Amygdalectomized Rats Research Articles

The amygdala modulates prefrontal cortex activity relative to conditioned fear.

Animals learn that a tone can predict the occurrence of an electric shock through classical conditioning. Mice or rats trained in this manner display fear responses, such as freezing behaviour, when they hear the conditioned tone. Studies using amygdalectomized rats have shown that the amygdala is required for both the acquisition and expression of learned fear responses. Freezing to a conditioned tone is enhanced following damage to the dorsal part of the medial prefrontal cortex, indicating that this area may be involved in fear reduction. Here we show that prefrontal neurons reduce their spontaneous activity in the presence of a conditioned aversive tone as a function of the degree of fear. The depression in prefrontal spontaneous activity is related to amygdala activity but not to the freezing response itself. These data indicate that, in the presence of threatening stimuli, the amygdala controls both fear expression and prefrontal neuronal activity. They suggest that abnormal amygdala-induced modulation of prefrontal neuronal activity may be involved in the pathophysiology of certain forms of anxiety disorder.

314 Spatial learning of amygdalectomized rats: Experimental model “emotional-cognitional interaction”

314 Spatial learning of amygdalectomized rats: Experimental model “emotional-cognitional interaction”

Differential Effects of Amygdala Lesions on Early and Late Plastic Components of Auditory Cortex Spike Trains during Fear Conditioning

In auditory fear conditioning, pairing of a neutral acoustic conditioned stimulus (CS) with an aversive unconditioned stimulus (US) results in an enhancement of neural responses to the CS in the amygdala and auditory cortex. It is not clear, however, whether cortical plasticity governs neural changes in the amygdala or vice versa, or whether learning in these two structures is determined by independent processes. We examined this issue by recording single-cell activity in the auditory cortex (areas Te1, Te1v, and Te3) of freely behaving, amygdalectomized rats using a movable bundle of microwires. Amygdala damage did not affect short-latency (0-50 msec) tone responses, nor did it interfere with conditioning-induced increases of these onset responses. In contrast, lesions of the amygdala interfered with the development of late (500-1500 msec) conditioned tone responses that were not present before conditioning. Furthermore, whereas onset conditioned responses in the control group remained elevated after 30 extinction trials (presentation of CS alone), onset responses in lesioned animals returned to their preconditioning firing level after approximately 10 extinction trials. These results suggest that the amygdala enables the development of long-latency (US anticipatory) responses and prevents the extinction of short-latency onset responses to threatening stimuli. The findings further suggest that auditory cortex cells may participate differently in explicit and implicit memory networks.

The EEG analysis of the interrelationships of structures of the thalamofrontal system during the recovery of conditioned reflex behavior of amygdalectomized rats.

The influence of a unilateral lesion of the basolateral amygdala (BLA) on instrumental reflexes and the EEG activity of the orbitofrontal cortex (OFC) and the dorsomedial nucleus of the thalamus (DMN) was investigated in experiments on rats. A decrease in the number of correct reactions and an increase in their latency over the course of the first two postoperative weeks was accompanied by an increase in the amplitude of the delta and theta rhythms in the EEG of the OFC and DMN, whereas in the following two weeks this change appeared only in the EEG of the OFC. The changes in the EEG reflecting new functional relationships between the structures of the injured system were more prolonged (more than a month) than the period of the recovery of the parameters of the reflexes. It is hypothesized that an important role in the foundation of the disturbance and recovery of the instrumental reflex behavior following destruction of the BLA belongs to the functional reorganization of connections between the limbic and thalamocortical structures of the brain.

LESIONS OF THE AMYGDALOID COMPLEX IMPAIR ACQUISITION OF SERIAL PATTERN LEARNING IN RATS

Normal and amygdala-lesioned rats were trained in a runway to respond to a three-element pattern ending in 2, 12, or 0 Noyes pellets (45 mg), respectively. The amygdalectomized rats' performance was inferior to that of normal controls during the early and middle stages of training, that is, amygdalectomized rats ran more slowly on rewarded trials and developed patterned running later than control rats. In the later stages of training, the lesioned rats demonstrated tracking of the series elements, reflected by differential running times similar to those of the control animals. Results are discussed in terms of some of the current theories involving the role of the amygdaloid complex in learning and reinforcement.

Transplantation of embryonal amygdalar tissue into the brain of amygdalectomized rats.

Transplantation of embryonal amygdalar tissue into the brain of amygdalectomized rats.

The collapse effect and delay of reinforcement with amygdalectomized rats

In Phase 1, alleyway run speeds of amygdalectomized rats given large (12 pellets) or small (2 pellets) magnitude of reward were initially faster for the large-magnitude group, with the small-magnitude group catching up (termed the collapse effect) early in training. The collapse effect for nonlesion groups given similar magnitudes of reward occurred also, but much later in training. In Phase 2, all animals were given the same number of pellets as in Phase 1 with the addition of a 60-sec goalbox delay of reinforcement. In the lesion animals, the brief increase in performance, due to such a shift, occurred later in training than it did for the non-lesion animals. Following the brief increase there was a large decrement in responding for all groups, but the performance decrement of the lesion groups combined was less than it was for the nonlesion groups combined. Thus, rats with amygdala lesions were less responsive to original, and to changes in, contingencies of reinforcement relative to control animals. The normal function of the amygdala is briefly discussed.

Runway performance of amygdalectomized rats: Magnitude of reinforcement and delay of food reward

In an alleyway, running speeds for amygdalectomized rats given large (12 pellets) or small (2 pellets) magnitude of reinforcement were initially faster for the large-magnitude group, but the small-magnitude group caught up (termed the collapse effect) in 20 trials. This is in contrast to intact animals, which typically exhibit the collapse effect anywhere between 50 and 100 trials. As such, control animals administered 20 trials showed the familiar form of responding—the speeds of the large-magnitude animals were reliably faster than those of the small-magnitude animals. With periodic increases in delay of food reward, from 0 to 45 sec in 15-sec increments, lesioned animals ran reliably faster than control animals, more so for the 30- and 45-sec delays. These results were viewed as supporting Richardson’s (1973) theory.

Effect of total amygdalectomy upon regulation of salt intake in rats

COX, J. R., C. E. CRUZ AND J. RUGER. Effect of total amygdalectomy upon regulation of salt intake in rats. BRAIN RES. BULL. 3(5) 431–435, 1978.—Sodium appetite was studied in rats with lesions destroying the entire amygdaloid nuclear complex. The rats were totally aphagic and adipsic for several days following lesioning but regained nearly normal levels of food and water intake about 2 to 3 weeks postoperatively. Intake of 3% saline was observed after induction of sodium appetite by treatment with a mineralocorticoid and a natriuretic agent. Rats with amygdaloid lesions generally manifested severe but not total loss of sodium appetite. Regulation of water intake was also moderately to severely impaired. Suggestive evidence was obtained that recovery of sodium appetite in amygdalectomized rats can be enhanced by postoperative experience with sodium appetite and saline reinforcement.

Amygdalectomy and mixed reinforcement schedule contrast effects

Four controls and four amygdalectomized rats were trained to leverpress on a mixed schedule of reinforcement in which 5 min of variable-interval reinforcement alternated with 5 min of extinction. Control animals increased responding in the variable-interval component over baseline rates (i.e., behavioral contrast), whereas amygdalectomized animals did not. No significant differences between groups were found during extinction. The lack of contrast effects in amygdaloid animals was attributed to a reduction in extinction-induced frustration.

The effect of bilateral ablation of the amygdala on endocrine function in the rat.

Bilateral electrolytic destruction of the amygdala in male rats does not significantly interfere with thyrotropin or corticotropin secretion by the pituitary, but gonadotropin production appears definitely reduced. The amygdalectomized rats were adipsic and aphagic.