MEDIAL GENICULATE LESIONS BLOCK AMYGDALAR AND CINGULOTHALAMIC LEARNING-RELATED NEURONAL-ACTIVITY

Citation
A. Poremba et M. Gabriel, MEDIAL GENICULATE LESIONS BLOCK AMYGDALAR AND CINGULOTHALAMIC LEARNING-RELATED NEURONAL-ACTIVITY, The Journal of neuroscience, 17(21), 1997, pp. 8645-8655
Citations number
81
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
17
Issue
21
Year of publication
1997
Pages
8645 - 8655
Database
ISI
SICI code
0270-6474(1997)17:21<8645:MGLBAA>2.0.ZU;2-F
Abstract
This study assessed the role of the thalamic medial geniculate (MG) nu cleus in discriminative avoidance learning, wherein rabbits acquire a locomotory response to a tone [conditioned stimulus (CS)+] to avoid a foot shock, and they learn to ignore a different tone (CS-) not predic tive of foot shock. Limbic (anterior and medial dorsal) thalamic, cing ulate cortical, or amygdalar lesions severely impair acquisition, and neurons in these areas develop training-induced activity (TIA): more f iring to the CS+ than to the CS-. MG neurons exhibit TIA during learni ng and project to the amygdala. The MG neurons may supply afferents es sential for amygdalar and cingulothalamic TIA and for avoidance learni ng. To test this hypothesis, bilateral electrolytic or excitotoxic ibo tenic acid MG nuclear lesions were induced, and multiunit recording el ectrodes were chronically implanted into the anterior and posterior ci ngulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei , and the basolateral nucleus of the amygdala before training. Learnin g was severely impaired and TIA was abolished in all areas in rabbits with lesions. Thus learning and TIA require the integrity of the MG nu cleus. Only damage in the medial MG division was significantly correla ted with the learning deficit. The lesions abolished the sensory respo nse of amygdalar neurons, and they attenuated (but did not eliminate) the sensory response of cingulothalamic neurons, suggesting the existe nce of extra geniculate sources of auditory transmission to the cingul othalamic areas.