonatally exposed to painful stimuli.

Twice daily for the first 15 days after birth, rats from the same litters were either placed for 5 sec on a hot plate (55 degrees C) (treated group), or on a plate maintained at body temperature (38 degrees C) (manipulated group). Controls were left undisturbed. When 90 days old, they were studied for pain threshold, open-field behavior, and two-way active avoidance learning and retention. Weight gain, pain threshold, open-field behavior, and active avoidance retention were not significantly different in the three groups. On the other hand, the rate of two-way active avoidance learning was significantly greater in treated rats. These results suggest that repeated neonatal exposure to painful stimuli, in rats raised under otherwise normal conditions, improves later active avoidance performance. The most likely mechanisms are discussed.

Acoustic Stimulation↗

PubMed1985

2-Amino-4-phosphonobutyric acid selectively blocks two-way avoidance learning in the mouse.

There seems to be ample evidence supporting the view that glutamate plays a significant role in the mammalian brain as a neurotransmitter. It is considered to be a likely transmitter candidate in one or more hippocampal pathways. Recently it has been visualized in excitatory, possibly glutamatergic, neurons in the hippocampus. Glutamate has been proposed to mediate memory formation. We wanted to see if blocking glutamate action by a specific glutamate antagonist could result in reduction of learning ability. 2-Amino-4-phosphonobutyric acid (APB) is an analogue of glutamic acid and has been used as a glutamate antagonist in electrophysiological studies on invertebrate neuromuscular junction, retina and hippocampus. We tested the influence of APB on the acquisition of two way avoidance learning in the shuttle box and on learning in the water maze. Our results show that intraperitoneal injection of APB led to a reduction in avoidance learning, whereas learning in the water maze was unaffected.

Aminobutyrates↗

PubMed1987

Passive-avoidance learning after medial septal lesions: effect of experience and the peripheral sympathetic nervous system.

Prior studies from our laboratory suggest that peripheral sympathetic ingrowth, which occurs in the hippocampus following medial septal lesions, is detrimental to the reaquisition of a spatial learning/memory task. To assess the generality of this finding we studied step-through passive-avoidance learning in animals with a medial septal lesion with or without superior cervical ganglionectomy under two experimental conditions. In the first condition, in which no prior experience with the task occurred, animals with a lesion demonstrated facilitation of learning. In the second condition, in which animals received pretraining with no shock prior to surgical manipulation, the behavior of animals with the lesion was similar to that of controls. No effect of ganglionectomy or initial sympathetic ingrowth was found in either condition. The results suggest that the effects of medial septal lesions on passive avoidance behavior are determined by the experimental condition and that early peripheral sympathetic ingrowth does not contribute either in a detrimental or beneficial fashion to passive avoidance learning.

Animals↗

PubMedDate not supplied

Enhanced passive avoidance learning and appetitive T-maze learning with post-trial rewarding hypothalamic stimulation.

Experiments were carried out to investigate the effects of post-trial reinforcing stimulation of the lateral hypothalamus on learning in rats. The reinforcing stimulation was always presented for a duration of 20--30 sec (0.2 sec on/0.8 sec off), and was administered either immediately, 30 sec delayed or 300 sec delayed after exposure to the learning situation. In experiment 1 post-trial stimulation led to improved passive avoidance learning of an alcove-avoidance task when presented 30 sec compared to immediately after the footshock. In Experiment 2 reversal learning of a one-way shuttle-box avoidance task was facilitated by 30 sec delayed, but not 300 sec delayed post-trial reinforcing stimulation. In Experiment 3 appetitive left-right discrimination was investigated using a T-maze task. Thirty sec delayed post-trial reinforcing stimulation presented contingent on errors facilitated learning of this task. Together, the 3 studies provide further support for the hypothesis that reinforcers directly influence labile memory processes (such as short-term memory) and thereby improve learning.

Animals↗

PubMed1979

Effects of fetal and early postnatal thiamin deficiency on avoidance learning in rats.

Thiamin deficiency was induced in two groups of young rats during two stages of growth: deficiency 1, from 8 days prepartum to 10 days postpartum or deficiency 2, from 1 to 18 days postpartum. The deficiency was reversed by thiamin injections for 5 days and return to a normal diet following which animals were tested at 35 days of age. Body weights at 21 and 36 days of age were not significantly reduced by the deficiency nor was brain weight affected. Activity levels were not significantly reduced by deficiency 1 but were reduced in deficiency 2. Both active and passive avoidance learning were significantly impaired in both deficiency 1 and 2, a finding which could not be attributed to alterations in pain sensitivity, motor ability or reduced activity levels. The results indicate that the developing brain is vulnerable to reduced thiamin intake and that the period of vulnerability may be different for activity and avoidance learning.

Aging↗

PubMedDate not supplied

Repeated toluene exposure and changes of response latency in shock avoidance learning.

Behavioral effects of repeated exposure to toluene were investigated. After 1, 3, and 6 weeks exposure to toluene at 1000 and 2000 ppm, all rats received shock avoidance training. Toluene-exposed rats could acquire shock avoidance learning and there was no significant difference between exposed rats and control rats. Analyzing response latencies (RLs) of avoidance responses, control rats shifted them to a longer RL and at last they learned to perform avoidance responses with specific RLs (3-4 sec). However, rats exposed to 1000 ppm toluene for 1 week and to 2000 ppm toluene for 1 week and 3 weeks, did not learn to respond with specific RLs. Rats exposed to 1000 ppm and 2000 ppm toluene for 6 weeks did not shift to longer RLs. It was suggested that repeated exposure to toluene vapor ranging up to 2000 ppm had no influence on the acquisition of shock avoidance learning, but caused some functional impairments of higher nervous functions.

Animals↗

PubMed1986

The effects of cholinergic drugs support an avoidance learning hypothesis of brief footshock-induced analgesia.

Rats were tested for tail-flick responses and then immediately subjected to footshock for 30 sec. This procedure induced analgesia, i.e. prolonged the latency of the tail-flick response, which was maximal immediately after the shock and decayed to normal levels within 2 hr. No analgesia occurred if either the analgesia test before the shock or the shock itself was omitted. The dependence of the analgesia on the association between the test before the shock plus the shock, suggests that this was a form of avoidance learning. The effects of drugs injected immediately after the shock were determined on latency of the tail-flick response, measured 2 hr later. Drugs known to improve memory, including physostigmine, pramiracetam and the muscarinic agonists, oxotremorine and RS 86, selectively induced analgesia in rats subjected to test before the shock plus the shock, thereby supporting a hypothesis of avoidance learning. Neostigmine and atropine methyl nitrate had no effect, indicating that the effects were mediated centrally. The learning effects were distinguishable from analgesia induced by drugs, since morphine increased analgesia regardless of the presence or absence of the test before shock or the shock. Also, naloxone, which had no effect per se, blocked analgesia induced by morphine but enhanced physostigmine-induced analgesia. Neither chlordiazepoxide nor D-amphetamine produced any changes in the latency of the tail-flick responses indicating that neither anxiolytic/muscle relaxant nor stimulant actions were involved.

Analgesia↗

PubMed1990

Effects of NMDA receptor antagonists on passive avoidance learning and retrieval in rats and mice.

The effects of NMDA antagonists on passive avoidance learning, shock sensitivity and locomotor activity were examined. Pre-training administration of the antagonists 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) in mice and rats resulted in impaired performance in a retention test 24 h later. No such impairment resulted from immediate post-training administration of either compound in either species. In addition neither compound, given only before the retention test, reduced the retention latencies of mice. In rats CPP was similarly ineffective whereas MK-801 reduced retention latencies, but only at a dose which significantly elevated locomotor activity at the time of the retention test. As assessed by vocalization threshold in mice and by the proportion of animals vocalizing in response to the passive avoidance training shock, neither compound produced analgesia. The vocalization threshold was, in fact, slightly reduced by both compounds. MK-801, but not CPP, stimulated locomotor activity in mice. These results indicate that in the passive avoidance task activation of NMDA receptors is involved in memory formation, but is not critical for the maintenance of memory or its retrieval.

Animals↗

PubMed1991

Genetic determinants of individual differences in avoidance learning: behavioral and endocrine characteristics.

Bidirectional genetic selection for good and poor active avoidance learning in a shuttle box has been carried out in three independent laboratories using remarkably similar discrete-trial training procedures. The resulting strains are known as the Roman High and Low Avoidance (RHA and RLA), the Syracuse High and Low Avoidance (SHA and SLA) and the Australian High and Low Avoidance (AHA and ALA) strains, respectively. An additional unidirectionally selected strain, known as the Tokai High Avoider (THA) strain was developed in Japan using a free-operant Sidman avoidance procedure in a Skinner box. This paper reviews the selection of the Syracuse strains, enumerates the various behavioral and endocrine characteristics of the strains, and compares them to the other similarly selected strains. The behavioral work suggests that genetic selection from diverse breeding stocks has resulted in common characteristics that differentiate the strains in the emotional, not learning, domain. The endocrine data, however, are somewhat at odds. The Syracuse strains differentiate one way with respect to endocrine function, and the Roman strains differentiate in the opposite way. We suggest, therefore, that the endocrine correlates are not tightly linked to the avoidance genotype. Genetic analysis of all of the selected strains for both the avoidance phenotype and the endocrine correlates will be needed to test this hypothesis.

Animals↗

PubMed1992

Effect of diazepam on successive negative contrast in one-way avoidance learning.

The effect of administration of diazepam on successive negative contrast in one-way avoidance learning was examined in rats. Contrast was induced by shifting rats from a large reward, 30 s spent in the safe compartment, to a small reward, 1 s spent in the safe compartment. IP administration of 2 mg/kg diazepam eliminated this negative contrast. Moreover, this effect is dose dependent, with doses of 2 and 2.5 mg/kg, but not 0.5 mg/kg, effective in reliably reducing contrast. These results suggest the existence of similar or common underlying mechanisms in both aversive and appetitive contrast effects; they are discussed in light of the current theories of frustrative nonreward and as a mean of studying the behavioral and biological mechanisms of anxiety.

Animals↗

PubMed1976

Stimulation of rat medial or sulcal prefrontal cortex during passive avoidance learning selectively influences retention performance.

Low-level unilateral electrical stimulation was delivered during passive avoidance learning through a bipolar electrode to the prefrontal cortex of the adult albino rat. No brain stimulation was applied during a retention test measured 24 h later. Ventromedial prefrontal cortex stimulation produced retention impairment over and above that observed with chronic electrode implantation. Sulcal cortex stimulation, in contrast, actually attenuated the retention deficit produced by chronic implantation in the sulcal cortex. Stimulation of an afferent common to both prefrontal regions, the dorsomedial thalamus, resulted in retention disruption, but stimulation of another common afferent, the locus coeruleus, did not. Acquisition of the inhibitory response was not affected by stimulation of any of the above brain regions. The present results demonstrate, again, that the functional role in memory of particular brain regions can be dissected by low-level electrical stimulation. The functional separation of rat sulcal and medial cortices revealed by the effects of stimulation suggests that these prefrontal subfields subserve different functions in the information storage process.

Animals↗

PubMed1990

Avoidance learning under hypo and hyperglycemia in rats.

Learning behaviour under different glycaemic conditions were studied in albino rats using an avoidance box. When insulin and glucose levels were low after fasting, animals showed delay in avoidance learning. But there was no change in acquisition of learning after hypoglacaemia induced by insulin. This difference in behaviour under hypoglycaemia of almost similar severity is possibly due to difference in its rate of induction and activation of counter regulatory neuro-endocrine mechanisms. Diabetic (alloxan) rats failed to improve learning. Besides, hyperglycemia, other factors like metabolic disturbances, cytotoxic effects of alloxan may have inhibited learning in this group. Hypo or hyperglycemia disturb the function of neuronal substrates responsible for learning and memory.

Animals↗