Effect of electrolytic and chemical lesion by ibotenic acid of the septal area on water and salt intake

• Published in: Brain research bulletin Vol. 47; no. 2; pp. 163 - 169
• Main Authors: Saad, Wilson Abrão, Camargo, Luiz Antonio de Arruda, Antunes-Rodrigues, José, Simões, Silvio
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.09.1998; Elsevier Science
• Subjects: Animals; Biological and medical sciences; Brain Mapping; Drinking - drug effects; Drinking - physiology; Electricity; Electrolytic lesion; Excitatory Amino Acid Agonists - pharmacology; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Ibotenic Acid - pharmacology; Ibotenic acid lesion; Male; Rats; Rats, Sprague-Dawley; Septal area; Septum Pellucidum - drug effects; Septum Pellucidum - pathology; Septum Pellucidum - physiology; Sodium Chloride; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Water; Water and salt intake; Ibotenic acid lesion; Septal area; Electrolytic lesion; Water and salt intake; Salt; Vertebrata; Mammalia; Feeding behavior; Rat; Septum nucleus; Rodentia; Central nervous system; Drinking; Water intake; Lesion; Brain (vertebrata)
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/S0361-9230(98)00057-4

Water and sodium chloride intake was studied in male Holtzman rats weighing 250–300 g that had been subjected to electrolytic and chemical lesions of the septal area (SA). Water intake increased in animals with electrolytic lesion of the SA bilaterally from 169.37 ± 8.55 (sham) to 214.87 ± 23.10 ml/5 days (lesioned). Water intake decreased after ibotenic acid lesion of the SA from 229.33 ± 27.60 to 127.33 ± 22.84 ml/5 days. Sodium chloride intake (1.5%) increased in animals with electrolytic lesion of the SA from 10.0 ± 1.73 to 15.5 ± 1.95 ml/5 days after lesion. Also sodium chloride (1.5%) intake increased after ibotenic acid injection into the SA to a greater extent (from 7.83 ± 1.25 to 14.33 ± 1.87 ml/5 days). The results indicate that the water intake response may be due to lesions that involve cell bodies and fibers of passage and that the sodium intake response can also be induced by lesions which involve only cell bodies. Finally, these results led us to conclude that the SA uses its cell bodies and afferent bodies and fibers for processing inputs mediating water intake and salt appetite and that the cells bodies of the SA are implicated in increased water intake.