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Lesions of the Ventral Lamina Terminalis Prevent Salt‐Induced Changes in the Responsiveness of Neurons in the Rostral Ventrolateral Medulla (RVLM)
Author(s) -
Stocker Sean D,
Adams Julye M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1169.1
Subject(s) - lamina terminalis , rostral ventrolateral medulla , medicine , endocrinology , chemistry , glutamate receptor , medulla , medulla oblongata , forebrain , blood pressure , anatomy , heart rate , hypothalamus , central nervous system , receptor
Sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to injection of L‐glutamate or GABA into the RVLM are enhanced during elevated dietary salt intake. The present study determined whether sodium‐sensing neurons of the forebrain lamina terminalis mediate these changes. Male Sprague‐dawley rats with or without lesions of the ventral lamina terminalis were given access to normal chow and either water or 0.9% NaCl for 14 days. Injection of L‐glutamate into the RVLM of control rats drinking 0.9% NaCl (57±2 ml/day, n=13) versus water (35±1 ml/day, n=11) produced greater changes in renal SNA (0.1nmol: 81±5 vs 52±5%; 1nmol: 123±8 vs 82±6%) and ABP (0.1nmol: 23±2 vs 10±1; 1nmol: 44±3 vs 24±1 mmHg). In marked contrast, injection of L‐glutamate in lesioned rats drinking 0.9% NaCl (56±7 ml/day, n=5) versus water (42±2 ml/day, n=5) showed similar increases in renal SNA (0.1nmol: 62±9 vs 57±11%; 1nmol: 87±4 vs 85±17%) and ABP (0.1nmol: 15±4 vs 15±3; 1nmol: 29±4 vs 31±5 mmHg). Similarly, injection of GABA produced greater depressor responses in control rats drinking 0.9% NaCl versus water (0.1nmol: −15±1 vs −7±1; 10nmol: −31±3 vs −15±1 mmHg, n>7), and this effect was prevented in lesioned rats (0.1nmol: −6±1 vs −7±1; 10nmol: −12±2 vs −15±1 mmHg, n=3). These findings suggest that increased dietary salt activates neurons in the forebrain lamina terminalis to enhance the responsiveness of RVLM neurons.