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PubMed1979

Stimulus and procedural determinants of the forgetting of conditioned fear.

Two studies investigated factors believed to influence the retention of acquired fear in rats. The results show clearly that the lack of forgetting over 24-hr interval reported by previous investigators is due to a depression of performance on the immediate test (3-min retention interval) resulting from the procedure of not handling the rats during conditioning but then handling them on every trial during the retention test. In accord with the McAllister's interpretation of related results, the depression of performance after short retention intervals may be due to a lack of generalization from training to the testing situation. As the retention interval is lengthened, the amount of generalization increases and escape performance improves on a relative basis. The nature of the retention function may be severely distorted by selection of an inappropriate paradigm for its evaluation.

Animals↗
PubMed1995

Conditioning of fear and conditioning of safety in rats.

In separate groups of rats forward and backward procedures for classical defensive conditioning were superimposed on on-going bar pressing for food. The forward conditioned stimulus elicited suppression of bar presses, indicating acquisition of fear. The backward stimulus paired with identical shock elicited behaviour typical for rats in a condition of safety and caused an increase of bar press rate. Enhancement of bar presses acquired in the course of backward conditioning was stable, immune to influences from unsignalled shocks presented in the same experimental context, and resistant to extinction when all shocks were discontinued. Properties of the employed variety of the backward conditioning procedure are discussed. When a brief shock overshadowed the onset of a backward stimulus, the remaining portion of the stimulus became a signal of safety.

Analysis of Variance↗
PubMed1999

Effect of subchronic lithium carbonate treatment on anxiolytic-like effect of citalopram and MKC-242 in conditioned fear stress in the rat.

We investigated the effect of citalopram [selective serotonin (5-HT) reuptake inhibitor] and MKC-242 (5-[3-¿(2S)-(1, 4-Benzodioxan-2-ylmethyl) amino¿propoxy]-1, 3-benzo-dioxol hydrochloride; a selective 5-HT(1A) receptor agonist) on the expression of conditioned freezing, an index of anxiety, following treatment with subchronic lithium carbonate (LiCO(3)). Male Sprague-Dawley rats were used in these experiments. Acute administration of citalopram (subcutaneously, s.c.) reduced freezing significantly at a high dose (30 mg/kg), while showing no effect at lower doses (3 and 10 mg/kg). Acute administration of MKC-242 (s.c.; 0.1-10 mg/kg) dose dependently reduced freezing. Subchronic LiCO(3) treatment (1 week; 0.05% or 0.2% LiCO(3) in diet; p.o.) showed no effect on freezing behavior. Acute treatment with both citalopram (3 and 30 mg/kg) and MKC-242 (1 mg/kg) after subchronic treatment with the higher, but not the lower concentration of LiCO(3) (1 week), reduced freezing markedly and significantly, as compared with either drug alone. These results suggest that subchronic LiCO(3) treatment enhanced the anxiolytic-like effects of these serotonergic drugs by facilitating central 5-HT neurotransmission at clinically therapeutic plasma lithium levels.

Animals↗
PubMed1979

Diazepam and flurazepam: effects on conditioned fear as measured with the potentiated startle paradigm.

Diazepam (0.3, 0.6, 1.2, or 2.5 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. Even the lowest dose tested (0.3 mg/kg) significantly attenuated potentiated startle. The effect was selective since the same doses did not depress baseline startle amplitude measured in the same animals in the same test session. A 2 X 2 design in which rats were trained and tested under the same or different drug condition (diazepam or saline) showed the results could not be explained by state-dependent learning. The primary effect of diazepam was to block expression of rather than acquisition of fear as measured by potentiated startle. Flurazepam (2.5, 10, or 20 mg/kg) also reduced potentiated startle selectively but was 6--8 times less potent than diazepam. These and other results suggest that the potentiated startle paradigm, as a measure of classical conditioning that involves no operant, might provide a useful adjunct to behavioral methods currently being used to analyze antianxiety compounds.

Animals↗
PubMed2006

Recovery of conditioned fear by a single postextinction shock: effect of similarity of shock contexts and of time following extinction.

Subjects in six experimental groups (n = 16 each) received one-trial passive avoidance (PA) training in which shock was delivered upon movement from a white wooden floor compartment to a black grid compartment. Then fear was extinguished (30 min) in the black compartment. After either 24 or 168 h, all the groups were treated in a room distinctively different from the training room. At each interval, one group received a shock in an apparatus similar to the conditioning box, another received a shock in a dissimilar apparatus, and another was placed in a neutral box. A PA test trial in the training apparatus indicated reinstatement of extinguished fear in all the groups given a postextinction shock except the 24-h dissimilar group. Control groups revealed that the extinction treatment was effective and that spontaneous recovery was not evident. The results were explained in terms of classical conditioning, stimulus generalization, and the broadening (flattening) of stimulus generalization gradients with time.

Animals↗
PubMedDate not supplied

Effects of conditioned fear and environmental novelty on plasma beta-endorphin in the rat.

The levels of rat plasma beta-endorphin-like immunoreactivity following a 30 min exposure to (1) an unfamiliar operant chamber, (2) an unfamiliar operant chamber providing a VI-5 second schedule of 3 mA, 1 sec footshocks, or (3) a familiar chamber providing no shocks, but previously paired with unavoidable shocks were compared to control values from animals left undisturbed in their familiar home cages. The shocked group showed ten-fold elevations of beta-endorphin-like immunoreactivity compared to the undisturbed control animals, while conditioned rats showed a smaller two-fold elevation when re-exposed to a chamber in which they had previously been shocked. Two of five rats exposed merely to an unfamiliar chamber showed elevations, but there was no statistically reliable group effect. Such procedures may be useful for controlled and parametric studies of the mobilization of pituitary or brain pools of beta-endorphin under conditions involving merely anticipation of pain rather than the actual activation of ascending nervous pain pathways.

Animals↗
PubMed1999

Conditioned fear attenuates light-induced suppression of melatonin release in rats.

Male rats were given 5 min of intermittent footshock, or were not shocked, for 3 or 5 consecutive days in a novel context at the midpoint of the dark phase of a 12:12-h light:dark cycle. Six days later, animals were reexposed to the context without footshock and received either a 5-min light pulse or were not disturbed. Reexposure to the context significantly increased plasma corticosterone in animals previously shocked there. Prior context-shock pairings significantly attenuated the suppression of melatonin by light, but did not affect basal levels of melatonin. These results suggest that the circuitry underlying the suppression of melatonin by light can be modified by changes in emotional state produced by aversive conditioning.

Animals↗
PubMedDate not supplied

Postextinction infusion of a mitogen-activated protein kinase inhibitor into the medial prefrontal cortex impairs memory of the extinction of conditioned fear.

We investigated whether postextinction training infusion of PD098059, a selective inhibitor of mitogen-activated protein kinase (MAPK) activation, into the medial prefrontal cortex, would impair retention of extinction learning in rats. We found that immediate, but not late (2 or 4 h), postextinction infusion of PD098059 provoked a full return of conditioned freezing. These results suggest that activation of prefrontal MAPK in early stages of postextinction training participates in processes that protect against spontaneous recovery of aversive responses.

Animals↗
PubMed2000

L -sulpiride, at antidepressant dosage, prevents conditioned-fear stress-induced gastric lesions in rats.

It has been previously shown that long-term treatment with low doses of l-sulpiride is highly effective in rat models of depression and of anticipatory anxiety/panic behavior. The present study was aimed at investigating whether the same treatment can prevent the ulcerogenic effect of repeated inescapable stresses. In adult rats, the repeated (7 consecutive days) exposure to an uncontrollable stressful condition (inescapable 2.5 mA scrambled shock for 60 s) produced the development of gastric lesions (multiple punctiform telangiectasias in all rats, with superficial erosions or more severe ulcerations in 10 out 13 rats; score 4.67 +/- 0.44). l-sulpiride, intraperitoneally injected once a day at an antidepressant dose level (4 mg kg(-1) per day), starting 21 days before the beginning of the 7-day sequence of inescapable punishments ( = 28 daily treatments), almost completely prevented the stress-induced gastric injury (score 1.67 +/- 0.29; P< 0.001 vs saline-treated rats, Mann-Whitney U test). These results show that, in rats, a long-term treatment with low doses of l-sulpiride prevents the development of gastric lesions induced by chronic exposure to uncontrollable stress.

Animals↗
PubMed2006

The role of the amygdala in the extinction of conditioned fear.

The amygdala has long been known to play a central role in the acquisition and expression of fear. More recently, convergent evidence has implicated the amygdala in the extinction of fear as well. In rodents, some of this evidence comes from the infusion of drugs directly into the amygdala and, in particular, into the basolateral complex of the amygdala, during or after extinction learning. In vivo electrophysiology has identified cellular correlates of extinction learning and memory in the lateral nucleus of that structure. Human imaging experiments also indicate that amygdaloid activity correlates with extinction training. In addition, some studies have directly identified changes in molecular constituents of the basolateral amygdala. Together these experiments strongly indicate that the basolateral amygdala plays a crucial role in extinction learning. Interpreted in the light of these findings, several recent in vitro electrophysiology studies in amygdala-containing brain slices are suggestive of potential synaptic and circuit bases of extinction learning.

Amygdala↗
PubMed2006

Neonatal treatment with a competitive NMDA antagonist results in response-specific disruption of conditioned fear in preweanling rats.

RATIONALE: The N-methyl-D-aspartate (NMDA) receptor has been implicated in processes of neurodevelopment, including cell proliferation, synaptogenesis, and apoptosis. Several studies have reported that administration of NMDA antagonists early in development can cause long-lasting changes in behavior. For example, Gould and Cameron [Behav Neurosci 111:49-56 (1997a)] have shown that a single injection of the competitive NMDA antagonist CGP 43487 on postnatal day (PD) 5 affected behavioral immobility in young rats exposed to the odor of a natural predator. OBJECTIVES: This experiment was undertaken to determine whether the behavioral effects previously reported would also be seen with conditioned cues. Both stimulus-elicited behavioral immobility (freezing) and changes in heart rate were recorded to examine impairments in responding across multiple measures. METHODS: Animals were given a single injection of 0, 2.5, or 5.0 mg/kg CGP 43487 on PD 5. On PD 20 subjects were given paired or unpaired presentations of either an olfactory or auditory conditioned stimulus (CS) with a 110-dB-white-noise unconditioned stimulus. CS-elicited freezing and changes in heart rate were measured. RESULTS: Pups treated with CGP exhibited impairments in conditioned freezing, but were unaffected in their expression of conditioned changes in heart rate, to both olfactory and auditory stimuli. CONCLUSIONS: These results indicate that neonatal treatment with an NMDA antagonist affects the expression of fear in a response-specific manner. The data suggest that antagonist-induced alterations in neural systems involved in the expression of freezing are affected by NMDA receptor blockade early in life.

2-Amino-5-phosphonovalerate↗
PubMed2003

Sleep after differing amounts of conditioned fear training in BALB/cJ mice.

Shock training and auditory cues associated with shock produce alterations in sleep that can be long-lasting in BALB/cJ (C) mice. We examined sleep in C mice after different amounts of shock training, and after cues with different strength cue-shock associations. Mice were implanted with transmitters for determining sleep via telemetry. After baseline sleep recording, the mice were trained (between 08:00 and 09:00 h) to associate a cue (tone) with footshock in either single shock training (SST: a single tone-shock pairing) or multiple shock training (MST: 15 tone-shock pairings) conditions. For testing, the mice were presented 15 cues (tone only) in their home cage between 10:45 and 11:00 h on post-training days 6, 13, 20, 27, and 34 (Cue 1 to Cue 5) following shock training. Sleep was recorded for two days after shock training or cue presentation. A separate group of mice received 15 tone-shock pairings and had their sleep recorded for 10 consecutive uninterrupted days. Both SST and MST mice showed decreases in rapid eye movement sleep (REM) after shock training, with the larger effect in the MST mice. Only MST mice showed significant reductions in REM in response to the fearful cues, and longer-term alterations in sleep could be observed even on the day after cue presentation. These results indicate that reminders of an aversive event can impact sleep for prolonged periods, and that the degree of the impact varies with amount of training.

Acoustic Stimulation↗
PubMed1995

Effects of a microinjection of morphine into the amygdala on the acquisition and expression of conditioned fear and hypoalgesia in rats.

A unilateral microinjection of morphine into the amygdala impaired the acquisition of fear and hypoalgesic responses in rats exposed to a heated floor in a hot-plate apparatus. This impairment was dose dependent, receptor specific, and not observed in rats microinjected with morphine into the caudal basolateral amygdala. A microinjection of morphine into the amygdala reduced the expression of fear responses and of naloxone-sensitive hypoalgesic responses, but did not reduce the expression of naloxone-insensitive hypoalgesic responses. The results document an involvement of opioidergic mechanisms in the amygdala in learned danger and of the amygdala in the control of opioid hypoalgesic responses. They also suggest that learned danger can activate antinociceptive mechanisms independently of the amygdala.

Amygdala↗
PubMed1997

Effects of electrolytic lesions of the medial prefrontal cortex or its subfields on 4-arm baited, 8-arm radial maze, two-way active avoidance and conditioned fear tasks in the rat.

The present study tested the effects of electrolytic lesions in two mPFC subregions, the dorsal anterior cingulate area (dACA) and prelimbic cortex, as well as the effects of a larger medial prefrontal cortex (mPFC) lesion which included both subregions, on 4-arm baited, 4-arm unbaited, 8-arm radial maze task and its reversal (Experiments 1 and 4), two-way active avoidance (Experiments 2 and 5) and conditioned emotional response (Experiments 3 and 6). Rats with large or small lesions of the mPFC learned the location of the 4 baited arms in the training and reversal stages of the radial maze task similarly to sham rats, indicating that these lesions did not affect animals' capacity to process and remember spatial information. dACA and mPFC lesions produced a transient deficit in the acquisition of the radial maze task, suggestive of an involvement of these regions in mnemonic processes. However, in view of the normal performance of these groups by the end of training and during reversal, this deficit is better interpreted as stemming from a difficulty to learn the memory-based strategy used to solve the task. Only mPFC lesion led to better avoidance performance at the beginning of training and tended to increase response during the presentation of a stimulus previously paired with shock, compared to sham rats. Both effects can be taken as an indication of reduced emotionality following mPFC lesion. The results are discussed in relation to known behavioral functions of the mPFC and the suggested functional specialization within this region.

Animals↗
PubMed1981

Associative learning in Aplysia: cellular correlates supporting a conditioned fear hypothesis.

Aversive associative learning in Aplysia california survives restraint of the animal and surgical exposure of the central nervous system. The learning is expressed in the intracellularly recorded activity of identified motor neurons mediating three different defensive behaviors: escape locomotion, inking, and siphon withdrawal. In each case, animals that had previously received paired training showed significant facilitation of synaptic input to motor neurons during test stimulation in the presence of the conditioned stimulus. Animals without such training showed no facilitation of input to the motor neurons. Resting potential and input resistance appeared unaffected by conditioning and were not altered by application of the conditioned stimulus. These results show that the conditioned facilitation of defensive responses cannot be explained by subthreshold actions of the conditioned stimulus on the motor neurons and support the hypothesis that Aplysia learn to associate the conditioned stimulus with a fearlike central state.

Action Potentials↗
PubMed2004

D-cycloserine and the facilitation of extinction of conditioned fear: consequences for reinstatement.

Several recent studies have reported that D-cycloserine (DCS), a partial N-methyl-D-aspartate agonist, facilitates extinction of learned fear in rats. Other studies have shown that representation of the unconditioned stimulus (US) can reinstate learned fear after extinction. This study examined whether this reinstatement effect occurs in Sprague-Dawley rats given DCS at the time of extinction. Results showed that saline-treated rats exhibited the reinstatement effect but DCS-treated rats did not (Experiments 1 and 2). This lack of reinstatement in DCS-treated rats was not due to residual effects of DCS on either US or context processing (Experiment 3). Overall, these results (a) raise questions about the mechanisms underlying DCS facilitation of extinction and (b) suggest that DCS might have substantial practical benefit.

Analysis of Variance↗