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The perirhinal cortex in the dog?s brain is composed of two traditional Brodmann?s areas: 35 and 36. Area 35 is situated along the entire rostro-caudal extent of the fundus of the posterior rhinal sulcus, whereas area 36 occupies its lateral bank. In this study, four subdivisions were distinguished in area 35 based on cytoarchitectonic differentiation. Area 36 is poorly developed in the dog?s brain and was divided into two subdivisions. The most characteristic features of area 35 are: a wide layer I, scattered cell clusters in layer II, and a prominent layer V containing a distinct population of large multiform neurons. Area 36 can be recognized by the presence of numerous cell clusters in layer II and increasing radial arrangement of neurons in deep layers of the area. Two fields of the postrhinal cortex were identified in the additional postrhinal gyrus, which is found in the fundus of the most caudal extent of the posterior rhinal sulcus.
EN
Reciprocal connections of amygdaloid nuclei with the temporal neocortex in the dog were investigated. Injections of fluorescent tracers and BDA into particular temporal areas were made in eleven dogs. The topographical arrangement of connections and variations in their density differentiate the temporal neocortex in the dog into a few regions. Among them, the cortex involving the anterior part of the ectosylvian gyrus did not send any amygdalopetal projection. The middle ectosylvian, dorsal zone of the posterior ectosylvian and the anterior part of the Sylvian gyrus were weakly connected with the amygdala. The cortical region involving the ventral zone of the posterior ectosylvian and composite posterior areas, as well as posterior Sylvian gyrus, was characterized by profuse connections with the amygdaloid complex. Corticoamygdaloid connections originate in the wide cortical area of the auditory cortex of the middle and dorsal part of the posterior ectosylvian gyrus as well as in the auditory association cortex located in the ventral ectosylvian, composite posterior and posterior Sylvian gyri. The connections showed a dorso ventral gradient of increasing density, in the direction of association fields. The most substantial projection taking rise from the ectosylvian posterior and posterior composite gyri terminated preferentially in the pericapsular sector of the lateral amygdaloid nucleus and, to a lesser degree, in its medial sector. Terminals of connections originating in the Sylvian gyrus occupied preferentially the intermediate part of the lateral nucleus, slightly more medially than that from the ectosylvian and posterior composite areas. Additionally, axonal terminals derived from the composite posterior and Sylvian posterior areas were observed in the basal parvocellular and magnocellular nuclei.Neocortical projections were reciprocated by amygdalofugal connections with two exceptions: the basal magnocellular nucleus was distinguished by a substantial amygdalofugal projection to the temporal neocortex focused on the dorsal Sylvian gyrus, and the central nucleus of the amygdala, in contrast, received an exclusively corticofugal projection.
EN
The main question of the study was: to what extent does a neonatal radiation-induced hippocampal lesion lead to emotional changes in adulthood? Acoustic startle response (ASR) was studied in two groups of adult rats. The rats from the first group (14 animals) were exposed to neonatal x-ray irradiation. Their ASR were compared with those from the 10 intact rats that formed a control group. The ASR was tested during two sessions with different illumination of the acoustic chamber. During the first session the rats were tested in the darkness while during the second test the acoustic chamber was illuminated with a 15 W bulb. Irradiation resulted in a significant reduction of granule cells of the hippocampus (about 55%). The lesion resulted in emotional and behavioral changes evidenced by modification of the ASR. The irradiated rats exhibited a significantly increased amplitude of the startle response. In contrast to the light condition, the darkness context caused a decline of the ASR amplitude in the control group and failed to elicit significant changes in the lesioned animals. The results support the hypothesis that hippocampal lesions disrupt motor inhibition.
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