Lesions of the commissural nucleus of tractus solitarii increase osmotic-induced activation of paraventricular and supraoptic hypothalamic nuclei.

University College Dublin (2009) Proc Physiol Soc 15, PC1

Poster Communications: Lesions of the commissural nucleus of tractus solitarii increase osmotic-induced activation of paraventricular and supraoptic hypothalamic nuclei.

G. T. Blanch1, A. H. Freiria-Oliveira1, E. Colombari1, J. V. Menani1, D. Murphy2, D. S. Colombari1

1. Physiology and Pathology, FOAr-UNESP, Araraquara, Sao Paulo, Brazil. 2. Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, United Kingdom.

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Neurons in the magnocellular division of paraventricular nucleus (PVN) and supraoptic nucleus (SON) of hypothalamus are activated by osmotic stimulus increasing the release of oxytocin and vasopressin, hormones that induce natriuresis, antidiuresis and vasoconstriction (McCann et al, 2003). PVN and SON receive important ascending neural connections from the nucleus of tractus solitarii (NTS) (Tribollet et al, 1985). Previously we have demonstrated that rats with lesions in the commissural subdivision of the NTS (commNTS) increased water intake, natriuresis and arterial pressure after intragastric 2 M NaCl load. Considering that the increase in arterial pressure in commNTS-lesioned rats is dependent on vasopressin, in the present study we investigated the effects of commNTS lesions on c-fos expression in the PVN and SON produced by intragastric hypertonic sodium load. Male Holtzman rats (300-320 g, n = 3-4/group) were anesthetized with ketamine (80 mg/kg of body weight, ip) combined with xylazine (7 mg/kg of body weight, ip) and submitted to electrolytic (1 mA x 10 s) or sham lesion of the commNTS. Fifteen days after lesions, rats received 2 ml of 2 M NaCl intragastrically, which increases plasma osmolality in 4% (Pereira et al, 2002) or 2 ml of 0.15 M NaCl. Two hours after sodium load, rats were deeply anesthetized with pentobarbital (50 mg/kg of body weight, ip), perfused with 4% paraformaldehyde and brains were removed. Imunohistochemistry for c-fos expression was performed in brain slices using DAB staining. Data are expressed as means ± SEM and analyzed by one-way ANOVA. In sham rats, intragastric 2 M NaCl induced c-fos expression in magnocellular PVN (70 ± 12 vs. 0.15 M NaCl: 8 ± 2 positive cells/section – each 150 μm bilateraly, p <0.05), parvocellular PVN (27 ± 4 vs. 0.15 M NaCl: 5 ± 1 positive cells/section, p <0.05) and SON (191 ± 12 vs. 0.15 M NaCl: 2 ± 1, positive cells/section, p <0.05). CommNTS lesions increased c-fos expression induced by intragastric 2 M NaCl in magnocellular and parvocellular PVN (139 ± 22 and 40 ± 27 positive cells/section, respectively, p <0.05 vs. sham) and SON (270 ± 11 positive cells/section, p < 0.05 vs. sham). Double labeling immunofluorescence demonstrated that a significant number of c-fos positive cells in PVN and SON in both commNTS- and sham-lesioned rats were oxytocinergic or vasopressinergic. The results show increased number of PVN and SON neurons activated by osmotic stimulus in commNTS-lesioned rats, which may have a correlation with the increased natriuresis and arterial pressure in commNTS-lesioned rats after hypertonic sodium load.



Where applicable, experiments conform with Society ethical requirements.

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