Median preoptic neurones projecting to the hypothalamic paraventricular nucleus respond to osmotic, circulating Ang II and baroreceptor input in the rat.
The present study sought to determine whether individual neurones of the median preoptic nucleus (MnPO) with axonal projections to the hypothalamic paraventricular nucleus (MnPO-PVN) respond to osmotic, circulating angiotensin II (Ang II), and baroreceptor stimulation. Hypertonic NaCl (0.75 or 1.5 osmol l(-1)) or Ang II (150 ng) was injected into the internal carotid artery (ICA). Baroreceptor stimulation was performed by i.v. injection of phenylephrine or sodium nitroprusside to increase or decrease arterial blood pressure, respectively. Of 65 MnPO neurones, 50 units were antidromically activated from the PVN with an average onset latency of 11.3 +/- 0.7 ms. Only 9.5% of MnPO-PVN neurones were antidromically activated from the PVN bilaterally. Type I MnPO-PVN neurones (n = 14) responded to osmotic but not Ang II stimulation. In 79% (11/14) of these type I neurones, the response was an increase in cell discharge. Type II MnPO-PVN neurones (n = 7) displayed a significant increase in cell discharge in response to ICA injection of Ang II but not hypertonic NaCl. Type III MnPO-PVN neurones (n = 16) responded to both ICA injection of hypertonic NaCl and Ang II. In 88% (14/16) of type III neurones, osmotic and Ang II stimulation each increased cell discharge. Type IV MnPO-PVN neurones (n = 13) displayed no change in cell discharge in response to ICA injection of hypertonic NaCl or Ang II. Baroreceptor stimulation altered the discharge in subpopulations of type I, II and III MnPO-PVN neurones (43-63% depending on neuronal type). Only one MnPO-PVN neurone responded solely to baroreceptor stimulation (type IV). In addition, a subset of type I, II and III neurones displayed a significant correlation with sympathetic nerve activity and/or the cardiac cycle. These findings suggest that a significant population of MnPO-PVN neurones respond to osmotic and circulating Ang II stimulation and thereby represents a neural substrate through which neurohumoral inputs are integrated within the forebrain lamina terminalis.
Stocker
Sean D
SD
Department of Physiology, University of Kentucky College of Medicine, Lexington, 40526-0298, USA. sdstoc3@email.uky.edu
Toney
Glenn M
GM
D000200:Action Potentials / Q000187:drug effects; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D004558:Electric Stimulation; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000145:classification* / Q000187:drug effects / Q000502:physiology; D009490:Neurosecretory Systems / Q000187:drug effects / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D009997:Osmotic Pressure; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D011301:Preoptic Area / Q000187:drug effects / Q000502:physiology*; D011311:Pressoreceptors / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012462:Saline Solution, Hypertonic; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D012462:Saline Solution, Hypertonic; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D009599:Nitroprusside; D010656:Phenylephrine