Effect of amygdalectomy on habituation and CER in rats

Spevack, Abraham A.; Campbell, Charles T.; Drake, Lawrence A.

doi:10.1016/0031-9384(75)90236-x

Cited by 49 publications

(21 citation statements)

References 24 publications

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“…The present results from the open field experiment are in good agreement with those obtained by Slotnick [34] and Coover et al [6], who generally reported less immobility in an open field, probably due to a reduction in the arousal of fear [2,6,34,35].…”

Section: Discussionsupporting

confidence: 93%

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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Section: Discussionsupporting

confidence: 93%

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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“…A central role of amygdalar neurons is indicated by findings that amygdala lesions impair the acquisition of conditioned immobility (LeDoux et al, 1988; Fanselow and K im, 1994;LeDoux, 1995), autonomic responding (Blanchard and Blanchard, 1972;Spevack et al, 1975;Kapp et al, 1979;Gentile et al, 1986;Iwata et al, 1986;Helmstetter, 1992) and fear-potentiated startle behavior (Davis, 1986(Davis, , 1992Hitchcock and Davis, 1987;Sananes and Davis, 1992). Also, amygdalar neurons exhibit associative, training-induced activity (TIA) during Pavlovian conditioning (Umemoto and Olds, 1975;Applegate et al, 1982;Pascoe and Kapp, 1985;Nishijo et al, 1988; Muramoto et al, 1993;McEchron et al, 1995;Quirk et al, 1995).…”

Section: Abstract: Limbic Thalamus; Cingulate Cortex; Amygdala; Learmentioning

confidence: 99%

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

Poremba

Gabriel

1997

J. Neurosci.

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This study assessed the role of the thalamic medial geniculate (MG) nucleus in discriminative avoidance learning, wherein rabbits acquire a locomotory response to a tone [conditioned stimulus (CS)ϩ] to avoid a foot shock, and they learn to ignore a different tone (CSϪ) not predictive of foot shock. Limbic (anterior and medial dorsal) thalamic, cingulate cortical, or amygdalar lesions severely impair acquisition, and neurons in these areas develop training-induced activity (TIA): more firing to the CSϩ than to the CSϪ. MG neurons exhibit TIA during learning and project to the amygdala. The MG neurons may supply afferents essential for amygdalar and cingulothalamic TIA and for avoidance learning. To test this hypothesis, bilateral electrolytic or excitotoxic ibotenic acid MG nuclear lesions were induced, and multiunit recording electrodes were chronically implanted into the anterior and posterior cingulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei, and the basolateral nucleus of the amygdala before training. Learning was severely impaired and TIA was abolished in all areas in rabbits with lesions. Thus learning and TIA require the integrity of the MG nucleus. Only damage in the medial MG division was significantly correlated with the learning deficit. The lesions abolished the sensory response of amygdalar neurons, and they attenuated (but did not eliminate) the sensory response of cingulothalamic neurons, suggesting the existence of extra geniculate sources of auditory transmission to the cingulothalamic areas. Key words: limbic thalamus; cingulate cortex; amygdala; learning; instrumental conditioning; anterior ventral nucleus; medial dorsal nucleusThere is currently a great interest in the neural circuitry underlying aversively motivated learning (for review, see Davis, 1992;Gabriel, 1993;Lennartz and Weinberger, 1994;LeDoux, 1995;McGaugh et al., 1995;. A central role of amygdalar neurons is indicated by findings that amygdala lesions impair the acquisition of conditioned immobility (LeDoux et al., 1988; Fanselow and K im, 1994;LeDoux, 1995), autonomic responding (Blanchard and Blanchard, 1972;Spevack et al., 1975;Kapp et al., 1979;Gentile et al., 1986;Iwata et al., 1986;Helmstetter, 1992) and fear-potentiated startle behavior (Davis, 1986(Davis, , 1992Hitchcock and Davis, 1987;Sananes and Davis, 1992). Also, amygdalar neurons exhibit associative, training-induced activity (TIA) during Pavlovian conditioning (Umemoto and Olds, 1975;Applegate et al., 1982;Pascoe and Kapp, 1985;Nishijo et al., 1988; Muramoto et al., 1993;McEchron et al., 1995;Quirk et al., 1995).An involvement of the medial geniculate (MG) nucleus in aversively motivated learning is indicated by the observation of TIA in the medial division of the MG nucleus (MGm) (Olds et al., 1972;Gabriel et al., 1975;Gabriel et al., 1976;Ryugo and Weinberger, 1978;Birt and Olds, 1981;Weinberger, 1982;Edeline, 1990;Edeline and Weinberger, 1992;McEchron et al., 1995), and by impaired conditioning in animals with MG lesions (Iwata et al., 198...

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“…This seems a possible, but precarious, foundation upon which to build such a biologically important function as fear conditioning, and, in any event, more issues came to plague the model (e.g., Ref. 11) Despite this accumulation of complications, the status of the amygdala as a major player in stimulus-consequence associations [12][13][14][15] , seems not to be in jeaopardy (e.g., Refs. 4 and 16), although the underlying brain circuitry and physiological mechanisms appear to require further investigation.…”

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confidence: 99%

The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

Zahm¹,

Trimble²

2008

CNS spectr.

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This review begins with a description of some problems that in recent years have beset an influential circuit model of fear-conditioning and goes on to look at neuroanatomy that might subserve conditioning viewed in a broader perspective, including not only fear, but also appetitive, conditioning. The paper then focuses on basal forebrain functional-anatomical systems, or macrosystems, as they have come to be called, which Lennart Heimer and colleagues described beginning in the 1970's. Yet more specific attention is then given to the relationships of the dorsal and ventral striatopallidal systems and extended amygdala with the dopaminergic mesotelencephalic projection systems, culminating with the hypothesis that all macrosystems contribute to behavioral conditioning.There is tremendous current interest in the neurobiological mechanisms underlying conditioned fear stemming in large part from an increasing prevalence in American culture of anxiety and panic disorders, not to mention PTSD 1 . By 2000, the relevant brain circuitry had seemed to be satisfactorily described 2 , but a number of serious caveats had been voiced the preceding year 3 , and an unraveling process accelerated thereafter. Indeed, current theory on the neural substrates of fear conditioning has entered into a state of reassessment 4 .The essential elements of fear conditioning are described by the observation that pairing neutral and fear-arousing stimuli causes the neutral one to gain meaning such that it can then drive an organism's voluntary and involuntary actions. Thus, behaviorally, rats exposed to a brief tone followed immediately by a footshock will soon, frequently after a single trial, come to "freeze" upon hearing the tone. In LeDoux's 2 model of this phenomenon, neuroplasticity reflecting the attachment of "significance" to a neutral stimulus, i.e., heralding the transformation of neutral to conditioned stimulus (CS), occurs in the amygdala, specifically its lateral nucleus (LA). According to LeDoux's model, LA projects to another part of the amygdala, the central nucleus (CeA), which, in turn sends out divergent descending projections to somatic and autonomic motor effectors in the brainstem, eliciting behavioral freezing and accompanying autonomic responses. Consistent with the model, [1] sensory inputs bearing information about the aversive and neutral (to be conditioned) stimuli converge in LA 5 , and [2] an increase in the efficacy of CS-related synapses corresponds to conditioning [6][7][8] . But, soon it was realized that the CeA consists of two parts, a medial division (CeAm) from which most of its descending projections arise and to which LA does not project, and a lateral one (CeAl) to which it does. While CeAl projects to CeAm and thus might serve as a relay interposed between LA and CeAm, the CeAl to CeAm projection is nearly exclusively inhibitiory (GABAergic) and thus would inhibit rather than activate outputs to brainstem. The model was accordingly adjusted to emphasize instead a projection from LA to amygda...

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Effect of amygdalectomy on habituation and CER in rats

Cited by 49 publications

References 24 publications

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

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

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

The Dopaminergic Projection System, Basal Forebrain Macrosystems, and Conditioned Stimuli

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