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PubMed1999

Role of brain-derived neurotrophic factor and presynaptic proteins in passive avoidance learning in day-old domestic chicks.

The consolidation of a one-trial passive avoidance learning task in the day-old chick involves a number of transient and longer-term biochemical processes, including increased release of glutamate. This study demonstrated that brain-derived neurotrophic factor, a proposed modulator of synaptic transmission and neurotransmitter release, is involved in the cascade associated with memory consolidation in the chick and that its actions were linked to modulation of expression of SNAP-25, syntaxin and synaptophysin, required for exocytosis. Intracerebral injections of 5 microl of antibodies to brain-derived neurotrophic factor into the left and right intermediate medial hyperstriatum ventrale resulted in a dose-dependent reduction in avoidance of an "aversive" bead by 3 h after training. Neurotrophin antibodies (0.5 microg/chick) administered between 1 h before, and up to 30 min after, training induced amnesia by 3 h which was sustained for at least 24 h. Injections of recombinant brain-derived neurotrophic factor (50 microg/ml; 0.5 microg/chick) just before training maintained avoidance in birds trained with a weaker aversant (10% methylanthranilate), such that chicks showed enhanced recall at times (24 h) beyond that when shorter-term forms of memory have decayed. In lysed synaptosomal membranes prepared from chicks injected with antibodies to brain-derived neurotrophic factor there was a decrease in expression of SNAP-25 and syntaxin in the left, but not the right, intermediate medial hyperstriatum ventrale, a region known to be associated with memory formation, which correlated with the decrease in neurotrophin concentration. Thus, these data indicate that brain-derived neurotrophic factor is involved in the formation of a long-term memory for an aversive stimulus and may function as a modulator of presynaptic proteins associated with exocytosis, enabling increases in neurotransmitter release.

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↗
PubMed1992

Active avoidance learning in old rats chronically treated with levocarnitine acetyl.

The aging laboratory animal is recognized as a suitable experimental model for the investigation on drugs potentially able to retard the age-dependent decline in cognitive functions. There is robust evidence that levocarnitine acetyl (ALCAR), the acetyl derivative of carnitine, when administered chronically, prevents some age-related deficits of the central nervous system, mainly at the hippocampal level. On the basis of this evidence and because learning of active avoidance was demonstrated to become impaired with age, we decided to investigate the effect of ALCAR in rats. For statistical evaluation of results, the Cluster Analysis technique was chosen. This procedure pointed out the great heterogeneity of the old population and allowed the classification of the animals into homogeneous groups according to their response pattern. The effect of ALCAR was evident in the higher number of treated old animals yielding escape responses, indicating that ALCAR can preserve, at least partially, learning and memory from the natural decay occurring with age.

Acetylcarnitine↗
PubMed1975

Dose-response effects of d-amphetamine on passive avoidance learning in the rat.

Trials and errors to learning a passive avoidance response were assessed in 63 albino rats injected subcutaneously with d-amphetamine, in amounts ranging from 0-7 mg/kg body weight. Both measures indicated dose-response effects on responding; animals under either low or high doses of d-amphetamine made significantly less errors and took significantly fewer trials to learn the response than did middle dosage animals. The scores of the lower and higher dosage animals did not differ from the nondrug control group. Results are discussed in terms of amphetamine stereotypy.

Animals↗
PubMed1990

[The development of theories of avoidance learning and its application to behavioral pharmacology].

How the development of theories changed the definition of avoidance behavior was discussed. Three major theories of avoidance learning; the two-process theory, the species-specific defense reactions hypothesis, and the cognitive expectancy theory were reviewed. Very few innovations were brought to the experimental apparatuses and procedures by which these theories were tested. The paradigms have been applied without any theoretical considerations. Therefore, I claim here that the modification or renewal of experimental paradigms will be needed to make suitable animal models for psychopharmacology.

Animals↗
PubMed1998

Timed active avoidance learning in lurcher mutant mice.

Lurcher mutant mice (+/Lc) which exhibit a massive loss of neurons in the cerebellar cortex and in the inferior olivary nuclei were subjected to an active avoidance learning task; the animals' avoidance response must occur within a small time window after a short or a long delay. The control mice needed a mean of 8.3 sessions of 10 trials (short delay group) and of 11.8 sessions (long delay group) and showed good retention after a 24 h interval. When subjected to the same number of sessions, the +/Lc mice were unable to learn the timing task. However, a subgroup of lurcher mutants was able to learn after a high number of sessions (25.4 sessions as a mean). There was no intergroup difference in the standard version of one-way active avoidance. These results indicate that the cerebellar cortex is involved in time processing during active avoidance. The cerebellum may be part of a loop including the cerebral cortex known to be involved in time perception. An alternative explanation is that the cerebellar mutant animals had persevering tendencies acquired during performance of the one-way avoidance task.

Animals↗
PubMed1997

Relative importance of odour and taste in the one-trial passive avoidance learning bead task.

The relative importance of taste and odour cues in a one-trial passive avoidance learning (PAL) task was examined. One-day-old chicks were presented with a small bead and different combinations of the taste and odour of methyl anthranilate (MeA). The chicks had received three consecutive pretraining trials where they were presented with white, red, and blue beads. They were then trained with a red bead presented in one of four possible conditions: dry and unscented, with the odour but not the taste of MeA, with the bitter taste but not the odour of MeA (the chicks' nostrils were occluded with a wax preparation), or with the taste and odour of MeA. Recall was tested 10 min after training by presenting a red and then a blue bead with no odour or taste added. The number of pecks made at the bead and the number of bouts of head shaking during each of the trials were scored. During testing, chicks that were trained with the odour of MeA alone pecked less at a red bead than at a blue bead, compared with chicks trained with a dry and unscented bead, indicating that they discriminated between the training bead and a bead of a different colour. There was no significant difference between the discrimination ratio of chicks trained with the odour, taste, or taste and odour of MeA. These results demonstrate that chicks can perform PAL using taste and/or odour cues.

Animals↗
PubMed1994

Transient benzodiazepine-GABAA receptor increase after a passive avoidance learning in synaptosomal membranes from chick forebrain.

One-day-old chicks were exposed to a one-time passive avoidance learning task. After chicks peak a bead dipped in a bitter-tasting liquid, they learn to stop pecking the bead. Radioligand binding analysis of [3H]flunitrazepam was performed on crude synaptosomal membranes from forebrains, at 10, 30, and 60 min post-training. Water-trained chicks (control) pecked a bead dipped in water, and they did not learn to stop pecking the bead. The water control was complemented with a methyl anthranilate fed control chick to demonstrate that taste per se does not affect the [3H]flunitrazepam binding. At 30 min in relation to 10 min post-training, the Bmax increased 31% in water-trained chicks and 56% in taste-trained chicks, with Bmax of the taste-trained chicks reaching a value 22% higher than that in water-trained chicks. The difference, attributable to the learning, disappeared at 60 min post-training, and at all times the affinity remained unchanged. The Bmax increase in water-trained chicks might be attributable to psychological stress accompanying the task and the Bmax increase in taste-trained chicks attributable to the learning in addition to the stress accompanying the task. The results suggest that the receptor increase associated with learning is involved in early stages of memory formation.

Animals↗
PubMed1991

Effects of cingulate cortical lesions on avoidance learning and training-induced unit activity in rabbits.

This study extends an ongoing analysis of the neural mediation of discriminative avoidance learning in rabbits. Electrolytic lesions encompassing anterior and posterior cingulate cortex (area 24 and 29) or ibotenic acid lesions in area 24 only were made prior to avoidance conditioning wherein rabbits learned to step in response to a tone conditional stimulus (CS+) in order to avoid a brief, response-terminated 1.5 mA. foot-shock unconditional stimulus (US). The US was presented 5 s after CS+ onset, in the absence of a prior stepping response. The rabbits also learned to ignore a different tone (CS-) not followed by the US. Multi-unit activity of the caudate and medial dorsal (MD) thalamic nuclei, projection targets of the cingulate cortex, was recorded during learning in all rabbits. Activity was also recorded in area 29 in the rabbits with area 24 lesions. Learning in rabbits with combined lesions was severely impaired and it was moderately retarded after lesions in area 24. MD thalamic and caudate training-induced neuronal discharge increments elicited by the CS+ were enhanced in rabbits with lesions, suggesting a suppressive influence of cingulate cortical projections on this activity. Early-, but not late-developing training-induced unit activity in area 29c/d was absent in rabbits with area 24 lesions, indicating that area 24 is a source of early-developing area 29 plasticity. These results are consistent with hypotheses of a theoretical working model, stating that: a) learning depends on the integrity of two functional systems, a mnemonic recency system comprised by circuitry involving area 24 and the MD nucleus and a mnemonic primacy system comprised by circuitry involving area 29 and the anterior thalamic nuclei; b) corticothalamic information flow in these systems suppresses thalamic CS elicited activity in trained rabbits; c) corticostriatal information flow is involved in avoidance response initiation. An absence of rhythmic theta-like neuronal bursts in area 29b in rabbits with area 24 lesions is attributable to passing fiber damage.

Animals↗
PubMed1990

Effects of concurrent manipulations of nicotinic and muscarinic receptors on spatial and passive avoidance learning.

The present study investigates the effects of concurrent manipulations of nicotinic and muscarinic cholinergic receptors on spatial and passive avoidance learning/retention in rats. Daily pretraining test injections of combinations of the subthreshold doses of muscarinic (scopolamine 0.3 mg/kg) and nicotinic (mecamylamine 2.5 mg/kg or 10 mg/kg) antagonists impaired acquisition of the water-maze task (WM). Drug-induced deficits were also observed during the retention trial: the groups injected with scopolamine 0.3 mg/kg, mecamylamine 10 mg/kg and scopolamine 0.3 mg/kg in combination with mecamylamine 2.5 mg/kg showed reduced spatial bias compared with controls. Single preretention test injections of the combination of subthreshold doses of mecamylamine (10 mg/kg) and scopolamine (0.8 mg/kg) impaired memory retrieval in WM. Combined pretraining injections of subthreshold doses of scopolamine (1.0 mg/kg) and mecamylamine (10 mg/kg) induced a severe passive avoidance impairment comparable to 2.0 mg/kg of scopolamine. However, preretention test injections did not impair passive avoidance retention. Either single or combined injections of hexamethonium (5.0 mg/kg, SC) and methylscopolamine (1.0 mg/kg) did not impair either passive avoidance or water-maze performance. The present results suggest that 1) nicotinic and muscarinic systems jointly modulate performance in spatial and avoidance learning tasks and 2) cholinergic antagonists affect acquisition functions more effectively than retention ability. These findings may be relevant to the clinical disorders, like Alzheimer's disease, which are associated with a loss of both cholinergic neurons and nicotinic receptors.

Animals↗
PubMed1999

Effects of suramin on hippocampal apyrase activity and inhibitory avoidance learning of rats.

The action of suramin on apyrase activity in hippocampal synaptosomes and its effects on retention of inhibitory avoidance learning were evaluated. Suramin, a P2-purinoceptor antagonist, significantly inhibited in a noncompetitive manner the ATP and ADP hydrolysis promoted by apyrase in hippocampal synaptosomes of adult rats. The Ki values obtained were 72.8 and 109 microM for ATP and ADP hydrolysis, respectively. Intrahippocampal infusion of suramin (0.01, 0.1, 1, and 10 microg) immediately posttraining, in a dose-dependent effect, significantly reduced the response latency during the retention test applied 24 h after the rats received step-down inhibitory avoidance training. The amnesic effects promoted by suramin probably occur by its antagonist action on hippocampal P2-purinoceptors and NMDA receptors. In view of the fact that ATP-metabolizing enzymes and P2-purinoceptors have similar binding domains, these results suggest that suramin can either alter ATP degradation and/or block purinergic neurotransmission.

Adenosine Triphosphate↗
PubMed1982

[The effects of hippocampal lesions on two types of avoidance learning in rats: effects on learning to be active or to be inactive].

Two experiments were conducted to study the effects of hippocampal lesions upon various behaviors of rats in both shock and shock-free situations. The main emphasis, however, was placed on the study of the effects of the lesion upon avoidance learning to be active and inactive. In Experiment I, partially hippocampectomized rats, as compared with the control rats, showed better performance in the avoidance task to be active, but groups did not differ in the avoidance task to be inactive. Having assumed that the latter result was due to the insensitivity of the stabilimeter device used to detect rat's movements, they were detected visually by an observer under a blind condition in Experiment II. Hippocampectomized rats were shown to be poorer than control rats in learning to avoid by being immobile. The results were discussed with reference to Issacson (1974) and Blanchard, Blanchard, Lee, and Fukunaga (1977). The results obtained in shock free situations did not differ significantly among groups. But there was some evidence showing the mean durations of freezing and immobility to be less per episode in hippocampectomized than control rats.

Animals↗
PubMed1979

Effect of p-chlorophenylalanine on avoidance learning of two differentially housed mouse strains.

The effect of p-chlorophenylalanine (PCPA) has been studied on the acquisition of avoidance learning and on brain concentrations of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and tryptophan of differentially housed male mice of Albino Swiss and DBA strains. The results obtained do not support the hypothesis that learning ability varies inversely with the concentration of brain 5-hydroxytryptamine. PCPA can appear as influencing learning ability of different strains of mice differentially housed, depending more on the emotional baseline of the animals than on brain 5-hydroxytryptamine modification.

5-Hydroxytryptophan↗
PubMed1989

Systemic injection of pirenzepine induces a deficit in passive avoidance learning in rats.

When injected IP, the M1 muscarinic receptor antagonist pirenzepine dose-dependently induced a deficit in passive avoidance learning in rats. This activity was optimal at 75 mg/kg injected 1 h before the acquisition session. The deficit induced by pirenzepine was antagonized by oxotremorine (0.03-0.3 mg/kg SC) and physostigmine (0.1 mg/kg SC), but not neostigmine. By comparison, under the same experimental conditions, physostigmine and oxotremorine also antagonized the deficit induced by an equipotent dose of scopolamine (0.5 mg/kg IP), although the activity of physostigmine appeared stronger against scopolamine than against pirenzepine. These results suggest that pirenzepine could produce a centrally-mediated behavioural disruption when injected systemically.

Animals↗
PubMed1977

Deficits in passive-avoidance learning following atropine in the developing rat.

The maturation of cholinergic inhibitory mechanisms that may be involved in passive-avoidance learning was studied in rats 14, 17, 21, 25, 28, and 34 days of age. Acquisition and extinction of the conditioned response were examined under saline and atropine sulfate (5 mg/kg). Learning was also tested following scopolamine hydrobromide injections (1, 4, 8 mg/kg) in rats 17 days of age and following alpha-methylatropine (5 mg/kg) in 17- and 34-day-old groups. In normal animals the rate of acquisition increased during ontogenesis, with a significant improvement between postnatal days 17 and 21, whereas the rate of extinction did not vary with age. Acquisition was impaired by atropine sulfate at all ages and even totally prevented in younger groups (14 and 17 days of age). It was also completely disrupted by scopolamine in 17-day-old rats. Extinction following acquisition under atropine was more rapid than after normal acquisition. Methyl-atropine was without effect. These results support the hypothesis of central cholinergic mechanisms involved in response suppression, already functioning in the rat 14 days of age and maturing mainly between the 17th and the 21st postnatal days.

Age Factors↗