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Results for “Avoidance Learning”

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PubMed1989

Effect of retraining trials on memory consolidation in weakly reinforced learning.

Day-old chicks given a single weakly reinforced (20% v/v methyl anthranilate in absolute ethanol) passive avoidance learning trial showed no evidence of long-term memory. A second learning trial given at 15 minutes after initial resulted in consolidation of the learning experience into long-term memory. The retention function resulting from two learning trials is similar to that observed with a single strongly reinforced learning trial, and consists of the stages postulated by Gibbs and Ng. With a dilution of 10% methyl anthranilate in ethanol, four training trials were needed to yield unequivocal evidence of long-term memory consolidation.

2,4-Dinitrophenol↗

PubMed1983

Strain specific cholinergic changes in response to stress: analysis of a time-dependent avoidance variation.

Investigators have established that the performance of an incompletely learned avoidance task is a U shaped function of the time since the original partial acquisition. Thus rats perform more poorly when retested at intermediate time intervals (1-8 hr) after training than they do when tested at longer post-acquisition intervals (24-48 hr). Studies have suggested that such time-dependent deficits are not related to changes in learning ability, but rather result from shock-induced motor suppression which interferes with active avoidance responding. Pharmacological studies utilizing drugs which effect cholinergic function have indicated that an inhibitory cholinergic system may be involved in mediating post-shock motor suppression. To obtain direct biochemical evidence for possible cholinergic mediation of post-shock motor suppression, measurements of high affinity choline uptake and acetylcholine turnover were made at varying time intervals following partial active avoidance training in F-344 rats. An increase in cholinergic function was found in the dorsal, but not the ventral hippocampus 30 min, 1 hr and 4 hr following acquisition training. These biochemical alterations were temporally correlated with deficits in active avoidance responding. We have reported that the immediate behavioral suppression observed in another rat strain (Sprague-Dawley, Zivic Miller Laboratories), which exhibits inferior active avoidance performance, is similarly correlated with cholinergic activation in the dorsal hippocampus [17]. These data support the hypothesis that the dorsal-hippocampal cholinergic system is involved in the mediation of stress-induced behavioral suppression.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1987

The effects of protein synthesis inhibition on structural changes associated with learning in the chick.

The effect of the protein synthesis inhibitor anisomycin on the structural changes associated with passive avoidance learning in the chick was investigated. Chicks were trained when they were 24 h old by allowing them to peck at a shiny bead coated with either water or the aversive-tasting substance methylanthranilate (MeA). Chicks which peck the MeA-coated bead will on subsequent testing avoid pecking a similar, but water-coated bead. Behavioural testing was carried out 12 h after training and immediately afterwards the chicks were killed and their brains prepared for electron microscopy. A specific region of the forebrain, the intermediate and medial part of the hyperstriatum ventrale (IMHV) was investigated. When the IMHV of the MeA trained chicks was compared with that of water-trained controls structural changes of the synapse were detected. These changes involved a significant increase in the mean length of the postsynaptic density (LPSD) of symmetrical synapses in the left IMHV. Chicks injected with 0.8 mg of anisomycin 30 min before training with a MeA-coated bead showed aversion for the shiny bead when tested 12 h later. Electron microscopic analysis of the IMHV from these amnestic chicks showed no evidence for the change in LPSD demonstrated in the water-injected controls. These results are discussed in relation to the nature of the memory trace induced by training on a passive avoidance task.

Animals↗

PubMed1998

Nitric oxide as a retrograde messenger during long-term potentiation in hippocampus.

Nitric oxide (NO) is widespread in the nervous system and is thought to play a role in a variety of different neuronal functions, including learning and memory (see other chapters, this volume). A number of behavioral studies have indicated that NO is involved in several types of learning such as motor learning (Yanagihara and Kondo, 1996), avoidance learning (Barati and Kopf, 1996; Myslivecek et al., 1996), olfactory learning (Okere et. al., 1996; Kendrick et al., 1997), and spatial learning (Holscher et al., 1995; Yamada et al., 1996) (for review of earlier papers see Hawkins, 1996). Moreover, NO is thought to be involved in neuronal plasticity contributing to these different types of learning in different brain areas including the cerebellum (chapter by R. Tsien, this volume) and hippocampus. In this chapter we review evidence on the role of NO in long-term potentiation (LTP), a type of synaptic plasticity in hippocampus that is believed to contribute to declarative forms of learning such as spatial learning.

Animals↗

PubMedDate not supplied

The role and mechanisms of action of glucocorticoid involvement in memory storage.

Adrenal steroid hormones modulate learning and memory processes by interacting with specific glucocorticoid receptors at different brain areas. In this article, certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation. By reviewing the work carried out in different learning models in chicks (passive avoidance learning) and rats (spatial orientation in the Morris water maze and contextual fear conditioning), a role for brain corticosterone action through the glucocorticoid receptor type on the mechanisms of memory consolidation is hypothesized. Evidence is also presented to relate post-training corticosterone levels to the strength of memory storage. Finally, the possible molecular mechanisms that might mediate the influences of glucocorticoids in synaptic plasticity subserving long-term memory formation are considered, mainly by focusing on studies implicating a steroid action through (i) glutamatergic transmission and (ii) cell adhesion molecules.

Animals↗

PubMed1990

Pentylenetetrazole kindling impairs learning in mice.

Repeated administration of 35 mg/kg body weight pentylenetetrazole (PTZ) induced a kindling phenomenon and an impairment of inhibitory avoidance learning. In contrast, a single administration of the same dose PTZ had no effect on learning. Kindled mice showed impaired habituation of exploratory activity. The results may be of relevance for antiepileptic drug testing.

Animals↗

PubMed1993

Lack of a temporal gradient of retrograde amnesia in rats with amygdala lesions assessed with the fear-potentiated startle paradigm.

It is well known that lesions of the hippocampal formation produce a temporally graded retrograde amnesia for certain types of memory. A similar pattern of results has been reported with amygdaloid lesions in avoidance learning (K.C. Liang et al., 1982). The present study examined the effects of posttraining amygdaloid lesions using a Pavlovian conditioning task, fear-potentiated startle, in which the amplitude of the acoustic startle reflex is increased when elicited in the presence of a cue (e.g., a light) previously paired with footshock. Electrolytic lesions of the amygdala given either 6 or 30 days after training blocked the expression of potentiated startle, indicating no temporal gradient of amnesia over these intervals in this paradigm. The effects of amygdaloid lesions on different measures of aversive learning are discussed.

Amygdala↗

PubMed1980

Failure of B6 deficiency to affect performance of aging rats in a passive avoidance task.

Male Fischer-344 rats from three age groups (6-7, 15-16, and 27-29 months) were given either a pyridoxine deficient diet or control diet for five weeks. Differences in body weight produced by the diets were evident in the youngest age groups but not in the oldest group in which all animals tended to lose weight. There was no evidence that diet or age affected performance during passive avoidance learning.

Aging↗

PubMed2005

Spatial learning of mice lacking a neuron-specific epidermal growth factor family protein, NELL2.

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains. We previously disrupted the NELL2 gene in mice by gene targeting and showed that long-term potentiation is enhanced in vivo in the dentate gyrus of NELL2-deficient mice. To further elucidate the physiological roles of NELL2, we performed a behavioral characterization of NELL2(-/-) and their heterozygous control mice. NELL2-deficient mice exhibited learning impairment in the Morris water maze task. However, we observed no difference in passive avoidance learning between NELL2(-/-) and NELL2(+/-) mice. These observations suggest that NELL2 plays an important role in hippocampus-dependent spatial learning and that emotional learning does not depend critically on NELL2.

Animals↗

PubMed2002

Reduction of cocaine place preference in mice lacking the protein phosphatase 1 inhibitors DARPP 32 or Inhibitor 1.

BACKGROUND: Modulation of protein phosphorylation by dopamine is thought to play an important role in drug reward. Protein phosphatase-1 (PP-1) is known to mediate some of the changes in neuronal signaling that occur following activation of the dopaminergic system. METHODS: Two endogenous inhibitors of PP-1 are dopamine and cyclic 3', 5' adenosine monophosphate-regulated phosphoprotein (DARPP-32) and Inhibitor-1 (I-1). Knockout mice lacking one or both of these PP-1 inhibitors were tested for responses to cocaine using in vivo amperometry and conditioned place preference. RESULTS: Presynaptic dopaminergic function appears to be unaffected by these mutations because stimulation-evoked changes in extracellular dopamine levels were unchanged between wild type mice and mice lacking one or both of these PP-1 inhibitors. In contrast, conditioned place preference to cocaine is reduced in mice lacking DARPP-32, I-1, or both phosphoproteins. This does not appear to be due to a learning deficit because mice lacking both DARPP-32 and I-1 show normal passive avoidance learning. CONCLUSIONS: These data imply that increased PP-1 function as a result of deficits in DARPP-32 or I-1 is sufficient to decrease the rewarding properties of cocaine. Furthermore, the mechanism for this altered cocaine place preference does not involve alteration of dopamine release or reuptake.

Animals↗

PubMed1986

Subtelencephalic locale of reinforcement and learning: looking for the minimal necessary structures.

This report summarizes 4 experiments which deal with the effects of surgical removal of the rat's telencephalic forebrain structures on performance of an inhibitory avoidance response, which was acquired either before or after the lesion was made. Two experiments provide evidence that inhibitory avoidance learning (using the single-trial up-hill avoidance task) is still possible after removal of all of the forebrain structures except for the hypothalamus. A third study using this preparation dealt with the question of whether this conditioned avoidance response can be eliminated as a consequence of it being punished. In a further experiment the conditioned avoidance response was established prior to ablation of the telencephalon plus thalamus. Recall of the conditioned response survived the lesion, suggesting that the avoidance response is also stored at a subtelencephalic level in the brain-intact animal.

Animals↗

PubMed2005

Avoidance behavior can function as a negative occasion setter.

The authors put forward the hypothesis that avoidance learning can result from the fact that participants learn (a) that a stimulus is followed by an unconditioned stimulus (US) when the avoidance behavior is not emitted and (b) that the stimulus is not followed by the US when the avoidance behavior is emitted. As such, avoidance behavior is assumed to function as a negative occasion setter. The results of a contingency judgment experiment involving 65 students showed that avoidance behavior indeed has the unique functional properties of a negative occasion setter (resistance to counterconditioning and selective transfer of modulation).

Association Learning↗

PubMed2001

Calcium channel antagonists enhance retention of passive avoidance and maze learning in mice.

Although a number of studies have shown that treatment with calcium channel antagonists (CCAs) can ameliorate impairments in learning and memory in aged animals, evidence for a general nootropic effect of CCAs in neurologically normal young adult animals is ambiguous. This study attempts to resolve some of this ambiguity by comparing the effects of several CCAs on retention of passive avoidance learning and acquisition and retention of appetitively motivated spatial discrimination learning in young adult mice. Animals were trained in a step through passive avoidance apparatus and, immediately after training, injected subcutaneously with different doses of nimodipine, nifedipine, amlodipine, flunarazine, diltiazem, or verapamil. Retention was tested 24 h after training. In the maze-learning task mice were treated with the same doses of the aforementioned CCAs immediately after a brief training session in a linear maze and retention was tested 24 h after training. The most effective dose of each agent in the maze-retention experiment was administered to additional groups of animals 1 h prior to training to determine the effects of CCAs on acquisition processes. The effects of central administration of CCAs were examined by intracerebroventricular injection of different doses of amlodipine immediately after passive avoidance training. Results showed (1) all peripherally administered drugs except verapamil facilitated retention of passive avoidance training in a dose-dependent manner, (2) all drugs dose dependently facilitated retention of linear maze learning, (3) all doses of the drugs (except verapamil) which facilitated maze retention also facilitated maze learning, and (4) central administration of the dihydropyridine amlodipine produced a dose-dependent facilitation of the retention of passive avoidance learning. These data indicate that drugs which block calcium channels can enhance retention of two different types of learning in mice.

Animals↗

PubMed1990

Facilitation of memory by peripheral administration of substance P and naloxone using avoidance and habituation learning tasks.

This paper summarizes results of a series of experiments dealing with the effects of the neuropeptide substance P (SP) on avoidance learning and habituation. Several doses of SP (0.5, 5, 50, 100, 250, 500 micrograms/kg) were administered posttrial intraperitoneally (IP). Three inhibitory one-trial avoidance tasks were used; uphill, step-down and step-through (alcove). Habituation was measured in an open field by recording the number of rearings. The posttrial injection of SP facilitated avoidance responses as well as reduced rearing in a dose- and time-dependent way. Pretraining and pretest injections (IP) of naloxone facilitated avoidance behavior and potentiated the action of SP, also in a dose-dependent manner. These results demonstrate that: a) peripheral posttraining administration of SP enhances memory; b) SP facilitates not only aversive or positively motivated learning tasks, but also habituation, which is a form of learning that involves neither positive nor negative reinforces; c) SP does not exert its effect by a long-lasting proactive action on performance during the testing trial; d) naloxone potentiates the SP posttraining effect. These data, therefore, suggest that memory-enhancing effects of SP are, at least in part, mediated via interactions between this peptide and endogenous opioid systems.

Animals↗

PubMed2006

Acute effects of maprotiline on learning, anxiety, activity and analgesia in male and female mice.

The acute effects of maprotiline (2.5, 5, 10, 15, 20 or 25 mg/kg) on learning, anxiety, activity and analgesia in male and female mice were evaluated. In addition to inhibitory avoidance learning, anxiety and locomotor activity were measured in the same animals using an elevated plus-maze. A study of the acute effects of maprotiline (15, 20 or 25 mg/kg) on analgesia was carried out in naive animals of both sexes. Maprotiline impaired inhibitory avoidance at doses of 15, 20 or 25 mg/kg. The highest dose produced an anxiolytic effect in females, and the doses of 20 and 25 mg/kg reduced locomotor activity. Analgesia was observed with the highest dose. The impairment of inhibitory avoidance by maprotiline would seem to be independent of the drug's influence on anxiety, is not shadowed by an instrumental performance deficit and, at least in the case of the highest dose, could be influenced by the drug's effects on analgesia. It is hypothesized that acquisition is the memory process principally affected by maprotiline, and in particular stimuli processing. The lack of sex differences in the effects of maprotiline on inhibitory avoidance supports the generalization of findings previously obtained only in males.

Analgesia↗

PubMed2002

BDNF-triggered events in the rat hippocampus are required for both short- and long-term memory formation.

Information storage in the brain is a temporally graded process involving different memory types or phases. It has been assumed for over a century that one or more short-term memory (STM) processes are involved in processing new information while long-term memory (LTM) is being formed. Because brain-derived neutrophic factor (BDNF) modulates both short-term synaptic function and activity-dependent synaptic plasticity in the adult hippocampus, we examined the role of BDNF in STM and LTM formation of a hippocampal-dependent one-trial fear-motivated learning task in rats. Using a competitive RT-PCR quantitation method, we found that inhibitory avoidance training is associated with a rapid and transient increase in BDNF mRNA expression in the hippocampus. Bilateral infusions of function-blocking anti-BDNF antibody into the CA, region of the dorsal hippocampus decreased extracellular signal-regulated kinase 2 (ERK2) activation and impaired STM retention scores. Inhibition of ERK1/2 activation by PD098059 produced similar effects. In contrast, intrahippocampal administration of recombinant human BDNF increased ERK1/2 activation and facilitated STM. The infusion of anti-BDNF antibody impaired LTM when given 15 min before or 1 and 4 hr after training, but not at 0 or 6 hr posttraining, indicating that two hippocampal BDNF-sensitive time windows are critical for LTM formation. At the same time points, PD098059 produced no LTM deficits. Thus, our results indicate that endogenous BDNF is required for both STM and LTM formation of an inhibitory avoidance learning. Additionally, they suggest that this requirement involves ERK1/2-dependent and -independent mechanisms.

Animals↗

PubMed1993

Effects of daily administration of methamphetamine on multiple active/passive avoidance performance in rats.

The effects of daily methamphetamine (M-Amp) treatment with (2 mg/kg/day, i.p.) were examined on multiple active/passive avoidance performance (MAP) in rats. After avoidance training, the animals were given M-Amp every day; on the days of learning sessions, which were on alternate days, the drug was administered at 15 min before the session. Daily administration of M-Amp produced enhancement of the number of respondings (running) as an excitatory dimension of behavior, disruption of immobilities as an inhibitory dimension, and impairment of successes as a discriminatory dimension, when compared with saline-treated rats. Following M-Amp withdrawal, recovery from these damages of learned behavior was observed, except the deterioration in the discriminative dimension. In conclusion, the MAP paradigm is good for assessing the behavioral effects of M-Amp treatment, making it easy to distinct the behavioral effects of M-Amp into excitatory-inhibitory and discriminative dimensions. It is important to distinguish the behavioral components induced by M-Amp, since the damage of learned avoidance performance consists of different dimensions in the M-Amp-treated rats. Impairment of discriminative behavior appears to demonstrate an attentional deficit, which may explain the behavioral disorderliness in M-Amp abusers who display no disturbance of apparent consciousness. These results are discussed with association of brain monoamine alterations.

Animals↗

PubMed1988

Stimulation and antagonism of opioid delta-receptors produce opposite effects on active avoidance conditioning in mice.

The effects of opioid delta-receptor activation on conditioning in a one-way active avoidance paradigm were investigated in mice. Peripheral administration of 30 and 100 micrograms/kg of [Leu5]enkephalin (LE) and 11.6 micrograms/kg of [D-Pen2,D-Pen5]enkephalin (DPDPE), a synthetic enkephalin analog with high delta-selectivity, impaired acquisition of avoidance responding. The dose response functions for both peptides were U-shaped. Deficits in responding were also present 24 hours after training, which suggests that the impaired performance observed during training was not an impairment in the ability of the mice to perform. Also, neither LE nor DPDPE decreased footshock sensitivity or open-field activity, which rules out analgesia and decreased activity levels as likely explanations for the deficits in conditioning. Finally, antagonizing endogenous ligands with the delta-selective antagonist ICI 154,129 enhanced acquisition, an effect opposite that produced by LE and DPDPE. The results suggest that activation of delta-receptors is normally involved in the modulation of active avoidance learning.

Animals↗