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PubMed2002

Successive positive contrast in one-way avoidance learning.

The main finding of these experiments was a positive contrast effect in one-way avoidance learning. Experiment 1 showed that increasing safety time during one-way avoidance training led to improved performance, surpassing that of a control group that had received the high reward (safe time) from the beginning of training. Experiment 2 showed that a similar positive contrast effect occurred when the time spent in the danger compartment before the onset of the warning signal was shortened. These results suggest that time spent in a safe context acts as a reinforcer of the avoidance response; however, its incentive value depends not only on its duration, but also on the length of the time spent in the danger compartment before the onset of the signal. Overall, results also suggest that the avoidance response is a mixture of flight (motivated by fear) and approach (to a safe place) behaviour. The specific weight of the flight or approach component may be a function of the time and the amount of activation of each emotional state (fear or relief) due to opponent homeostatic compensatory processes that occur in the danger and safe compartments during one-way avoidance learning.

Animals↗
PubMed1988

Inhibition of long-term memory formation by anti-ependymin antisera after active shock-avoidance learning in goldfish.

Ependymins are acidic glycoprotein constituents of goldfish brain cytoplasm and extracellular fluid which are known to participate in biochemical reactions of long-term memory formation. In earlier experiments, anti-ependymin antisera were found to cause amnesia when injected into goldfish brain ventricles after the acquisition of a vestibulomotoric training task. To investigate whether they also inhibit memory consolidation after other learning events the anti-ependymin antisera were injected after an active shock-avoidance learning paradigm, as follows: goldfish were trained in a shuttle-box to cross a barrier in order to avoid electric shocks (unconditioned stimulus) applied shortly after a light signal (conditioned stimulus). Anti-ependymin antisera blocked retention of the learned avoidance when injected 0.5, 4.5 or 24 h after acquisition of the new behavior. They had no effect, however, when injected 72 h after learning. Apparently, long-term memory was already consolidated at this point. Antisera injected 0.5 or 72 h prior to training, also did not influence learning or memory. Thirteen percent of the goldfish fled the light stimulus spontaneously. These fish therefore did not experience the unconditioned stimulus and thus were unable to learn the task. When they were treated with the anti-ependymin antisera and tested 3 days later, the spontaneous escape reaction was not affected (active control group). The ability of anti-ependymin antisera to inhibit memory consolidation and their efficacy after administration at specific time intervals are very similar for the active shock-avoidance learning and for the vestibulomotoric training. We conclude that ependymins are not task-specific, but serve a general function in biochemical reactions essential for long-term memory formation.

Animals↗
PubMed1982

Action of substance P and an SP-hexapeptide analogue on avoidance learning in rats.

The effects of Substance P (SP) (Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-MetNH2) and of a SP hexapeptide analogue (SP-A) (Lys-Phe-Ile-Gly-Leu-MetNH2) on active avoidance learning were investigated in spontaneously hypertensive rats (SHR) and Wistar rats. Active avoidance learning was slower in SHR than in Wistar rats. SP-A "normalized" the slower active avoidance learning in SHR, whereas SP did not. Some possible causes of this difference as well as the mechanism of the normalizing effect of SP-A are discussed.

Animals↗
PubMed1988

Does avoidance learning only depend on mossy fiber distribution?

Rats and mice with a poor active avoidance behavior in the shuttle box exhibit a larger extent of the zone innervated by mossy fibers in the infrapyramidal area of the hippocampal sector CA3. The question arose whether only these differences in the amount of inputs from granular cells do correlate with poor avoidance learning, or whether cholinergic septal inputs are likewise related to behavioral performance. Inbred and non-inbred rats with low and high avoidance scores were used. Freezing sections were alternately used for TIMM-staining and for the histochemical visualization of the acetylcholinesterase activity. In comparison with "good avoidance learners" the rats with "poor active avoidance performance" exhibited a larger zone of mossy fibers and a lower activity of acetylcholinesterase in the investigated field. A significant inverse correlation between mossy fiber innervation and cholinergic septal inputs could be established. Our findings suggest that poor avoidance learning does not simply depend on mossy fiber distribution but seems to be dependent rather on the relation between mossy fiber innervation and cholinergic septal inputs.

Acetylcholinesterase↗
PubMed1980

Effects of a substance P-analogue on blood pressure and avoidance learning of rats with spontaneous hypertension.

A shortened and modified eledoisin-hexapeptide sequence (Lys-Phe-Ile-Gly-Leu-MetNH2) was tested for their action on avoidance learning and blood pressure of rats with spontaneous hypertension (SH-rats) and intact Wistar rats. Both groups were 10, 14, and 26 weeks of age. Disorders of avoidance learning and elevation of blood pressure were likely to aggravate along with growing age of SH-rat. The used eledoisin-hexapeptide sequence is related to the essential C-terminal pentapeptide sequence of Substance P (SP). After injection of the used hexapeptide at doses of 250 microgram/kg intraperitoneally disorders in avoidance learning were completely eliminated from ten-week SH-rats or conditionally for SH-rats aged 14 and 26 weeks. Elevated blood pressure in SH-rats aged 26 weeks was reduced by the hexapeptide from 220 Torr to approximately 190 Torr. Blood pressure in SH-rats aged 14 weeks, originally about 180 Torr, was almost unaffected by the hexapeptide. Blood pressure went up from about 150 Torr to 190 in ten-week-old Sh-rats. A hypothesis was made about the mode of action of Substance P and related peptides.

Animals↗
PubMed1976

Effect of midbrain raphe lesion on avoidance learning in aggressive mice.

Lesion of the midbrain ventral raphe nucleus greatly improves the avoidance-learning efficiency of normal and isolated-aggressive Albino Swiss mice. Since the lesion of this brain area selectivity lowers the forebrain concentration of 5-hydroxytryptamine (5-HT), implications of the role of brain 5-HT in avoidance-learning acquisition are discussed.

Aggression↗
PubMed1997

Effects of nicotine on active avoidance learning in rats: sex differences.

Nicotine, a cognition enhancer and a drug of abuse, exerts its central actions through neuronal nicotinic acetylcholine receptors which show sexual dimorphism. This study tested the effects of nicotine on active avoidance learning in male and female rats. Three month-old Sprague-Dawley rats received varying doses of nicotine (0.2, 0.4 and 0.6 mg/kg) or saline s.c. before active avoidance learning trials (15 trials/day) for a period of 5 days. Behavioural testing was continued after the termination of nicotine treatment once a week for four weeks. Nicotine improved acquisition of active avoidance learning in a dose-dependent manner. In male rats nicotine was active at all doses tested whereas, in females, learning performance deteriorated at a dose of 0.6 mg/kg. In conclusion, nicotine pre-treatment affects active avoidance in a sexually dimorphic and dose-dependent manner.

Animals↗
PubMed1985

Evidence for a role of brain serotonergic neurotransmission in avoidance learning.

This thesis has analyzed the role of brain serotonergic (5-HT) neurotransmission in avoidance learning in the male rat using neurochemical, pharmacological and behavioural approaches. The acute and long-term effects of p-chloroamphetamine (PCA) on one-way and two-way active avoidance (AA) acquisition and retention and passive avoidance (PA) retention and on central monoamine concentrations were examined in the male rat. The effects of PCA were compared with the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA). To characterize the effects of PCA the following neurotoxins were used: 5,6- and 5,7-dihydroxytryptamine (5,6- and 5,7-DHT) and N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). The concentrations of biogenic monoamines and their metabolites in discrete brain regions were determined by high pressure liquid chromatography with or without electrochemical detection. The effects on 5-HT receptors in vitro and in vivo were measured by ligand binding studies (using 3H-5-HT and 3H-ketanserin as radioligands) and with behavioural techniques, respectively. Administration of the 5-HT releasing compound PCA prior to training (pre-training) produced a dose- and time-related impairment of one-way AA acquisition and retention and PA retention. A series of studies indicated that the avoidance learning deficits caused by PCA are produced by release of 5-HT, resulting in stimulation of postsynaptic 5-HT receptors. For instance, the avoidance deficit was blocked by pretreatment with the 5-HT uptake inhibitors alaproclate and zimeldine, which inhibit the 5-HT release induced by PCA. The avoidance deficits could not be related to changes (direct or indirect) in NA and DA transmission. Lesion experiments in combination with biochemical analyses provided evidence that the avoidance deficit caused by PCA involves 5-HT terminals of the forebrain, while the descending 5-HT projections seem to play a minor role. The AA acquisition deficit induced by PCA appears to be mediated via stimulation of 5-HT2 receptors, whereas the PA retention is mediated via 5-HT1 receptors. Analysis of the PCA-induced AA deficit indicated that it is mediated by non-associative factors. Thus, the performance of the PCA-treated rats was susceptible to interference from extratask contextual stimuli. Pre-training administration of PCA was found to produce a time-dependent loss in memory retention (PA retention) in animals which had acquired the response. This finding indicates that serotonin also has a role in associative learning processes e.g. in the way information is processed in the rat brain following acquisition.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

[Effects of chlordiazepoxide on passive avoidance learning in Wistar-Imamichi and F344/Du strain rats].

The present study was designed to investigate the effects of chlordiazepoxide (CDP; 5 and 10 mg/kg, ip) on one-trial step-through passive avoidance learning in Wistar-Imamichi (W-I) and F344/Du (F) strain rats. Step-through latency and the time spent in safety-box were significantly longer in W-I than F rats. The number of animals that attained the 300-s criterion was also larger in W-I than F rats. Therefore, it was concluded that W-I rats showed superior performance in the passive avoidance task as compared to F rats. Taken together, these and the previous results (Iwasaki et al, 1984) that F rats acquired the active avoidance learning more easily than W-I rats, the differences of performance in the two strains would reflect differences of strain-specific response patterns in aversive situations, but not of learning ability. Further, CDP produced a dose-dependent state-dependency in W-I but not in F rats. These strain differences in the effect of CDP were considered to derive from differences in sensitivity to the drug, rather than in the baseline performance level, because comparable strain differences in drug effect were reported in active avoidance learning.

Animals↗
PubMed2000

The action of pituitary adenylate cyclase activating polypeptide (PACAP) on passive avoidance learning. The role of transmitters.

In the present study, the action of PACAP 38 on one-way passive avoidance learning was investigated. PACAP-38 was administered into the lateral brain ventricle and the latency of the passive avoidance response was measured 24 h later. In order to study the possible roles of various neurotransmitters in mediating the action of PACAP on the consolidation of passive avoidance learning, the animals were pre-treated with receptor blockers in doses that per se proved to be ineffective. PACAP facilitated the learning, the consolidation of learning and the retrieval of the passive avoidance response. The following receptor blockers attenuated the action of PACAP on this consolidation: haloperidol, phenoxybenzamine, propranolol and methysergide. An antagonist of PACAP 38, PACAP 6-38, and also nitro-L-arginine (the latter blocks the enzyme nitric oxide synthase) thereby inhibiting the formation of NO from L-arginine, completely blocked the action of PACAP 38 on consolidation. The following receptor blockers were ineffective: naloxone, bicuculline and atropine. The presented data suggest that PACAP 38 is able to improve the learning and memory processes in a passive avoidance paradigm. In this action, the PACAP 38 receptor and NO are important mediators. Dopaminergic, alpha- and beta-adrenergic mediation and serotonin receptors modified the action of PACAP 38, but they are probably not of great importance.

Adrenergic beta-Antagonists↗
PubMed1989

Effort and stress influence the effect of lesion of the habenula complex in one-way active avoidance learning.

Previous studies which have examined the effects of lesions of the habenula on active avoidance learning have not provided unambiguous support for response deficits. Moreover, interpretation of early studies is confounded by large lesions which damaged adjacent structures. We report the effects of smaller circumscribed lesions of the habenula complex on a simple one-way active avoidance paradigm in three separate experiments in which the required operant was a step or jump onto an elevated platform. In the first study involving avoidance of shock of low intensity (0.5 mA) with an average long intertrial interval of 8 minutes, lesioned animals were not significantly different from sham operated controls. However, in following experiments in which stress levels were increased by raising the shock intensity and reducing the intertrial-interval, or in which the operant was made considerably more demanding by raising the height the animals had to jump to make an avoidance response, there were large lesion induced deficits in avoidance responding. The absence of significant differences between lesioned and sham operated controls in escape latencies suggested no lesion induced impairment of the response to the shock. It is suggested that the data not only support an effect of habenular lesions on active avoidance learning but also are consistent with a previous suggestion that the functional effects of lesion of the habenula on behaviour are effected through changes in dopaminergic function.

Animals↗
PubMed1992

Successive negative contrast in one-way avoidance learning in rats.

In three experiments, successive negative contrast was examined in one-way avoidance learning. Reward magnitude in first (pre-shift) and second (post-shift) phases was manipulated by time spent in the safe compartment. Experiment 1 demonstrated that when time in the danger compartment was held constant, a group shifted from a large reward--30 sec spent in the safe compartment--to a small reward--1 sec--showed poor performance and longer response latency than a group conditioned with the small reward in both phases. Experiment 2 replicated this effect with a less intense shock and also demonstrated that a group shifted from large to small reward performed more poorly than a group exposed to large reward--30 sec--in both phases. Finally, Experiment 3 showed that changes in intertrial interval, defined as total time spent in the safe compartment and the danger compartment before the onset of the warning signal, were not responsible for this contrast effect. These results suggest that time spent in a safe place can act as appetitive incentive during one-way avoidance learning.

Animals↗