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At least 775 records · Page 43Linked to original sources
PubMed1991

Sympathoadrenal effects on extinction of rewarded running in the rat.

Two groups of rats underwent adrenal demedullation or sham surgery before being trained to run in a straight runaway for food reward at a short intertrial interval (90 s). Half of each group of animals were then injected IP with the sympathetic neurotoxin, 6-hydroxydopamine HBr (6-OHDA; 30 mg/kg); the remainder received saline vehicle. After 3 more days of acquisition training, running was extinguished over 12 trials in all rats. Running times were similar in all groups at the start of extinction. In saline-injected animals, extinction proceeded more slowly in the demedullated than in the sham-operated group, but this effect was largely abolished by 6-OHDA. Consistent with previous results, there was evidence that 6-OHDA facilitated extinction, irrespective of adrenal demedullation, but this effect was most apparent in the time taken to emerge from the start-box. The rats were killed two days after the end of the experiment; cardiac noradrenaline levels were depleted by 83% of control values in 6-OHDA-treated animals. The results suggest that the adrenal medulla and sympathetic neurones have opposing and interacting effects on the response to nonreward.

Adrenal Glands↗
PubMed1992

Effects of brain natriuretic peptide-32 on the extinction of active avoidance behavior in rats. Transmitter-mediated action.

Three doses of porcine brain natriuretic peptide (pBNP-32) were tested in regards to the extinction of active avoidance behavior following injection into the lateral brain ventricle in rats. This peptide delayed the extinction of the active avoidance reflex in a dose-dependent manner. To clarify the involvement of transmitters in the action of the peptide, the animals were pretreated with different receptor blockers in doses that did not affect the behavior of the animals in this learning paradigm. Dopaminergic, cholinergic, and alpha- and beta-adrenergic blockers effectively blocked the delaying action of pBNP-32, whereas GABAergic, serotoninergic, and opiateergic blockers were ineffective. The data suggest that the delaying action of pBNP-32 on the extinction of active avoidance behavior is mediated via dopaminergic and alpha- and beta-adrenergic neuromediations.

Animals↗
PubMed1976

Extinction-induced mirror responding as a baseline for studying drug effects on aggression.

Pigeons worked individually in a chamber containing a response key and a mirror. Responding on the key was controlled by a multiple schedule in which a brief period of continuous food reinforcement alternated with a 5 min period of extinction. Under baseline conditions, aggressive behavior (responding on the mirror) occurred at the onset of each extinction period. After 10 saline control sessions, 5 mg/kg of chlordiazepoxide was injected IM 30 min presession for 60 daily sessions. The drug initially produced a marked decrease in aggressive behavior but had little or no effect on key pecking. The aggressive behavior generally remained suppressed during the chronic drug regimen and returned to control levels when the drug was withdrawn. It was concluded that the technique of extinction-induced mirror responding in pigeons provides a stable, sensitive and recoverable baseline for objectively assessing selective drug effects on aggression.

Aggression↗
PubMed1977

Protein synthesis inhibition and memory for pole jump active avoidance and extinction.

This study utilizes a pole jump active avoidance task to investigate the effects of protein synthesis on memory formation. An extinction training procedure for this task is also described. Amnesia for extinction is produced by inhibition of protein synthesis and is also demonstrated by active responding, so it is clear that there is no general impairment sufficient to disrupt motor skill, motivation, or retrieval of stored memories. It was found that while inhibition of protein synthesis in brain for 2 hr did not produce amnesia, inhibition for 6 to 8 hr did. These results demonstrate that for both shock-motivated learning and non-shock motivated extinction learning, the duration of inhibition of protein synthesis is important in determining whether amnesia occurs. We conclude that inhibition of cerebral protein synthesis can best account for amnesia induced by anisomycin, cycloheximide, and acetoxycycloheximide.

Animals↗
PubMed1986

Effect of LSD on acquisition, maintenance, extinction and differentiation of conditioned responses.

Three experiments were conducted to compare the effects of LSD (30 nmol/kg) on the acquisition, maintenance, extinction and differentiation of the rabbit's classically conditioned nictitating membrane response. LSD significantly enhanced the acquisition of conditioned responses to tone and light conditioned stimuli as compared with vehicle injected controls (Experiments 1 and 2), but had no detectable effect on differential conditioning in Experiment 3. The conditioned responses acquired under LSD in Experiments 1 and 2 exhibited some unusual features in that: they were more rapidly extinguished under continued injections of LSD; they demonstrated a significant decrement when animals were switched from LSD to vehicle during maintenance; and they were virtually eliminated when animals were switched from LSD to vehicle during extinction. In contrast, conditioned responses acquired under saline injections in Experiments 1 and 2 were not affected when animals were switched to LSD injections during either maintenance or extinction. These results of Experiments 1 and 2 were interpreted as indicating that LSD produces an asymmetrical state-dependent learning.

Acoustic Stimulation↗
PubMed1986

Haloperidol induces a partial reinforcement extinction effect in rats: implications for a dopamine involvement in food reward.

The hypothesis that dopamine antagonist drugs attenuate the reinforcing properties of food was investigated in hungry rats trained to traverse a straight runway for food reward. Testing consisted of a single trial per day during which latencies to leave the start box and to traverse the alley were recorded. In each experiment, a reinforcement phase lasting 30 consecutive days was immediately followed by a 21 day extinction phase. The runway responses of animals that experienced intermittent food reward during the reinforcement phase of the experiments, was later found to be more resistant to extinction than those of continuously reinforced animals. This "partial reinforcement extinction effect" (PREE) was also observed in animals that experienced periodic reductions in the quantity, but not quality, of food reward. Intermittent pretreatment with 0.15 mg/kg of haloperidol during the reinforcement phase produced a PREE that was indistinguishable from that produced by reward omission on those same trials. Control groups for motor debilitation and for non-associative drug effects did not demonstrate a PREE. These results are consistent with the view that central dopamine substrates play a role in the neural basis of food reward.

Animals↗
PubMed1983

The neurochemistry and pharmacology of extinction behavior.

The role of various neurotransmitter systems in the brain in extinction behavior is examined. An attempt is made to suggest psychological mechanisms (such as attention, secondary reinforcement or internal inhibition) by which the neurotransmitter systems or drugs act to produce the observed alteration in extinction behavior. The putative neurotransmitters acetylcholine, noradrenaline, dopamine, serotonin, endorphins and the peptides are reviewed, as are pharmacological agents such as the benzodiazepines, the barbiturates, the psychodelics, the neuroleptics, the psychomotor stimulants and cannabinoids. Other treatments and factors are considered such as peripheral hormones and the adrenal-pituitary axis. It is suggested that the noradrenergic system may be involved in the expression of extinction behavior by a role in selective attention, the dopamine system via an involvement with secondary reinforcement, the cholinergic system by a mechanism of response inhibition and the barbiturates and benzodiazepines by a block of nonreward.

Acetylcholine↗
PubMed1990

Effect of anxiolytics and antidepressants on extinction and negative contrast.

Anxiolytics, particularly the benzodiazepines and barbiturates tend to retard, but not prevent, extinction, promote recovery from negative contrast, and elevate S- responding in discrimination training. Anxiolytics, administered during acquisition, tend to eliminate the partial reinforcement extinction effect, but this result is substantially influenced by parametric considerations. Behaviors that are energized in extinction may have a different pharmacological profile than behaviors that decline. Conclusions regarding the effects of antidepressants must be more tentative but, in general, acutely administered antidepressants are relatively ineffective in all of these paradigms. However, antidepressants may enhance the efficiency of responding on DRL schedules whereas anxiolytics tend to disrupt such behavior.

Animals↗
PubMed1988

Differential hippocampal and cortical cholinergic activation during the acquisition, retention, reversal and extinction of a spatial discrimination in an 8-arm radial maze by mice.

Possible differentiation of the intervention of cholinergic septohippocampal and magnocellular forebrain (NBM) projections to cortex during learning and memory processes has been investigated directly using mice. High-affinity choline uptake velocities in the hippocampus and cortex were analyzed, in parallel, at various periods during the acquisition, over 8 days, as were the subsequent retention, reversal and extinction of a spatial discrimination in an 8-arm radial maze. Initial acquisition induced an immediate (30 s) and long-lasting (approx. 3 h) increase in mean hippocampal (+33%) and cortical (+23%) cholinergic activities. The time course of this activation was structure-dependent and correlations of hippocampal-cortical cholinergic activities showed large and consistent alterations as a function of time after training. Cholinergic activation in both brain regions was observed immediately following each daily training session with amplitudes which did not vary significantly in spite of a progressive daily increment in performance. Following acquisition mice were tested for retention, reversal and extinction: 30 s following the retention session, cholinergic activation was observed in both cortex and hippocampus, with magnitudes similar to those observed at the end of acquisition. However, in the reversal and extinction groups, a treatment-dependent attenuation of cholinergic activation was observed which was accompanied by a significant loss of correlation of cholinergic activity between these two brain regions. The results are discussed in relation to the concepts of reference and working memory and also to novelty, stress, arousal and frustrative non-reward. The data constitute direct experimental evidence for a differential involvement of cholinergic septohippocampal and NBM-cortical projections in learning and memory processes.

Animals↗
PubMed1981

Arginine vasopressin and a vasopressin antagonist peptide: opposite effects on extinction of active avoidance in rats.

Systemic injection or arginine vasopressin (AVP) (1 micrograms/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5 : 1. At a dose of 100 micrograms/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction. Injections of dPTyr-(Me)AVP into the lateral ventricle were ineffective except at a dose of 10 micrograms/rat. These results confirm previous reports of the effect of vasopressin on delaying extinction of avoidance behavior, but suggest a site of action distant from the lateral ventricle.

Animals↗
PubMed1985

Effects of peripherally injected vasopressin and des-glycinamide vasopressin on the extinction of a spatial learning task in rats.

An elevated eight-arm radial maze was employed to study the effects of neuropeptide administration on the spatial learning abilities of food-deprived rats. Following 18 days of reinforced training, each animal was briefly exposed to the maze with no food available in any of the eight food-cups. Immediately after this preliminary trial, animals were injected with a single subcutaneous dose of either saline, arginine vasopressin (AVP: 1.0 or 5.0 micrograms/kg), or an AVP analog with only weak endocrinological activity, des-gly-arginine vasopressin (DG-AVP: 1.0, 5.0 or 10.0 micrograms/kg). Additional extinction trials were conducted at 2, 4, 6 and 8 h post-injection. These tests consisted of individually placing an animal on the empty maze and recording the number of arms chosen in a 5-min period. In this situation, animals learn that food is no longer present in the maze and, consequently, extinguish responding. Vasopressin potentiated this radial maze extinction behavior while DG-AVP produced behavioral results directionally opposite to those predicted by a memory facilitation hypothesis. In a subsequent experiment, vasopressin had no effects on unconditioned locomotor activity measured 2 and 4 h post-injection. These results suggest that: vasopressin improved the learning that occurred during extinction of conditioned appetitive behaviors, these vasopressin effects on conditioned behavior were independent of any unconditioned, sedative or non-specific actions of the peptide, and peripheral endocrinological responses may be necessary to demonstrate memory-enhancing effects following peripherally administered AVP.

Animals↗
PubMed1986

The contingent negative variation (CNV) to fear-related stimuli in acquisition and extinction.

Contingent Negative Variation (CNV) in anticipation of phobic and neutral slide material was recorded in Acquisition of a learned association between tone pitch and slide type, and in Extinction (following removal of slide presentation). In phobic volunteers, no clear CNV differentiation between 'phobic' and control condition was apparent in either Acquisition or Extinction. For Control subjects, a different pattern entirely has been demonstrated, with anticipation of the neutral condition giving rise to a larger CNV than anticipation of the 'phobic' condition (in Acquisition). In addition, Extinction led to a reversal of this CNV amplitude relationship, with the tone previously associated with the phobic slide producing a DC-shift which was larger than that following the tone previously paired with the neutral slide. The results are compatible with a dynamic model of CNV generation according to which CNV amplitude is positively related to an expectancy for reward or non-punishment but inversely related to an expectancy for punishment or non-reward.

Adult↗
PubMedDate not supplied

Vasopressin analog delays extinction of classically conditioned bradycardia.

Albino rabbits were subjected to Pavlovian (classical) conditioning and extinction of concomitant heart rate and eyeblink responses. Sixty minutes before each of three extinction sessions animals were treated with 5 or 20 micrograms/kg of deamino-dicarba-arginine-8-vasopressin or saline. Vasopressin treatment delayed extinction of bradycardiac conditioned responses but did not affect concomitant eyeblink conditioned responses. It was concluded that classically conditioned autonomic responses may be useful tools for studying the effects of peptides on learning.

Animals↗
PubMedDate not supplied

Differential effects of DGAVP on acquisition and extinction of active avoidance behavior.

DGAVP facilitates consolidation and retrieval of active and passive avoidance behavior. In this study it was tested whether the long-term behavioral effects of DGAVP are the consequence of an initial increase in behavioral arousal during the learning phase. Animals that were preestimated in an open field test to be low active showed a lower number of conditioned avoidance responses (CAR's) during acquisition and extinction of a shuttle-box task than high active rats. DGAVP was administered 40 min prior to the 1st acquisition session. The immediate effect of DGAVP was a shift in the bell-shaped curve of the relation between arousal and performance (13); an increase in acquisition performance was observed with a low dose of DGAVP (0.1 microgram), while a decrease was found with a high dose of DGAVP (1 microgram). A dose-dependent inhibition of extinction was found in both low and high active animals. These results suggest an immediate effect of DGAVP on the rate of acquisition behavior, which may be a direct consequence of its arousing properties, and a long-term effect on extinction, indicating the formation of memory traces specific for vasopressin-related neuropeptides.

Animals↗
PubMed1979

Forebrain noradrenaline depletion blocks the release by chlordiazepoxide of behavioral extinction in the rat.

The interaction between chlordiazepoxide (CDP) and forebrain noradrenaline (NA) was investigated in rats with bilateral radiofrequency lesions of the noradrenergic dorsal tegmental bundle (DTB). Forebrain NA was reduced to 35% of control by the DTB lesions; hypothalamic NA and dopamine were unchanged. Rats were trained on a straight alley runway task for food reward. During extinction of the runway task, CDP significantly increased extinction responding in sham lesion animals but not in DTB lesion animals. Thus, CDP was ineffective in increasing resistance to extinction responding in the runway task in animals with significant depletion of forebrain NA.

Animals↗
PubMed1993

Extinction of emotional learning: contribution of medial prefrontal cortex.

Stimuli associated with painful or otherwise unpleasant events acquire aversive emotional properties in animals and humans. Subsequent presentation of the stimulus alone (in the absence of the unpleasant event) leads to the eventual extinction of the aversive reaction. Although the neural basis of emotional learning has been studied extensively, considerably less is known about the neural basis of emotional extinction. In the present study, we show that the medial prefrontal cortex plays an important role in the regulation of fear extinction in rats, a finding that may help elucidate the mechanisms and, possibly, the treatment of disorders of uncontrolled fear, such as anxiety, phobic, panic and posttraumatic stress disorders in humans.

Animals↗
PubMedDate not supplied

The extinction of naturally occurring conditioned reactions in psychoactive substance users: analog studies.

In the present series of studies we develop an analog approach for the study of conditioned reactions to drug stimuli. The analog we study is the naturally occurring conditioned reaction of salivation at the sight of a lemon. We show that this conditioned reaction can be extinguished, that spontaneous recovery occurs, and that the conditioned reaction increases after "relapse." Further, we show that massed extinction trials lead to greater extinction than do spaced trials. This analog provides an approach that can be used to develop cue-exposure treatments that minimize spontaneous recovery from extinction and reduce the likelihood of relapse.

Adolescent↗
PubMed1993

Limits of habituation and extinction: implications for relapse prevention programs in addictions.

Problems in the application of exposure techniques to the management of long term dishabituation in addicts are discussed in the light of human and animal evidence. Extinction and habituation of responses to drug cues or drug aftereffects are unstable and strongly dependent on context, thus limiting the effectiveness of cue exposure treatments in the prevention of relapse. Several strategies are suggested to improve the stability of extinction and habituation in order to enduringly prevent relapse in addictions. (i) Warning patients about the episodic resurgence of unexpected urges or cravings precipitated by conditioned contexts and exposing them to such contexts. (ii) To obtain a maximum protection against relapse, extinction should 'recreate' all the original learning contexts (i.e. all possible drug cues). (iii) The behavioral chains involved in self administering drugs ought to be incorporated into cue exposure treatments (without permitting consummatory responses) in order to decrease their signal value as cues for drugs.

Animals↗