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Smardencas A, Denton DA, McKinley MJ. Hyperdipsia in sheep bearing lesions in the medial septal nucleus. Brain Res. 2020;1752:147223doi: 10.1016/j.brainres.2020.147223.
Smardencas, A., Denton, D. A., & McKinley, M. J. (2021). Hyperdipsia in sheep bearing lesions in the medial septal nucleus. Brain research, 1752147223. https://doi.org/10.1016/j.brainres.2020.147223
Smardencas, A, et al. "Hyperdipsia in sheep bearing lesions in the medial septal nucleus." Brain research vol. 1752 (2021): 147223. doi: https://doi.org/10.1016/j.brainres.2020.147223
Smardencas A, Denton DA, McKinley MJ. Hyperdipsia in sheep bearing lesions in the medial septal nucleus. Brain Res. 2021 Feb 01;1752:147223. doi: 10.1016/j.brainres.2020.147223. Epub 2020 Dec 23. PMID: 33358728.
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Brain Res. 2021 Feb 01;1752:147223. doi: 10.1016/j.brainres.2020.147223. Epub 2020 Dec 23.

Hyperdipsia in sheep bearing lesions in the medial septal nucleus.

Brain research

A Smardencas, D A Denton, M J McKinley

Affiliations

  1. Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic 3010, Australia. Electronic address: [email protected].
  2. Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic 3010, Australia; Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Vic 3010, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Vic 3010, Australia. Electronic address: [email protected].
  3. Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic 3010, Australia; Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Vic 3010, Australia; Department of Physiology, University of Melbourne, Melbourne, Vic 3010, Australia. Electronic address: [email protected].

PMID: 33358728 DOI: 10.1016/j.brainres.2020.147223

Abstract

Previous experiments in rodents showed that ablation of the septal brain region caused hyperdipsia. We investigated which part of the septal region needs ablation to produce hyperdipsia in sheep, and whether increased drinking was a primary hyperdipsia. Following ablation of the medial septal region (n = 5), but not parts of the lateral septal region (n = 4), daily water intake increased from ~2.5-5 L/day up to 10 L/day for up to 3 months post-lesion. In hyperdipsic sheep, plasma osmolality increased on the first day post-lesion and body weight fell, suggesting that initial hyperdipsia was secondary to fluid loss. However hyperosmolality was not sustained long-term and plasma hypo-osmolality persisted from 0.5 to 3 months post-lesion. Acute dipsogenic responses to intravenous hypertonic saline, intravenous or intracerebroventricular angiotensin II, water deprivation for 2 days, or feeding over 5 h were not potentiated by medial septal lesions, showing that the rapid pre-systemic inhibitory influences that cause satiation of thirst upon the act of drinking were intact. However, hyperdipsic sheep continued to ingest water when hyponatremic (plasma [Na] was 127-132 mmol/l) and plasma osmolality was 262-268 mosmol/kg due to retention of ingested fluid resulting from intravenous infusion of vasopressin administered to maintain a basal blood level of antidiuretic hormone. The results show that septal lesion-induced hyperdipsia is not due to disruption of acute pre-systemic influences associated with drinking water that initiates rapid satiation of thirst. Rather, inhibitory influences of hyponatremia, hypo-osmolality or hypervolemia on drinking appear to be disrupted by medial septal lesions.

Copyright © 2020 Elsevier B.V. All rights reserved.

Keywords: Angiotensin; Hyponatremia; Medial septum; Pre-systemic factors; Primary hyperdipsia; Thirst

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