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Results for “fear conditioning”

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PubMed1991

Effects of NMDA receptor antagonists and sigma ligands on the acquisition of conditioned fear in mice.

Recent studies have shown that several compounds known to act as competitive or non-competitive antagonists of NMDA receptors can disrupt learning in rodents. The present study was carried out to investigate the effects of a range of NMDA antagonists, acting at several sites in the NMDA receptor complex, on the acquisition of learned fear in mice. Dose-related disruptions of learning were produced by the non-competitive antagonists phencyclidine, dizocilpine, dextromethorphan and (+) and (-)N-allylnormetazocine. The (+) enantiomer of N-allylnormetazocine was approximately twice as potent as the (-) enantiomer. The competitive NMDA receptor antagonist, CGS 19755, also blocked the acquisition of learned fear as did the non-specific glutamate antagonist riluzole. In contrast, the anti-ischaemic drugs ifenprodil and SL 82.0715, which probably act as NMDA antagonists through an effect on the polyamine site, had no effect on learning up to doses which substantially reduced locomotion. The sigma receptor ligand DTG was also inactive. These results confirm that both competitive and non-competitive NMDA antagonists disrupt learning but indicate that the extent to which such an effect is observed may depend on the site at which the compounds act within the receptor complex. Activity at sigma receptors is unrelated to the effect on learning.

Animals↗
PubMed1979

Morphine and naloxone: effects on conditioned fear as measured with the potentiated startle paradigm.

Morphine (0.6 to 10 mg/kg) produced a dose-dependent reduction of the potentiated startle effect where acoustic startle amplitude is normally increased in the presence of a light previously paired with a shock. The effect was selective since the same doses did not appreciably depress baseline levels of startle. Naloxone (2 mg/kg) did not significantly affect potentiated startle, but antagonized the ability of morphine (10 mg/kg) to block potentiated startle. Morphine did not block potentiated startle by accelerating extinction. The advantages of this paradigm for studying fear or anxiety were discussed.

Animals↗
PubMed1989

Fear conditioning, meaning, and belongingness: a selective association analysis.

Twenty-three subjects rated the belongingness of pairs of conditionable (photographic slides) and unconditioned (e.g., shock, tone, human scream) stimuli. Forty new subjects were then classically conditioned, using rating-defined high (angry face/scream) and low (landscape/scream) belongingness pairs. Finger-pulse responses to the high-belongingness pairs showed superior acquisition and resistance to extinction. Another 40 subjects were conditioned to compound stimuli: a slide (either landscape or angry face) that was the same over trials, and a yellow or blue background that was the discriminant cue for the unconditioned stimulus (scream). When the angry face (the high-belongingness slide) was the invariant part of the compound, relatively poorer differential pulse-volume and skin-conductance conditioning was observed. Thus, depending on the task, a priori belongingness rendered stimuli selectively conditionable, either enhancing or inhibiting visceral response associations.

Association↗
PubMed1999

Theoretical mechanisms underlying the trial-spacing effect in Pavlovian fear conditioning.

Contemporary explanations of the trial-spacing effect (TSE) were evaluated. Experiment 1 revealed, in rats given tone-footshock trials with 15-, 60-, or 900-s intertrial intervals (ITIs), a direct relationship between freezing to the tone and ITI (the TSE) but an inverted U-shaped relationship between freezing to the training context and ITI. In Experiment 2, footshock preexposure eliminated the TSE that otherwise occurs across 15- to 60-s ITIs but had no effect on the TSE that occurs across 60- to 900-s ITIs. In Experiments 3 and 4, neither (a) increasing posttraining exposure to the training context in rats trained with 60-s ITIs nor (b) reducing between-trial exposure to this context in rats trained with 900-s ITIs influenced freezing to the tone. These findings suggest that the TSE obtained in this research is due to more than 1 mechanism: 1 responsible for the TSE that occurs with ITIs less than approximately 60 s and another responsible for the TSE that occurs with ITIs greater than this. Although the perceptual-defensive-recuperative model may correctly describe the former mechanism, none of the theories tested seems to correctly describe the latter.

Animals↗
PubMed2003

Stimulation of medial prefrontal cortex decreases the responsiveness of central amygdala output neurons.

In extinction of auditory fear conditioning, rats learn that a tone no longer predicts the occurrence of a footshock. Recent lesion and unit recording studies suggest that the medial prefrontal cortex (mPFC) plays an essential role in the inhibition of conditioned fear following extinction. mPFC has robust projections to the amygdala, a structure that is known to mediate the acquisition and expression of conditioned fear. Fear conditioning potentiates the tone responses of neurons in the basolateral amygdala (BLA), which excite neurons in the central nucleus (Ce) of the amygdala. In turn, the Ce projects to the brainstem and hypothalamic areas that mediate fear responses. The present study was undertaken to test the hypothesis that the mPFC inhibits conditioned fear via feedforward inhibition of Ce output neurons. Recording extracellularly from physiologically identified brainstem-projecting Ce neurons, we tested the effect of mPFC prestimulation on Ce responsiveness to synaptic input. In support of our hypothesis, mPFC prestimulation dramatically reduced the responsiveness of Ce output neurons to inputs from the insular cortex and BLA. Thus, our findings support the idea that mPFC gates impulse transmission from the BLA to Ce, perhaps through GABAergic intercalated cells, thereby gating the expression of conditioned fear.

Action Potentials↗
PubMed2004

Temporary inactivation of the nucleus accumbens disrupts acquisition and expression of fear-potentiated startle in rats.

Recent research suggests that in addition to its prominent role in appetitive learning, the nucleus accumbens (NAC) may also be involved in fear conditioning. In the present study, we investigated whether temporary inactivation of the NAC, by injection of tetrodotoxin (TTX), affects acquisition and expression of conditioned fear, as measured by fear-potentiated startle (FPS). TTX injection into the NAC totally blocked acquisition and markedly decreased expression of conditioned fear to a discrete visual conditioned stimulus (CS). Interestingly, temporary inactivation of the NAC did not affect shock sensitization of startle, indicating that both the perception of the shock and short-term contextual conditioning was not affected by intra-accumbal TTX injection. Taken together, these results show that the NAC is crucial for acquisition and expression of long-term conditioned fear, as measured by fear-potentiated startle, to discrete CSs, but not short-term conditioned fear to a context.

Anesthetics, Local↗