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PubMed2004

Temporal encoding in fear conditioning revealed through associative reflex facilitation.

Temporal encoding in Pavlovian fear conditioning was examined through conditional facilitation of the short-latency (Rl) component of the rat eyeblink reflex. Rats were fear-conditioned to a tone conditional stimulus (CS) with either a 3- or 9-s interstimulus interval (ISI) between CS onset and the onset of the grid-shock unconditional stimulus (US). Rl facilitation was tested over 2 days, in counterbalanced order, at a latency of 3 s and 9 s from CS onset. CS-produced Rl facilitation, the conditional response (CR), was 3-4 times larger when the test latency equaled the conditioning ISI. These results, coupled with the known neurophysiology of Rl facilitation, suggest that this CR could disclose differences in the time course of CS-generated output from the amygdala when driven by cortical versus subcortical CS-CR pathways.

Animals↗
PubMed2005

Perinatal nutritional iron deficiency permanently impairs hippocampus-dependent trace fear conditioning in rats.

Many studies show that iron deficient (ID) children are at risk for poor cognitive development. This suggests that learning and cognitive centers in the brain, such as the hippocampus, may be compromised by developmental ID. The present study used a heart rate trace fear conditioning procedure in rats to show that perinatal nutritional ID impairs hippocampus-dependent learning. This procedure requires rats to associate a conditioned stimulus and a fearful unconditioned stimulus, which are separated by a trace interval. Rats were started on ID or control (CN) diets 10 days prior to birth, and learning was assessed on post natal day (PND)-28. The ID pups were impaired in trace fear coniditioning, but an ID control group was not impaired in a non-trace basic fear conditioning procedure that does not depend on the hippocampus. Another group was switched from ID to CN diet on PND-31, and this group also showed impairments in trace fear conditioning when tested during early adulthood (i.e. PND-63). Separate control tests show that ID may produce skeletal motor deficits. The ID-induced learning impairments in this study, however, were not due to altered motor activity because learning was assessed using non-motor heart rate responses.

Animal Nutritional Physiological Phenomena↗
PubMed2006

Membrane excitability and fear conditioning in cerebellar Purkinje cell.

In a previous study it has been demonstrated that fear conditioning is associated with a long-lasting potentiation of parallel fiber to Purkinje cell synaptic transmission in vermal lobules V and VI. Since modifications of intrinsic membrane properties have been suggested to mediate some forms of memory processes, we investigated possible changes of Purkinje cell intrinsic properties following the same learning paradigm and in the same cerebellar region. By means of the patch clamp technique, Purkinje cell passive and active membrane properties were evaluated in slices prepared from rats 10 min or 24 h after fear conditioning and in slices from control naïve animals. None of the evaluated parameters (input resistance, inward rectification, maximal firing frequency and the first inter-spike interval, post-burst afterhyperpolarization, action potential threshold and amplitude, action potential afterhyperpolarization) was significantly different between the three studied groups also in those cells where parallel fiber-Purkinje cell synapse was potentiated. Our results show that fear learning does not affect the intrinsic membrane properties involved in Purkinje cell firing. Therefore, at the level of Purkinje cell the plastic change associated with fear conditioning is specifically restricted to synaptic efficacy.

Action Potentials↗
PubMed1986

Zimelidine does not antagonise the effects of alcohol or diazepam on the acquisition of conditioned fear in mice.

Recent work has suggested that, in man, the specific inhibitor of serotonin reuptake, zimelidine, can block the effects of ethanol on memory processes without affecting psychomotor performance decrements produced by ethanol. The present study was carried out to investigate whether a similar interaction between ethanol and zimelidine could be observed in mice. Using a 2-trial conditioned fear test known to be sensitive to the effects of benzodiazepines and similar drugs, it was found that ethanol, administered before the first trial, produced a dose-related disruption of fear conditioning as shown on the second trial. In a second experiment several doses of zimelidine were administered at the same time as a dose of either ethanol or diazepam. No evidence was obtained for a zimelidine-induced antagonism of the effects of either ethanol or diazepam.

Animals↗
PubMed1997

Enhancement of morphine analgesia in rats following removal from contextual conditioned fear cues.

1. Previous studies have shown that morphine analgesia is enhanced when analgesia testing is conducted in an environment that has been previously paired with shock, but not in a novel or neutral environment. 2. Two experiments were conducted to assess if enhanced morphine analgesia could be demonstrated in a neutral context if rats were first exposed to conditioned fear cues. This was done by pre-exposing rats to a context previously paired with shock and testing for enhanced morphine analgesia in a neutral context immediately following removal from the conditioned fear context. To determine if conditioned analgesia contributed to the enhanced morphine analgesia, rats were tested for analgesic responsiveness immediately following removal from conditioned fear cues, prior to morphine administration. 3. In Experiment 1, although conditioned analgesia was not observed, a small enhancement of morphine analgesia was demonstrated in an neutral context in rats pre-exposed to conditioned fear cues, compared to non-conditioned controls. 4. In Experiment 2, which employed more sensitive test procedures, a strong enhancement of morphine analgesia was observed in a neutral context only in those rats that demonstrated conditioned analgesia.

Analgesia↗
PubMed1999

Effects of conditioned fear stress on serotonin neurotransmission and freezing behavior in rats.

In an attempt to clarify the role of the brain serotonergic system in the psychopathology of anxiety, we examined the effect of a psychological stress, conditioned fear stress, on extracellular serotonin (5-hydroxytryptamine, 5-HT) concentrations in the rat medial prefrontal cortex using the method of in vivo microdialysis, while simultaneously observing conditioned fear stress-induced freezing behavior, an index of anxiety. Conditioned fear stress increased extracellular 5-HT levels in the medial prefrontal cortex, and this 5-HT level increase was followed by a resolution of the freezing behavior. A dose of 10 mg/kg of a selective 5-HT reuptake inhibitor, citalopram, administered 60 min before exposure to conditioned fear stress increased extracellular 5-HT concentrations immediately and potently, reducing freezing behavior. These findings strongly suggest that facilitation of brain 5-HT neurotransmission decreases anxiety, which is in agreement with the clinical reports that selective 5-HT reuptake inhibitors are effective in the treatment of anxiety disorders.

Animals↗
PubMed1978

Antinociception following lesion-induced hyperemotionality and conditioned fear.

Hyperemotionality and antinociception (during hyperemotional states) followed lesioning of the septal area in rats. Both of these behaviors showed parallel decreases with daily handling as well as significant positive correlations between them. Tail-flick latencies were also elevated when fear was conditioned to the environmental cues associated with the tail-flick procedure. Fear-induced antinociception trials. These results are interpreted as demonstrations of the behavioral activation of endogenous antinociceptive mechanisms and are in agreement with the postulates of centrifugal control of nociception of the gate control theory of pain.

Animals↗
PubMed2004

Non-specific effect of fear conditioning and specific effect of social defeat on social recognition memory performance in female rats.

The so called "emotion learning" literature describes the ability of distressing and aversive unconditioned stimuli to classically condition a learned avoidance response. In order to investigate the impact of experience with noxious stimuli in one conditioning context on learning and memory performance in a separate, non-aversively motivated task, juvenile recognition ability was examined in adult female rats exposed previously to one of two environmental stressors. In particular, experimental adult rats were either socially defeated by exposure to an aggressive conspecific rat or fear conditioned using single or multiple pairings with footshock prior to performance of the social recognition task. Experiment 1 established that repeated exposure to a single juvenile resulted in social memory formation reflected in decreased social investigation from the first to the second exposure. Experiment 2 documented that both single and multiple pairings of an environment with footshock produced robust freezing behavior (90-95% suppression of activity). In addition, fear conditioning produced a non-specific 5-60% increase in social investigation time in both single and multiple-pairing fear conditioned groups which confounded the ability of the social recognition measure to assess effects of fear conditioning on learning and memory performance per se. In contrast, Experiment 3 documented that when social recognition memory performance was impaired to 85% of control levels by imposition of a 2 h delay, exposure to a social defeat stressor reinstated optimal social recognition memory performance. These findings suggest that the after effects of fear conditioning include non-specific alteration of social investigation whereas exposure to conspecific aggression enhances subsequent social recognition memory.

Aggression↗
PubMed2006

Dual activation of cardiac sympathetic and parasympathetic components during conditioned fear to context in the rat.

1. The present study investigates the contribution of the sympathetic and vagal parasympathetic systems to the tachycardic response of long-lasting (40 min) conditioned fear responses to context. 2. The conditioned fear response evoked by re-exposure to a footshock chamber was tested 10 min after intravenous injection of the beta-adrenoceptor antagonist propranolol (2 mg/kg) or the muscarinic antagonist atropine methyl nitrate (2 mg/kg) in rats implanted with radiotelemetric probes. 3. Compared with saline controls, the drugs did not change the behavioural component of the response (freezing, 22 kHz ultrasonic vocalizations) or its pressor component (+28 mmHg). 4. Propranolol abolished the tachycardic response of fear, whereas atropine more than doubled it (from +75 to +175 b.p.m. above resting baseline). 5. The results demonstrate that both sympathetic and vagal parasympathetic outflows to the heart are strongly activated during conditioned fear. The vagal activation may act to hold back cardiac acceleration while the animal waits for the aversive stimulus to come.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Differential fear conditioning induces reciprocal changes in the sensory responses of lateral amygdala neurons to the CS(+) and CS(-).

In classical fear conditioning, a neutral sensory stimulus (CS) acquires the ability to elicit fear responses after pairing to a noxious unconditioned stimulus (US). As amygdala lesions prevent the acquisition of fear responses and the lateral amygdaloid (LA) nucleus is the main input station of the amygdala for auditory afferents, the effect of auditory fear conditioning on the sensory responsiveness of LA neurons has been examined. Although conditioning was shown to increase CS-evoked LA responses, the specificity of the changes in responsiveness was not tested. Because conditioning might induce nonspecific increases in LA responses to auditory afferents, we re-examined this issue in conscious, head-restrained cats using a differential conditioning paradigm where only one of two tones (CS(+) but not CS(-)) was paired to the US. Differential conditioning increased unit and field responses to the CS(+), whereas responses to the CS(-) decreased. Such changes have never been observed in the amygdala except in cases where the CS(-) had been paired to the US before and fear responses not extinguished. This suggests that fear conditioning is not only accompanied by potentiation of amygdalopetal pathways conveying the CS(+) but also by the depression of sensory inputs unpaired to noxious stimuli.

Acoustic Stimulation↗
PubMed1998

Contributions of anterior perirhinal cortex to olfactory and contextual fear conditioning.

The present experiments examined the effects of excitotoxic lesions of anterior perirhinal cortex (PRH) on the expression of fear conditioned to an explicit olfactory CS and to the context in which CS-US pairing took place. Animals with anterior PRH lesions exhibited an attenuation of fear conditioned to the explicit CS, but no attenuation of fear conditioned to the training context. These data replicate previous findings in our laboratory examining the effects of aspirative lesions of anterior PRH, and are consistent with the notion that this cortical region comprises a critically important component of the neural system mediating the acquisition and/or expression of associations between olfactory cues and footshock.

Analysis of Variance↗
PubMed1999

Suppression of conditioned fear by administration of CCKB receptor antagonist PD135158.

In order to examine the involvement of CCK in the formation of anxiety, we have investigated whether CCKB receptor antagonist PD135158 suppressed conditioned fear stress. Rats were individually subjected to 30 min of inescapable electric footshock in a chamber with a grid floor. First, the rats were individually subjected to 30 min of footshock. Twenty-four h after the footshock, the rats were again placed in the chamber and observed for 5 min without shocks. PD135158 was administered 30 min before placing the rats in the chamber again. Secondly, PD135158 was administered 30 min before footshock. Thirdly, PD135158 was administered 5 min after footshock. Administration of PD135158 30 min before conditioned fear stress significantly reduced freezing behavior. Administration of PD135158 30 min before footshock also significantly reduced freezing behavior. But, administration of PD135158 5 min after footshock did not significantly reduce freezing behavior. PD135158 blocked not only the acquisition but also the expression of conditioned fear. These results suggest that the CCKB receptor might play an important role in conditioned fear stress and that it might be related to anxiety.

Animals↗
PubMed2006

WIN 55212-2 impairs contextual fear conditioning through the activation of CB1 cannabinoid receptors.

The memory deficits induced by cannabinoid agonists have been found in several behavioral paradigms. Nevertheless, there is evidence that not all types of memory are impaired after cannabinoid administration. The aim of this study was to investigate whether the cannabinoid agonist WIN 55212-2 (WIN) is able to influence the acquisition of fear conditioning using tone and contextual versions. For tone-fear conditioning, male Wistar rats were placed in the conditioning chamber and after 3 min, a sound (CS) was presented for 10s that terminated with a 1-s electric footshock (1.5 mA). For contextual-fear conditioning, a similar procedure was used but no sound was presented. Twenty-four hours after, the animals were re-exposed to the respective CS (tone or conditioning chamber) and the freezing behavior was registered. A subsequent experiment investigated a possible state-dependent effect of WIN by administering WIN or control solution 30 min before conditioning and before testing. WIN (2.5 and 5.0 mg/kg) administered i.p. 30 min before impaired contextual fear conditioning but did not modify the freezing behavior elicited by tone presentation. These animals did not show any state-dependent effects of WIN. Further, the impaired contextual conditioning was prevented by preadministration of SR141716A (1.0 mg/kg, i.p.) or SR147778 (1.0 mg/kg, i.p.), selective cannabinoid CB1 receptor antagonists. The present findings highlight that cannabinoid agonists effects are selective for the hippocampus-dependent aversive memories in rats. This effect appears to be related to the activation of CB1 cannabinoid receptors and confirms that cannabinoids might provide a novel approach for the treatment of unpleasant memories.

Analgesics↗
PubMed2006

The role of gastrin-releasing peptide on conditioned fear: differential cortical and amygdaloid responses in the rat.

RATIONALE: Bombesin (BB), an amphibian peptide, was shown to affect the expression of the stress response. However, the physiological role of the mammalian counterparts of BB in mediating anxiety and fear responses remain to be characterized. OBJECTIVE: This study examined the effects of gastrin-releasing peptide (GRP), a mammalian analogue of BB, and its receptor antagonist, BW2258U89, on conditioned emotional response (CER), using fear conditioning. MATERIALS AND METHODS: The effects of these compounds on contextual and cued fear conditioning were assessed after direct bilateral infusions into the prelimbic (PrL) cortex, infralimbic (IL) cortex or central nucleus of the amygdala (CeA). RESULTS: GRP (300 ng) microinjected into each of the three target nuclei significantly reduced freezing to contextual cues. Similarly, in the cued portion of CER, GRP administered to the IL cortex significantly reduced freezing. Administration of BW2258U89 resulted in dose-dependent and site-specific effects. At the IL cortex, the 50 ng dose decreased freezing to both contextual and cued fear conditioning. At the CeA, the 300 ng dose also decreased freezing, but at the 50 ng dose, it increased contextual freezing. At the PrL cortex, BW2258U89 did not affect freezing. CONCLUSIONS: These results illustrate that (1) GRP system(s) can significantly affect the expression of learned fear, (2) some of the relevant brain sites mediating these effects include the PrL, IL and the CeA, and (3) such effects may be dependent upon whether responses were evoked by environmental contextual fear cues or by specific auditory cues that were explicitly paired with an aversive stimulus.

Amygdala↗
PubMed2000

Spatial learning, contextual fear conditioning and conditioned emotional response in Fmr1 knockout mice.

Fmr1 knockout mice are an animal model for fragile X syndrome, the most common form of heritable mental retardation in humans. Fmr1 knockout mice exhibit macro-orchidism and cognitive and behavioural deficits reminiscent of the human phenotype. In the present study additional behavioural and cognitive testing was performed. Knockouts and control littermates were subjected to a spatial learning test using a plus-shaped water maze. Animals had to learn the position of a hidden escape platform during training trials. The position of this platform was changed during subsequent reversal trials. Previously reported deficits in reversal learning were replicated, but we also observed significant differences during the acquisition trials. A plus-shaped water maze experiment with daily changing platform positions failed to provide clear evidence for a working memory impairment, putatively underlying the spatial learning deficits. Two different test settings were used to examine the reported deficit of Fmr1 knockout mice in fear conditioning. Conditioned fear responses were observed in a contextual fear test, and the ability to acquire an emotional response was tested by means of response suppression in a conditioned emotional response procedure. Neither protocol revealed significant differences between controls and knockouts.

Acoustic Stimulation↗
PubMed2000

Effects of inescapable shock and conditioned fear on the release of excitatory and inhibitory amino acids in the locus coeruleus.

We investigated the importance of endogenous amino acids in the locus coeruleus in inescapable electric shock and conditioned fear. In naive rats and in rats exposed to noise (N), light (L) and electric shock (S) or to N + L only, the locus coeruleus was superfused with artificial cerebrospinal fluid through a push-pull cannula and the release of GABA, taurine, glutamate, aspartate, serine and glutamine was determined in the superfusate by HPLC after derivatization with o-phthaldialdehyde. Locomotor activity, arterial blood pressure and heart rate were telemetrically monitored. The placement of naive rats or conditioned rats from their home cage to a chamber provided with a grid-floor for shock virtually did not change the release rates of the amino acids in the locus coeruleus. Motility was enhanced in naive and conditioned rats to a similar extent. Blood pressure and heart rate were enhanced in conditioned rats only. Exposure to N + L + S for 5 min greatly enhanced the release rates of all determined amino acids in the locus coeruleus. In conditioned rats the increase in release of most amino acids lasted longer than in naive rats. Electric shock also enhanced motility, blood pressure and heart rate. In conditioned rats, motility and cardiovascular changes were more pronounced and/or lasted longer than in naive rats. Exposure of conditioned rats to the conditioned stimuli N + L for 5 min led to an increased release of taurine and aspartate. The enhanced release of taurine lasted 30 min. Exposure to N + L did not affect the release rates of amino acids in naive rats. N + L did not influence motility but arterial blood pressure and heart rate were elevated in conditioned rats. The findings show that inescapable electric shock enhances the release of several amino acids in the locus coeruleus, while conditioned fear selectively increases the outflow of taurine and aspartate. Moreover, conditioned fear prolongs the response of excitatory and inhibitory amino acids to electric shock. The results suggest that an excitatory amino acid (aspartate) and an inhibitory amino acid (taurine) of the locus coeruleus are implicated in conditioned fear.

Amino Acids↗
PubMed2001

Neurobiology of Pavlovian fear conditioning.

Learning the relationships between aversive events and the environmental stimuli that predict such events is essential to the survival of organisms throughout the animal kingdom. Pavlovian fear conditioning is an exemplar of this form of learning that is exhibited by both rats and humans. Recent years have seen an incredible surge in interest in the neurobiology of fear conditioning. Neural circuits underlying fear conditioning have been mapped, synaptic plasticity in these circuits has been identified, and biochemical and genetic manipulations are beginning to unravel the molecular machinery responsible for the storage of fear memories. These advances represent an important step in understanding the neural substrates of a rapidly acquired and adaptive form of associative learning and memory in mammals.

Amygdala↗
PubMed2000

Fear conditioning in C57/BL/6 and DBA/2 mice: variability in nucleus accumbens function according to the strain predisposition to show contextual- or cue-based responding.

The contribution of the nucleus accumbens shell, the dorsal hippocampus, and the basolateral amygdala to contextual and explicit cue fear conditioning was assessed in C57BL/6 (C57) and DBA/2 (DBA) mice showing differences in processing contextual information associated with consistent but non-pathological variations in hippocampal functionality. Mice from both strains with bilateral ibotenic acid or sham lesions located in each area were introduced in a conditioning chamber and exposed twice to the pairing of a tone (2 x 8 s, 2000 Hz, 80 dB) with a shock (2 s, 0.7 mA). On the following day, mice were first exposed to the training context then to the tone in a different context. Freezing behaviour was scored in all situations. C57 showed more freezing to the context than to the tone whereas DBA showed more freezing to the tone than to the context. In C57, both nucleus accumbens and hippocampal lesions impaired acquisition of contextual fear conditioning but paradoxically improved acquisition of cue fear conditioning, whereas amygdala lesions disrupted performance in every task. In DBA, nucleus accumbens lesions, like amygdala lesions, impaired acquisition of both contextual and cue fear conditioning, whereas hippocampal lesions did not produce any effect. The parallelism between the effect of nucleus accumbens and hippocampus lesions in C57, and between the effect of nucleus accumbens and amygdala lesions in DBA points to a variability in nucleus accumbens function according to the strain specialization to develop context- or cue-based responding.

Acoustic Stimulation↗