Taurine selectively modulates the secretory activity of vasopressin neurons in conscious rats.
Previous experiments have shown that a 10-min forced swimming session triggers the release of vasopressin from somata and dendrites, but not axon terminals, of neurons of the hypothalamic-neurohypophysial system. To further investigate regulatory mechanisms underlying this dissociated release, we forced male Wistar rats to swim in warm (20 degrees C) water and monitored release of the potentially inhibitory amino acids gamma amino butyric acid (GABA) and taurine into the hypothalamic supraoptic nucleus using microdialysis. Forced swimming caused a significant increase in the release of taurine (up to 350%; P < 0.05 vs. prestress release), but not GABA. To reveal the physiological significance of centrally released taurine, the specific taurine antagonist 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide was administered into the supraoptic nucleus via retrodialysis. Administration of this antagonist caused a significant increase in the release of vasopressin within the supraoptic nucleus and into the blood both under basal conditions and during stress (up to 800%; P < 0.05 vs. basal values), without affecting hypothalamic or plasma oxytocin. Local administration of the GABA(A) receptor antagonist bicuculline, in contrast, failed to influence vasopressin secretion at either time point. In a separate series of in vivo electrophysiological experiments, administration of the same dosage of the taurine antagonist into the supraoptic nucleus via microdialysis resulted in an increased electrical activity of identified vasopressinergic, but not oxytocinergic, neurons. Taken together our data demonstrate that taurine is released within the supraoptic nucleus during physical/emotional stress. Furthermore, at the level of the supraoptic nucleus, taurine inhibits not only the electrical activity of vasopressin neurons but also acts as an inhibitor of both central and peripheral vasopressin secretion during different physiological states.
Engelmann
M
M
Institut für Medizinische Neurobiologie, Otto-von-Guericke-Universität Magdeburg, Leipziger Str. 44. D-39120 Magdeburg, Germany. mario.engelmann@medizin.uni-magdeburg.de
Ludwig
M
M
Singewald
N
N
Ebner
K
K
Sabatier
N
N
Lubec
G
G
Landgraf
R
R
Wotjak
C T
CT
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001581:Benzothiadiazines / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology; D003243:Consciousness / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000378:metabolism*; D010121:Oxytocin / Q000097:blood / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism* / Q000503:physiopathology; D013495:Supraoptic Nucleus / Q000187:drug effects / Q000378:metabolism*; D013550:Swimming / Q000502:physiology; D013654:Taurine / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014667:Vasopressins / Q000097:blood / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D001581:Benzothiadiazines; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D014667:Vasopressins; D013654:Taurine; D001224:Aspartic Acid; D018698:Glutamic Acid; D010121:Oxytocin; D005680:gamma-Aminobutyric Acid; C032946:6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide; D001640:Bicuculline