“…The idea that activation of the amygdala may produce patterns of limbic neural activity leading to the characteristic response pattern in novelty/fear situations is consistent with studies showing that lesions of this structure reduce the behavioral signs of fear displayed by rats placed into fear-producing situations (Blanchard & Blanchard, 1971Kemble & Tapp, 1968;Pellegrino, 1968). Amygdaloid lesions would, according to the present interpretation, eliminate or reduce the source of the neural bias that produced this pattern of responding.…”
Food-deprived rats were placed individually into a novel test cage containing food pellets for 5 min per day for 4 days. Detailed observation of their behavior showed that the rats ate more and explored less each day, and that there was a consistent pattern of the component behaviors of exploration in all rats. Over the next 5 days, the same experimental procedure was followed, except that the rats were given low-level stimulation of the basolateral area of the amygdala. During the stimulation phase, the rats exhibited the same patterns of behavior as they did during the nonstimulation phase, and the components of evoked exploration were highly similar to those observed during normal exploration. Additional groups of rats stimulated in the lateral or ventromedial areas of the hypothalamus exhibited behavior patterns which did not resemble the patterns of normal or amygdaloid-stimulation-evoked exploration. The data suggest that the amygdala may function as a part of a neural circuit which mediates the exploration that occurs in response to novelty. This would account for the well-known finding that amygdaloid stimulation interrupts various appetitive behaviors.
“…The idea that activation of the amygdala may produce patterns of limbic neural activity leading to the characteristic response pattern in novelty/fear situations is consistent with studies showing that lesions of this structure reduce the behavioral signs of fear displayed by rats placed into fear-producing situations (Blanchard & Blanchard, 1971Kemble & Tapp, 1968;Pellegrino, 1968). Amygdaloid lesions would, according to the present interpretation, eliminate or reduce the source of the neural bias that produced this pattern of responding.…”
Food-deprived rats were placed individually into a novel test cage containing food pellets for 5 min per day for 4 days. Detailed observation of their behavior showed that the rats ate more and explored less each day, and that there was a consistent pattern of the component behaviors of exploration in all rats. Over the next 5 days, the same experimental procedure was followed, except that the rats were given low-level stimulation of the basolateral area of the amygdala. During the stimulation phase, the rats exhibited the same patterns of behavior as they did during the nonstimulation phase, and the components of evoked exploration were highly similar to those observed during normal exploration. Additional groups of rats stimulated in the lateral or ventromedial areas of the hypothalamus exhibited behavior patterns which did not resemble the patterns of normal or amygdaloid-stimulation-evoked exploration. The data suggest that the amygdala may function as a part of a neural circuit which mediates the exploration that occurs in response to novelty. This would account for the well-known finding that amygdaloid stimulation interrupts various appetitive behaviors.
“…But conflicting data exist in literature on the behavioral effects of amygdaloid lesions with respect to avoidance learning since Robinson [29] reported an impaired acquisition of avoidance behavior in amygdaloid lesioned rats, which was confirmed by Horvath [12], Goddard [8], McKew et al [22], Coover et al [6] and Molino [23], whereas Kemble and Tapp [17] and King [18] could not observe a disturbance in active avoidance behavior of rats following amygdalectomy and Grossman [10] suggests that lesions in each of the 6 major subdivisions of the amygdaloid complex induce facilitatory effects on active avoidance behavior. Besides cholinergic components of the amygdaloid complex may be involved in the mediation of escape-avoidance behavior [9], whereas a role for an amygdala /3-adrenergic system in memory processes has been suggested as well [7].…”
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
“…In previous research employing male rats, we have repeatedly failed to note amygdaloid lesion effects on simple active avoidance tasks (Kemble & Tapp, 1968; Kemble, Note 1). Since two-way avoidance acquisition is enhanced in female rats following some small amygdaloid lesions (Grossman, Grossman, & Walsh, 1975), it is possible that sex by lesion interactions would emerge in a more complex task.…”
Amygdaloid lesions decreased the latency of male rats to initiate consumption of a novel food but increased latencies among females. Lesions also depressed the rate of postoperative weight gain of male but not female subjects. Female rats showed shorter latencies on three other ingestional and grooming measures and more rapid acquisition of a passive avoidance task. There were no lesion effects or lesion by sex interactions on these measures. There were also no group differences or interactions in the acquisition of a simple active avoidance task. Further investigations of sex differences in amygdaloid function are suggested.Recent evidence indicates that the amygdaloid complex is sexually dimorphic in a number of its features. Sex differences in cell body volume of the central and medial amygdala which are abolished by neonatal castration have been noted by Staudt and Dorner (1976). Dimorphism in amygdaloid uptake of methionine in adult mice (MacKinnon, 1973) and puberal rats (Ter Haar & MacKinnon, 1975) and estradiol uptake in neonatal rats (Westley & Salam an , 1977) has also been demonstrated. Baum and Goldfoot (1975) also found that amygdaloid lesions in perpuberal male ferrets reduced blood and testis levels of testosterone and retarded body growth. Such lesions in prepuberal females hastened the onset of first estrous and had no effect on body growth. Raisman (1974) has shown that amygdaloid efferents in the stria terminalis, while not themselves dimorphic, synapse on sexually differentiated neurons within the preoptic area. Kling (1974) has also reported increased aggression in female, but not male, monkeys following amygdaloid lesions. Little attention, however, has been directed toward a systematic comparison of lesion effects on behavior in the two sexes. The present experiment explored this possibility.
METHOD
SubjectsSubjects were 16 male and 16 female rats supplied by the Holtzman Company (Madison, Wisconsin). Male rats weighed 437-515 g and females 250-295 g at the time of surgery. All subjects were of equivalent age. Eight rats of each sex sustained amygdaloid lesions; two received control operations and six sustained scalp incisions. Three female rats (one amygdaloid and two control) died during surgery. Except where noted, rats received ad-lib access to Purina Lab Chow and water throughout the experiment.
Surgery and HistologyUsing pentobarbital anesthesia (45 mg/kg), amygdaloid lesions were produced by passing 2.0-mA anodal dc through At the conclusion of testing, 24-micron coronal sections were prepared through the lesion area of each experimental rat and stained with thionin.
ProceduresReactivity to novel foods. Latency to consume a single piece of presweetened cereal (Froot Loops), a small (10 x lOx 5 mm, ±2 mm) piece of apple (Washington Delicious), and a single piece of lettuce leaf (approximately 2 cm') was measured in the home cage. The novel food was placed in a 3.8-cm-diam dish in the rat's cage, and latency to begin and complete consumption of the novel food was recorded by stopwatc...
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