Lesions in the amygdala and the frustration effect

Henke, Peter G.; Maxwell, Deborah

doi:10.1016/0031-9384(73)90137-6

Cited by 60 publications

(50 citation statements)

References 12 publications

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“…This result is incompatible with studies that report terminal acquisition differences between amygdalectomized animals and controls on such tasks as behavior contrast (e.g., Henke, 1972) or the frustration effect (e.g., Henke & Maxwell, 1973), both of which utilize internally produced representations of cues for responding. Perhaps what is being observed here is a recovery of function toward specific nuclei.…”

Section: Discussioncontrasting

confidence: 81%

Single-alternation pattern running in amygdalectomized rats

Goomas

1982

Psychobiology

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Amygdalectomized and nonlesioned rats were administered alternated reinforced and nonreinforced trials in an alleyway. Animals with amygdala lesions showed slower response speeds during earlier stages of training. As training continued, reinforced-trial speed, characteristically faster than nonreinforced-trial speed in normal animals, was delayed in the lesioned animals. Once the lesioned animals exhibited pattern running, there were no differences between them and the nonlesioned group. These results were discussed in terms of Richardson's (1973) theory. 368The most common example of pattern running is the faster reinforced-trial than nonreinforced-trial speed that ultimately occurs when reinforced and nonreinforced trials are alternated (Bloom & Capaldi, 1961;Capaldi, 1967). Here, single-alternation patterning occurs because "a characteristic cue is produced by reinforcement (SR), as is by nonreinforcement (SN), and under a single-alternation schedule, SR always occurs on nonreinforced trials and so is the S-cue, while SN always occurs on reinforced trials and so is the S+ cue" (Capaldi, 1979, p, 64). According to this analysis, pattern running may be described as discriminative running based on internal memory cues provided by a nonrandom schedule of reinforcement.According to Richardson (1973), the normal function of the amygdala is to incorporate and integrate internally produced representations of cues and stimuli into new behavior patterns; lesioning the amygdala results in the disruption of these internally generated representations. Support for Richardson's theory is derived from studies in which the acquisition or retention of a task by lesioned subjects is dependent upon the utilization of either external environmental stimuli or internal cues. Consider the former case. Amygdaloid ablation does not interfere with rather complex tasks so long as the correct response is cued by an external environmental stimulus. For example, the acquisition of a go/no-go discrimination cued by a light and the reversal of this discrimination were not disrupted in lesioned rats (Pellegrino, 1968). On the other hand, for those tasks whose performance depends on internally formed cues for the correct response, a lesion deficit is observed. ported that lesions of the basolateral region of the nucleus impaired performance on a timing task (DRL-20) relative to performance by a control group of rats (seealso Pubols, 1966). Likewise, Schartzbaum and Poulos (1965) reported that amygdalectomized monkeys did worse on a discrimination reversal task than did the control animals. It appears , then, that the amygdaloid lesion deficit is observed when internally generated representations of cues (e.g., timing task or discrimination reversal), rather than external stimuli (e.g., light), are being utilized for the correct response.The purpose of this experiment was, first, to further extend those investigations that had incorporated internally produced cues into their manipulations in the study of the amygdala and, second, to test the ...

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Section: Discussioncontrasting

confidence: 81%

Single-alternation pattern running in amygdalectomized rats

Goomas

1982

Psychobiology

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“…Amygdaloid damage has been shown to interfere with response suppression [25], to prevent the formation of induced taste aversion [16,21,24], to attenuate emotional and/or emotional reactions in a number of situations [8,11,15], to eliminate self-punitive behavior [27], to produce significant learning deficits for passive avoidance conditioning [34] and to induce an increase in sniffing, rearing and exploration [6,37].…”

Section: Discussionmentioning

confidence: 99%

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Greidanus

Croiset

Bakker

et al. 1979

Physiology & Behavior

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VAN WlMERSMA GREIDANUS, T. B., G. CROISET, E. BAKKER AND H. BOUMAN. Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4_m) on avoidance behavior. PHYSIOL. BEHAV. 22(2) 291-295, 1979.-Lesions in the amygdaloid complex result in an increased activity of rats in open field behavior in that generally more exploration and rearing is observed as compared with sham-operated animals. No effect of the lesion was observed on acquisition and extinction of an active avoidance response, but the amygdala lesions block the inhibitory effect of the neuropeptides vasopressin and ACTH4_~,, on extinction of a conditioned avoidance response. Searching for the CNS sites of action of these neuropeptides in relation to avoidance behavior several brain areas appear to be involved in their inhibitory effects on extinction of an active avoidance response. Implantation studies point to the posterior thalamic area including the parafascicular nuclei as a site of action of ACTH [43] as well as vasopressin [47]. Lesion studies however indicated that this parafascicular area is less essential for vasopressin in relation to its inhibitory effect on avoidance extinction than for ACTH4_., [48]. Subsequent experiments in which additional limbic structures were destroyed such as the rostral septal area [42,49] and the dorsal hippocampal complex [44] revealed that these structures are important for the behavioral effects of vasopressin and ACTH4-1o. From these data it has been suggested that the limbic system needs to be intact in order to allow the neuropeptides vasopressin and ACTH4-10 to display their inhibitory action on active avoidance extinction.Since the amygdaloid complex is an essential part of the limbic system the present study was performed in which the effects of the behaviorally active vasopressin analogue desglycinamide-lysine-8-vasopressin (DG-LVP) [40] and of ACTH4_,, on extinction of an active avoidance response were studied in animals with lesions in the amygdala nuclei. In addition the effect of the amygdaloid lesion itself was studied on exploratory behavior. METHOD AnimalsMale rats of an inbred Wistar strain weighing 130-150 g were used for the experiments. Stereotaxic lesions were made bilaterally in the amygdaloid complex using radiofrequency lesioning. The procedure in the sham-operated rats was identical to that in the amygdaloid lesioned animals except for the current. In the lesioned rats bilateral electrolytic lesions were placed in the baso-lateral amygdala by passing a 2 mA anodal current through the uninsulated 0.5 mm tip of a stainless steel electrode for 40 sec. A rectal cathode completed the circuit. With the incisor bar set 5 mm above the interaural plane and using bregma at the zero point, the following coordinates were employed: posterior -1.0 ram, lateral 4.7 mm and ventral -8.5 mm. ProcedureAfter recovery from the operation, which usually took

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“…The amygdala has been implicated in mediating the behavioral phenomenon, termed "the reinforcement-omission effect" or "frustration effect," that occurs when an animal trained to respond for a positive reinforcer unexpectedly finds that the reinforcer is omitted following the operant response previously associated with reinforcer procurement (Amsel and Roussel, 1952;Henke, 1973;Henke and Maxwell, 1973;Dudley and Papini, 1997;Abler et al, 2005;Ernst et al, 2005). Hull (1952) first described this behavioral phenomenon, stating that "the abrupt cessation of a customary reinforcement" results in an initial, transient increase in operant responding.…”

Section: Bla Involvement In Expression Of "The Frustration Effect"mentioning

confidence: 99%

Amygdala Neural Encoding of the Absence of Reward during Extinction

Tye¹,

Cone²,

Schairer³

et al. 2010

J. Neurosci.

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The basolateral amygdala complex (BLA) has been identified as a critical structure mediating fear extinction. However, little is known about the functional role of neurons in the BLA during the extinction of a reward-seeking behavior. Here, we used in vivo electrophysiology procedures in freely moving rats to investigate whether and how the BLA encodes the extinction of responding for sucrose. We recorded 330 neurons from 15 rats during a within-session extinction procedure following training under a partial reinforcement schedule. Several distinct populations of neurons change their response profiles as the rat ceases to respond for the omitted reinforcer. One population of neurons (32 of 330; 10%), which responded selectively to port entries in the presence, but not the absence, of sucrose during maintenance, subsequently developed a phasic response to port entries in the absence of sucrose during the extinction epoch only. The relative proportion of these "reinforcement-omission" neurons per rat was correlated with response intensity during extinction, as well as with the rate at which reward-seeking behavior was extinguished. A subpopulation of neurons responded with opposite phasic changes in activity to port entries in the presence of sucrose and to port entries during extinction, demonstrating that BLA neurons may contribute to the detection of value differences between expected and actual outcomes. Another population of neurons (47 of 330; 14%) responded to the empty port only during extinction. Because BLA neural correlates reflect the omission of an expected reward, these neuronal populations may contribute to the expression of behavior during extinction.

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Lesions in the amygdala and the frustration effect

Cited by 60 publications

References 12 publications

Single-alternation pattern running in amygdalectomized rats

Single-alternation pattern running in amygdalectomized rats

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Amygdala Neural Encoding of the Absence of Reward during Extinction

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