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At least 847 records · Page 47Linked to original sources
PubMed2006

Repeated withdrawal from ethanol spares contextual fear conditioning and spatial learning but impairs negative patterning and induces over-responding: evidence for effect on frontal cortical but not hippocampal function?

Repeated exposure of rats to withdrawal from chronic ethanol reduces hippocampal long-term potentiation and gives rise to epileptiform-like activity in hippocampus. We investigated whether such withdrawal experience also affects learning in tasks thought to be sensitive to hippocampal damage. Rats fed an ethanol-containing diet for 24 days with two intermediate 3-day withdrawal episodes, resulting in intakes of 13-14 g/kg ethanol per day, showed impaired negative patterning discrimination compared with controls and animals that had continuous 24-day ethanol treatment, but did not differ from these animals in the degree of contextual freezing 24 h after training or in spatial learning in the Barnes maze. Repeatedly withdrawn animals also showed increased numbers of responses in the period immediately before reinforcement became available in an operant task employing a fixed-interval schedule although overall temporal organization of responding was unimpaired. Thus, in our model of repeated withdrawal from ethanol, previously observed changes in hippocampal function did not manifest at the behavioural level in the tests employed. The deficit seen after repeated withdrawal in the negative patterning discrimination and over-responding in the fixed-interval paradigm might be related to the changes in the functioning of the cortex after withdrawal.

Animals↗
PubMed1999

The absence of relation between anxiety sensitivity and fear conditioning using 20% versus 13% CO2-enriched air as unconditioned stimuli.

Anxiety sensitivity has been implicated as a risk factor in the development and maintenance of anxiety and fear-related disorders. Indeed, persons who score high on the anxiety sensitivity index (ASI) are generally more responsive to biological challenge procedures such as CO2-inhalation that directly evoke the feared bodily events. One would expect, therefore, that persons high on anxiety sensitivity should be more conditionable and hence more likely to acquire fears, than persons low on anxiety sensitivity when CO2-enriched air is used as an unconditioned stimulus (UCS). Undergraduates (N = 96), scoring high, medium and low on the ASI received 8 repeated 20-s inhalations of either 20 or 13% CO2-enriched air (UCSs) paired with one of three CSs differing in fear-relevance (snake, heart and flowers). Several autonomic and self-report measures were assessed. Contrary to expectation, electrodermal and cardiac conditioned responses failed to discriminate between ASI groups. Yet, SUDS and severity and frequency of DSM-IV panic symptoms varied reliably as a function of anxiety sensitivity. Overall, the findings suggest that anxiety sensitivity is related to subjective fear-related complaints, but not autonomic responding and conditionability. We discuss clinical and theoretical implications for understanding the place fo anxiety sensitivity in fear onset.

Adolescent↗
PubMed1992

Comparison of neuroendocrine and behavioral effects of ipsapirone, a 5-HT1A agonist, in three stress paradigms: immobilization, forced swim and conditioned fear.

Ipsapirone is an anxiolytic drug and a serotonin1A (5-HT1A) agonist. The aim of the present study was to investigate the effects of low doses of ipsapirone on the hormonal and behavioral response to three stress procedures: immobilization, forced swim and conditioned emotional response (CER). We examined the effect of ipsapirone (0.1, 0.5 or 1.0 mg/kg) on plasma renin concentration (PRC), adrenal corticotropic hormone (ACTH), corticosterone, prolactin and defecation in rats exposed to immobilization, forced swim or CER stress. All three stressors significantly elevated all the hormone levels (P less than 0.01). Immobilization-induced elevations of PRC, and corticosterone were inhibited by the highest doses of ipsapirone (0.5 and 1 mg/kg, i.p.). However, ipsapirone did not modify the immobilization-induced elevations of plasma ACTH, prolactin or defecation. Ipsapirone was relatively ineffective at reducing the endocrine responses to forced swim. Ipsapirone reduced some, but not all of the hormonal responses to CER stress. CER-induced elevations of corticosterone and prolactin were not inhibited by ipsapirone. However, the ACTH response to CER was significantly (P less than 0.01) inhibited by all doses of ipsapirone and the highest dose of ipsapirone attenuated the renin response. In contrast with the hormonal responses, ipsapirone inhibited all of the behavioral responses to CER stress. Ipsapirone inhibited CER-induced freezing behavior and defecation, while dose-dependently reversing the suppressive effect of CER on exploring, grooming and rearing behaviors. In conclusion, there is a dissociation between the influence of ipsapirone on the endocrine and behavioral responses to CER stress. Ipsapirone also has differential effects on the neuroendocrine response to the three stressors studied. Ipsapirone was most effective in attenuating the hormonal responses to CER, followed by immobilization and swim stress. Of the hormones studied, the stimulation of renin secretion after exposure to the three stressors was most sensitive to ipsapirone, while corticosterone and prolactin were the least sensitive to ipsapirone.

Animals↗
PubMed1987

Evidence of Pavlovian conditioned fear following electrical stimulation of the periaqueductal grey in the rat.

Stimulation of the periaqueductal grey (PAG) has been used to support aversive conditioning in a variety of species with several experimental paradigms. However, it has not been clearly demonstrated whether the behavioral changes produced by PAG stimulation in these paradigms are mediated by associative or nonassociative mechanisms. The present studies demonstrate that electrical stimulation of the PAG in the rat may be used to support associative learning in a Pavlovian paradigm. In each experiment, a fully controlled conditional emotional response (CER) procedure was used to examine the unconditional aversive properties of PAG stimulation. In Experiment 1a, weak associative conditioning was observed when a light CS was paired with PAG stimulation over 6 conditioning trials. In Experiment 1b, robust associative conditioning was obtained with a light CS when 18 conditioning trials were used. In Experiment 2, robust associative conditioning was demonstrated with a tone CS when 6 conditioning trials were used. The results parallel those found when other aversive stimuli are used as a UCS (e.g., footshock or intraorbital air puff), and because the present experiments included the proper control procedures the results clearly indicate that the behavioral changes produced by PAG stimulation are mediated by associative Pavlovian learning mechanisms rather than nonassociative mechanisms such as sensitization or pseudoconditioning. The present technique may be useful for assessing the neuroanatomical and neurochemical substrates underlying the aversive effects of brain-stimulation, and for screening the effects of drugs on the conditional and unconditional responses produced by such stimulation.

Acoustic Stimulation↗
PubMed1996

Contribution of ventral tegmental area dopamine neurons to expression of conditional fear: effects of electrical stimulation, excitotoxin lesions, and quinpirole infusion on potentiated startle in rats.

Potentiated startle was used in this study to determine the fear-motivational functions of the ventral tegmental area (VTA). In Experiment 1, electrical stimulation of the VTA increased acoustic startle amplitudes. In subsequent experiments fear-potentiated startle was assessed following axon-sparing N-methyl-D-aspartic acid (NMDA) lesions of the VTA and after bilateral intra-VTA infusion of the dopamine (DA) D2/3 receptor agonist quinpirole. The NMDA lesions produced substantial cell loss in the medial ventral tegmentum and suppressed fear expression. Similarly, inhibition of DA neuronal activity associated with locally administered quinpirole blocked fear-potentiated startle. It was suggested that VTA neurons and their forebrain DA projections regulate levels of aversive emotional arousal within the amygdala-based fear system.

Acoustic Stimulation↗
PubMedDate not supplied

Spared anterograde memory for shock-probe fear conditioning after inactivation of the amygdala.

Previous studies have shown that amygdala lesions impair avoidance of an electrified probe. This finding has been interpreted as indicating that amygdala lesions reduce fear. It is unclear, however, whether amygdala-lesioned rats learn that the probe is associated with shock. If the lesions prevent the formation of this association, then pretraining reversible inactivation of the amygdala should impair both acquisition and retention performance. To test this hypothesis, the amygdala was inactivated (tetrodotoxin; TTX; 1 ng/side) before a shock-probe acquisition session, and retention was tested 4 d later. The data indicated that, compared with rats infused with vehicle, rats infused with TTX received more shocks during the acquisition session, but more importantly, were not impaired on the retention test. In Experiment 2, we assessed whether the spared memory on the retention test was caused by overtraining during acquisition. We used the same procedure as in Experiment 1, with the exception that the number of shocks the rats received during the acquisition session was limited to four. Again the data indicated that amygdala inactivation did not impair performance on the retention test. These results indicate that amygdala inactivation does not prevent the formation of an association between the shock and the probe and that shock-probe deficits during acquisition likely reflect the amygdala's involvement in other processes.

Amygdala↗
PubMed1981

Contextual conditioning and the US preexposure effect in conditioned fear.

A series of five experiments was carried out in which fear of context caused by exposure to shocks was manipulated by signaling the shocks with a discrete stimulus, signaling the days during which shocks occurred with a session-long stimulus, or switching the context between exposure and the subsequent test. All these manipulations influenced fear of the context in the manner predicted by the Rescorla-Wagner associative model. Following this, all the rats were given conditioning trials with shock and a different discrete stimulus. All preexposure treatments produced consistent and reliable interference with conditioning with the exception of signaling the shocks with a discrete stimulus, which greatly reduced interference. These results are interpreted as being consistent both with a cognitive explanation of the US exposure effect, which claims that animals learn that shocks are unpredictable during conditioning and this knowledge retards future conditioning when they are predictable, and with an adaptation explanation, which claims that unpredictable shocks produce chronic fear and this fear through either a change in adaptation level or through emotional exhaustion renders the shocks less reinforcing during the conditioning test.

Adaptation, Psychological↗
PubMed2006

Synaptically released zinc gates long-term potentiation in fear conditioning pathways.

The functional role of releasable Zn2+ in the central nervous system remains unknown. Here we show that zinc transporter 3 (ZnT-3), which maintains a high concentration of Zn2+ in synaptic vesicles and serves as a marker for zinc-containing neurons, is enriched in the lateral nucleus of the amygdala and in the temporal area 3 of the auditory cortex, an area that conveys information about the auditory conditioned stimulus to the lateral nucleus of the amygdala, but not in other conditioned stimulus areas located in the auditory thalamus. Using whole-cell recordings from amygdala slices, we demonstrated that activity-dependent release of chelatable Zn2+ is required for the induction of spike timing-dependent long-term potentiation in cortical input to the amygdala implicated in fear learning. Our data indicate that synaptically released Zn2+ enables long-term potentiation at the cortico-amygdala synapses by depressing feed-forward GABAergic inhibition of principal neurons. This regulatory mechanism, implicating pathway-dependent release of Zn2+, may serve an essential control function in assuring spatial specificity of long-lasting synaptic modifications in the neural circuit of a learned behavior.

Animals↗
PubMed1991

Evaluation of a psychophysiological model of classical fear conditioning in anxious patients.

Skin conductance variables have been compared in 30 anxious patients and 30 controls to investigate the extent to which anxiety is associated with increased autonomic arousal, reduced habituation or enhanced aversive conditioning. Skin conductance level, variability (spontaneous fluctuations) and response amplitudes to tones were significantly greater in patients than controls. Habituation of skin conductance responses to a series of ten innocuous tones (80 dB, 1 s) did not differ between the groups. Aversively conditioned skin conductance responses were measured to a further series of ten tones after a conditioning trial in which a loud white noise (100 dB) followed tone 11. All subjects showed enhanced (conditioned) responses to the tones after the conditioning trial, but patients did not show greater conditioning than controls. The results indicate that anxious neurotic out-patients have greater sweat gland activity and reactivity than controls but fail to demonstrate differences in central mechanisms of habituation or conditioning.

Acoustic Stimulation↗
PubMed1997

Projections from the lateral part of the central amygdalar nucleus to the postulated fear conditioning circuit.

The lateral part of the central nucleus projects densely to only three regions: the medial part of the central nucleus, restricted parts of the bed nuclei of the stria terminalis, and the parabrachial nucleus in the pons. The possible role of the lateral central amygdalar nucleus in circuitry mediating conditioned emotional responses is discussed; changing neuropeptide levels in the lateral part may act as a 'gain control' for reversible long-term modulation (LTM) of medial part output.

Amygdala↗
PubMed2002

Unconscious amygdalar fear conditioning in a subset of chronic fatigue syndrome patients.

Here, a novel hypothesis for chronic fatigue syndrome (CFS) is proposed. CFS may be a neurophysiological disorder focussing on the amygdala. During a 'traumatic' neurological event often involving acute psychological stress combined with a viral infection or other chemical or physiological stressor, a conditioned network or 'cell assembly' may be created in the amygdala. The unconscious amygdala may become conditioned to be chronically sensitised to negative symptoms arising from the body. Negative signals from the viscera or physiological, chemical and dietary stressors, become conditioned stimuli and the conditioned response is a chronic sympathetic outpouring from the amygdala via various brain pathways including the hypothalamus. This cell assembly then produces the CFS vicious circle, where an unconscious negative reaction to symptoms causes immune reactivation/dysfunction, chronic sympathetic stimulation, leading to sympathetic dysfunction, mental and physical exhaustion, and a host of other distressing symptoms and secondary complications. And these are exactly the symptoms that the amygdala and associated limbic structures are trained to monitor and respond to, perpetuating a vicious circle. Recovery from CFS may involve projections from the medial prefrontal cortex to the amygdala, to control the amygdala's expressions. I shall firstly discuss predisposing, precipitating, and perpetuating factors involved in the possible etiology of chronic fatigue syndrome (CFS), followed by the patient's experience of the illness. Finally, I shall look at a suggested explanation for the symptoms of CFS.

Amygdala↗