title: Central neural pathway mediating splanchnic osmosensation.
abstract: To determine the central neural pathway which carries splanchnic osmosensory information to vasopressin (AVP) neurons in the hypothalamus, bilateral electrolytic lesions were placed in the ascending catecholaminergic fiber bundle, the locus coeruleus (LC), the locus subcoeruleus (subLC), the lateral parabrachial nucleus (LPB), the caudal periaqueductal gray (PAG) and the median preoptic nucleus (MPO). Six and seven days later, plasma AVP levels, plasma osmolality, mean arterial pressure and heart rate were measured following gastric infusion of hypertonic (598 mosm/kg; 2 ml/4 min) or isotonic (290 mosm/kg) saline in conscious rats with indwelling tail artery catheters and nasogastric tubes. The most effective pontine lesions, which were located in the ventral locus subcoeruleus (vsubLC) approximately 1.0 mm below the LC, decreased the AVP response to hypertonic gastric infusion by 59.7% (P less than 0.05) as compared to sham-lesioned controls. In addition, unilateral vsubLC lesions dramatically reduced the catecholamine innervation of the ipsilateral paraventricular nucleus (PVN), as qualitatively determined with dopamine beta-hydroxylase immunocytochemistry, suggesting that a pathway ascending with catecholaminergic fibers was disrupted. Lesions of the MPO were also very effective, decreasing the AVP response to hypertonic saline infusion by 60.3% (P less than 0.05), suggesting that the MPO is an integral relay center in this pathway. On the other hand, LC, LPB and PAG lesions were ineffective. Systemic plasma osmolality or cardiovascular factors did not mediate the AVP response. These results demonstrate, for the first time, that splanchnic osmotic information is transmitted to the hypothalamus via pathways within the ascending catecholaminergic fiber bundles, the MPO is a relay center where peripheral and central osmotic information may be integrated, and the LC, LPB, and PAG are not part of the splanchnic osmotic pathway.
authors.affiliation: Neuroscience Program, University of Virginia Medical Center, Charlottesville 22908.
authors.forename: M S
authors.initials: MS
authors.lastname: King
authors.forename: A J
authors.initials: AJ
authors.lastname: Baertschi
mesh_terms: D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000502:physiology*; D001921:Brain / Q000502:physiology*; D004299:Dopamine beta-Hydroxylase / Q000032:analysis; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology*; D013152:Splanchnic Circulation / Q000502:physiology*; D013153:Splanchnic Nerves / Q000502:physiology*; D014882:Water-Electrolyte Balance
chemical_list: D012462:Saline Solution, Hypertonic; D001127:Arginine Vasopressin; D012965:Sodium Chloride; D004299:Dopamine beta-Hydroxylase