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At least 19 recordsLinked to original sources
PubMed1992

Differential contribution of amygdala and hippocampus to cued and contextual fear conditioning.

The contribution of the amygdala and hippocampus to the acquisition of conditioned fear responses to a cue (a tone paired with footshock) and to context (background stimuli continuously present in the apparatus in which tone-shock pairings occurred) was examined in rats. In unoperated controls, responses to the cue conditioned faster and were more resistant to extinction than were responses to contextual stimuli. Lesions of the amygdala interfered with the conditioning of fear responses to both the cue and the context, whereas lesions of the hippocampus interfered with conditioning to the context but not to the cue. The amygdala is thus involved in the conditioning of fear responses to simple, modality-specific conditioned stimuli as well as to complex, polymodal stimuli, whereas the hippocampus is only involved in fear conditioning situations involving complex, polymodal events. These findings suggest an associative role for the amygdala and a sensory relay role for the hippocampus in fear conditioning.

Amygdala↗
PubMed1992

Potentiation or diminution of discrete motor unconditioned responses (rabbit eyeblink) to an aversive pavlovian unconditioned stimulus by two associative processes: conditioned fear and a conditioned diminution of unconditioned stimulus processing.

In two experiments using the rabbit conditioned eyeblink preparation, the conditions under which a Pavlovian conditioned stimulus (CS) potentiates or diminishes the unconditioned response (UR) were examined. The results indicated that, after discrimination training (CS+ vs. CS-), the CS+ diminished UR amplitude at the training interstimulus interval (ISI). When CS+ trials were segregated into trials on which a conditioned response (CR) did or did not occur, the CS+ diminished the UR when it elicited a CR, but not when a CR failed to occur. When the CS-unconditioned stimulus (US) interval was lengthened to 10 s, the CS+ reliably potentiated the eyeblink UR on CR trials but did not potentiate responding on trials on which a CR was absent. The results are discussed in terms of the modulatory effects and temporal properties of conditioned fear and an associatively produced decrement in US processing.

Animals↗
PubMed1991

N-methyl-D-aspartate receptor antagonist APV blocks acquisition but not expression of fear conditioning.

The role of N-methyl-D-aspartate (NMDA) receptors in Pavlovian fear conditioning was examined using the NMDA antagonist DL-2-amino-5-phosphonovaleric acid (APV). Either APV (5 micrograms/rat) or saline was administered before the training phase, the testing phase, or both. APV completely blocked acquisition but not expression of fear conditioning. The L enantiomer of APV did not affect the acquisition of conditional fear. To separate encoding from consolidation processes, APV was administered either before or immediately after the footshock unconditional stimulus (US) during the training phase. The results indicate that APV must be present during the US to produce its effects on fear conditioning. The behavioral effect of the drug is not due to analgesic action because APV did not alter pain sensitivity. The data suggest that NMDA receptors are critical for the acquisition but not expression of fear conditioning. These effects on fear conditioning are parallel to the in vitro effects of APV on the acquisition but not expression of long-term potentiation (LTP) and suggest that endogenously generated NMDA-dependent LTP participates in the neural plasticity underlying fear conditioning.

2-Amino-5-phosphonovalerate↗
PubMed1992

Equipotentiality of thalamo-amygdala and thalamo-cortico-amygdala circuits in auditory fear conditioning.

The goal of the present study was to examine the contribution of thalamo-amygdala and thalamo-cortico-amygdala projections to fear conditioning. Lesions were used to destroy either the thalamo-cortico-amygdala projection, the thalamo-amygdala projection, or both projections, and the effects of such lesions on the acquisition of conditioned fear responses (changes in arterial pressure and freezing behavior) to a tone paired with footshock were measured. In each group of animals examined, a large lesion of the acoustic thalamus, including all nuclei of the medial geniculate body and adjacent portions of the posterior thalamus, was made on one side of the brain to block auditory transmission to the forebrain at the level of the thalamus on that side. In this way, experimental lesions could be made on the contralateral side of the brain. Thus, animals with thalamo-amygdala pathway lesions received a large lesion of the acoustic thalamus on one side. Contralaterally, only the nuclei that project to the amygdala (the medial division of the medial geniculate body, the posterior intralaminar nucleus, and the suprageniculate nucleus) were selectively destroyed, leaving much of the thalamo-cortico-amygdala projection intact. For thalamo-cortico-amygdala pathway lesions, the acoustic thalamus was destroyed on one side and temporal and perirhinal cortices were ablated contralaterally. In these animals, thalamo-amygdala projections were intact on the side of the cortical lesion. Destruction of either pathway alone had no effect on auditory fear conditioning. However, combined lesions of the two sensory pathways disrupted conditioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMedDate not supplied

Differential effects of selective opioid peptide antagonists on the acquisition of pavlovian fear conditioning.

Pretreatment with opioid antagonists enhances acquisition of Pavlovian fear conditioning. The present experiments attempted to characterize the type of opioid receptor responsible for this effect using a procedure that assessed the fear of rats to a chamber previously associated with electric shock (1 mA, 0.75 s). Freezing, a species-typical immobility, was employed as an index of fear. Two mu opioid antagonists, CTOP (40 ng) and naloxonazine (10 micrograms), enhanced conditioning. On the other hand, the kappa antagonist nor-binaltorphimine reduced conditioning. Two delta antagonist treatments (16-methyl cyprenorphine and naltrindole) had no reliable effect on acquisition. Thus the enhancement of conditioning appears to be mediated by mu receptors. Previous research has shown that the conditional fear produced by these procedures caused an analgesia that is also mediated by mu receptors. It is argued that the enhancement effect occurs because of an antagonism of this analgesia and that the analgesia normally acts to regulate the level of fear conditioning.

Animals↗
PubMed1992

One-trial backward excitatory fear conditioning transfers across contexts.

One path to human phobia may be one-trial backward fear conditioning. Human phobias transfer readily across contexts. However, animal studies of one-trial backward fear conditioning have yet to demonstrate such transfer. The present study sought to do so. It used a lick-suppression procedure with 84 naive male albino rats. Two conditioning contexts, designated O and V, were crossed factorially with two test contexts, O and V. Within each cell of the factorial design, rats received in the conditioning context either a single 12 sec tone backward paired with a single 4 sec 1 mA shock or the same tone explicitly unpaired with shock. Fear of context and fear of tone were subsequently assessed in terms of the suppression of licking that they evoked. Test results suggested that (1) the rats discriminated between contexts O and V, and (2) despite such discrimination, one-trial backward fear conditioning transferred across the two contexts. The results enhance the plausibility of one-trial backward fear conditioning as a source of human phobia.

Animals↗
PubMed1992

Bilateral destruction of neocortical and perirhinal projection targets of the acoustic thalamus does not disrupt auditory fear conditioning.

The present study examined whether complete bilateral destruction of auditory cortex would interfere with auditory fear conditioning in rats. Complete destruction of auditory cortex required lesions of temporal neocortical and perirhinal periallocortical areas. Fear conditioning was assessed by measuring freezing and arterial pressure responses elicited by an acoustic stimulus after pairing with footshock. Animals with complete bilateral lesions of auditory cortex showed conditioned arterial pressure and freezing responses comparable to those of unoperated controls. In contrast, bilateral destruction of the acoustic thalamus interfered with the conditioning of both responses. These results demonstrate that the auditory cortex is not required for the conditioning of fear responses to simple acoustic stimuli and add to the growing body of evidence that fear conditioning can be mediated by subcortical (amygdaloid) projections of the acoustic thalamus.

Acoustic Stimulation↗
PubMed1992

Stimulation at a site of auditory-somatosensory convergence in the medial geniculate nucleus is an effective unconditioned stimulus for fear conditioning.

The medial division of the medial geniculate nucleus (MGm) and the posterior intralaminar nucleus (PIN) are necessary for fear conditioning to an auditory conditioned stimulus (CS), receive both auditory and somatosensory input, and project to the amygdala, which is involved in production of fear conditioned responses. If CS-unconditioned stimulus (US) convergence in the MGm-PIN is critical for fear conditioning, then microstimulation of this area should serve as an effective US during classical conditioning, in place of standard footshock. Guinea pigs underwent conditioning (40-60 trials) using a tone as the CS and medial geniculate complex microstimulation as the US. Conditioned bradycardia developed when the US electrodes were in the PIN. However, microstimulation was not an effective US for conditioning in other parts of the medial geniculate or for sensitization training in the PIN or elsewhere. Learning curves were similar to those found previously for footshock US. Thus, the PIN can be a locus of functional CS-US convergence for previously for footshock US. Thus, the PIN can be a locus of functional CS-US convergence for fear conditioning to acoustic stimuli.

Amygdala↗
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↗
PubMed1992

Frequency-specific receptive field plasticity in the medial geniculate body induced by pavlovian fear conditioning is expressed in the anesthetized brain.

Fear conditioning modifies the processing of frequency information; receptive fields (RF) in the auditory cortex and the medial geniculate body (MGB) are altered to favor processing the frequency of the conditioned stimulus (CS) over the pretraining best frequency (BF) and other frequencies. This experiment was designed to determine whether brief conditioning in the waking state produces RF plasticity that is expressed under general anesthesia. Guinea pigs bearing electrodes in the MGB received 20 trials of tone-shock pairing in a single training session. RFs were determined with animals under ketamine anesthesia before conditioning and 1-3 hr and 24 hr after conditioning. Frequency-specific RF plasticity was evident for both postconditioning periods: The BF shifted toward or to the CS frequency, responses to the BF decreased, and responses to the CS increased. Broadly tuned cells developed greater RF plasticity than narrowly tuned neurons. The results demonstrate that the specific neuronal results of brief learning experiences can be expressed in the anesthetized brain.

Amygdala↗
PubMed1992

Selective impairment of long-term but not short-term conditional fear by the N-methyl-D-aspartate antagonist APV.

Previous research has indicated that the competitive N-methyl-D-aspartate (NMDA) antagonist APV (DL-2-amino-5-phosphonovalerate) prevents the Pavlovian conditioning of fear to contextual stimuli when tested 24 hr, but not immediately, after training. The present study investigated this differential time-dependent effect of APV on fear conditioning. Rats were given either APV or saline and presented with 3 footshocks in a distinctive chamber. Promptly after the shock, rats that had received APV exhibited a species-typical fear response-freezing. However, the freezing lasted for only a short period of time (less than 3 min) compared with that of controls. An immediate-shock procedure showed that freezing was entirely a conditional response to the chamber. In addition, the results of a savings test suggest that APV impairs storage rather than retrieval processes. These results indicate that there are two temporally distinct associative fear processes, a short-term NMDA-independent conditional fear and a long-term NMDA-dependent conditional fear.

2-Amino-5-phosphonovalerate↗
PubMed1991

Efferent pathway of the amygdala involved in conditioned fear as measured with the fear-potentiated startle paradigm.

Fear-potentiated startle in the rat is a measure of conditioned fear that is blocked by lesions of the central nucleus of the amygdala. In a companion study, Rosen, Hitchcock, Sananes, Miserendino, and Davis (1991) demonstrated a direct anatomical projection from the central nucleus to the brainstem startle reflex circuit. In the present study, fear-potentiated startle was blocked by lesions that interrupted this pathway at 3 different levels or by a crossed lesion that interrupted the pathway at its source on one side and at a more caudal level on the other side. Although synaptic relays have not been ruled out entirely, the data suggest that the direct projection from the central nucleus of the amygdala to the startle circuit mediates the expression of fear-potentiated startle. These findings are consistent with the literature indicating that efferent projections from the central nucleus to various brainstem structures are involved in the expression of several conditioned fear responses.

Amygdala↗
PubMed1992

Contribution of the amygdala to learning and performance of conditional fear.

The amygdaloid complex appears to be an essential component in the neural systems mediating some forms of aversive Pavlovian conditioning. The relative contribution of this structure to acquisition and performance during fear conditioning was assessed by making temporary lesions in the amygdala prior to training or retention testing in a single-trial Pavlovian conditioning preparation. Microinjection of lidocaine HCl (5.0%, 1.0 microliters) into the amygdala prior to the presentation of a CS signalling footshock resulted in a significant attenuation of the performance of conditional fear, as indexed by the amount of time rats spent engaged in defensive freezing behavior during the retention session. However, similar treatment with lidocaine prior to the training session, during which the CS and UCS were paired, resulted in only a weak reduction in subsequent responding. Thus, while both acquisition- and performance-related processes take place within the amygdala, it appears that the latter are more sensitive to disruption using the present procedures. These results are discussed in terms of the general role played by this structure in aversive learning and motivational processes.

Amygdala↗
PubMed1992

Associative regulation of Pavlovian fear conditioning: unconditional stimulus intensity, incentive shifts, and latent inhibition.

Conditional stimuli (CS) associated with painful unconditional stimuli (US) produce a naloxone-reversible analgesia. The analgesia serves as a negative-feedback regulation of fear conditioning that can account for the impact of US intensity and CS predictiveness on Pavlovian fear conditioning. In Experiment 1 training under naloxone produced learning curves that approached the same high asymptote despite US intensity. Shifting drug treatment during acquisition had effects that paralleled US intensity shifts. In Experiment 3 naloxone reversed Hall-Pearce (1979) negative transfer using a contextual CS, indicating that conditional analgesia acquired during the CS-weak-footshock phase retards acquisition in the CS-strong-footshock phase. Experiment 5 used a tone CS in both a latent-inhibition and a negative-transfer procedure. Only negative transfer was blocked by naloxone. Therefore, negative transfer but not latent inhibition is mediated by a reduction of US processing.

Animals↗
PubMed1976

Fear-dependent variations in continuous avoidance behavior of pigs. II. Effects of diazepam on acquisition and performance of Pavlovian fear conditioning and plasma corticosteroid levels.

Previously acquired continuous avoidance performance of pigs in a shuttle-box was modified by a Pavlovian fear-conditioning procedure. Diazepam (1 mg/kg) given before the Pavlovian conditioning session prevented the increase in corticosteroids and the impairment of performance in the subsequent test session before the presentation of the fear signal. Diazepam given before the Pavlovian conditioning session and/or the test session did not prevent the increase of response to the CS presentation; however, the temporal pattern of increase differed according to the drug condition: the diazepam treatment on the day of the test significantly delayed the peak of responding to the CS; in pigs treated with diazepam on the day of Pavlovian conditioning and with saline on the day of test, the increase of response was diffuse instead of being localized to the CS presentation period. Pigs treated with diazepam both during learning and performance of fear conditioning showed some evidence of performance facilitation. Usual unitary interpretations cannot account for such results which would appear to be the net result of several intermingled effects among which state-dependent learning, acquisition deficit, and performance facilitation seem to be of importance.

Adrenal Cortex Hormones↗
PubMed1992

N-methyl-D-aspartate receptor antagonist MK-801 impairs learning but not memory fixation or expression of classical fear conditioning in goldfish (Carassius auratus).

The amnestic effects of the noncompetitive antagonist MK-801 on visually mediated, classic fear conditioning in goldfish (Carassius auratus) was examined in 5 experiments. MK-801 was administered 30 min before the training session on Day 1 to look for anterograde amnestic effects, immediately after training to look for retrograde amnestic effects, and before the training or test session, or both, to look for state-dependence effects. The results showed that MK-801 produced anterograde amnesia at doses that did not produce retrograde amnesia or state dependency and did not impair the expression of conditioned or unconditioned branchial suppression responses (BSRs) to the conditioned stimulus. The results indicate that MK-801 disrupts the mechanism of learning of the conditioned stimulus-unconditioned stimulus relation. Evidence is also presented that the learning processes that are disrupted by MK-801 occur during the initial stage of BSR conditioning.

Animals↗
PubMed1976

Fear-dependent variations in continuous avoidance behavior of pigs. I. Lack of effect of diazepam on performance of discriminative fear conditioning.

Pigs trained to avoid shocks by crossing a barrier in a shuttle-box according to a continuous avoidance procedure were submitted to a Pavlovian discriminative fear-conditioning procedure in which a tone was always followed by unavoidable shock (CS+) and another tone never followed by shock (CS-). The presentation of the CS+ on a test session in the shuttle-box induced an increase of the response rate while the CS- decreased the performance. Diazepam (1 mg/kg) administered before the test session did not modify the changes in avoidance response to each CS.

Animals↗
PubMed1976

Simultaneous and backward fear conditioning as a function of number of CS-UCS pairings.

Four experiments examined the possibility that the outcome of simultaneous and backward fear conditioning procedures might depend upon the number of CS-UCS pairings. A punishment procedure will rats as subjects and shock as the UCS was used; the amount of suppression produced by response-contingent CS presentations indexed the strength of acquired fear. Experiments 1, 3, and 4 examined the suppressive tendencies of simultaneous-and backward-trained CSs after 0, 10, 20, 40, 80, and 160 pairings. The pattern of data suggested that initial pairings have the effect of increasing suppressive tendencies of the CS, while subsequent pairings decrease them. In addition, evidence of fear inhibition was found after 160 pairings in the case of the backward paradigm. Experiment 2 examined several nonassociative accounts based upon differential shock exposure. Groups given 10 pairings or 80 pairings were compared to ggroups given 10 pairings plus 70 shock-alone presentations. The results indicated that number of pairings, rather than number of UCS occurrences, is the important factor in decreasing the initial suppression. The evidence for eventual inhibition in the backward paradigm suggests that this occurs through the acquisition of inhibitory tendencies which are antagonistic to the previously conditioned excitation.

Animals↗