The osmoreceptor complex in the rat: evidence for interactions between the supraoptic and other diencephalic nuclei.
1. Experiments were undertaken to provide evidence for the existence of a circuit of neuronal interconnections between the supraoptic nucleus (SON), the ventral anteroventral third ventricular region (including the organum vasculosum of the lamina terminalis; ventral AV3V) and the median preoptic nucleus (MnPO), and to determine the importance of these connections in the osmotic control of the neuronal activity of the SON. Extracellular recordings were made in the urethane-anaesthetized male rat from neurones in one of these three sites, while the other two sites were electrically stimulated. 2. During recording from the SON, electrical stimulus pulses applied either to the ventral AV3V or to the MnPO were followed by orthodromic excitation (OD+) or initial short-duration inhibition followed by long-duration excitation (OD- +) of most SON neurones (44/48). The latency of OD+ or OD+ component of OD- + response produced by electrical stimulation of the MnPO was significantly (paired t test, P less than 0.01) shorter than that by the stimulation of the ventral AV3V. None of the neurones we recorded in the SON was activated antidromically by stimulation of either the ventral AV3V or the MnPO. Pressure injection of lidocaine (10%, 50 nl) into the MnPO reversibly depressed the OD+ effect after stimulation of the ventral AV3V in all the SON neurones tested (11/11), while injection of lidocaine into the ventral AV3V did not affect the OD+ effect after stimulation of the MnPO in most neurones (7/9). Both types of observation are consistent with the presence of an excitatory input to SON through the MnPO. 3. Pressure injection of lidocaine into both the ventral AV3V and the MnPO reversibly blocked the activation of SON neurones following an I.P. injection of 1.5 M-NaCl (1 ml) (ventral AV3V 11/11; MnPO, 10/10 cells tested). Injection of lidocaine at both sites, however, did not prevent activation of SON neurones by hypovolaemia (2 ml of blood was withdrawn through a cannula in the right atrium: ventral AV3V, 4/5; MnPO, 4/4 cells tested). The integrity of connections in the ventral AV3V and MnPO thus appeared to be essential for osmotic activation of the SON. 4. Of the 119 ventral AV3V neurones which were tested for their response to electrical stimulation of the SON, forty-nine neurones showed orthodromic excitation (OD+; n = 33) or initial inhibition followed by excitation (OD- +; n = 16). Thirty of the forty-nine OD+ or OD- + neurones also showed antidromic excitation (AD) after electrical stimulation of the MnPO.(ABSTRACT TRUNCATED AT 400 WORDS)
Honda
K
K
Department of Physiology, Fukui Medical School, Matsuoka, Japan.
Negoro
H
H
Dyball
R E
RE
Higuchi
T
T
Takano
S
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D004027:Diencephalon / Q000502:physiology*; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology; D009995:Osmosis; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology; D010904:Pituitary Gland, Posterior / Q000502:physiology; D011301:Preoptic Area / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012684:Sensory Thresholds / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology; D013495:Supraoptic Nucleus / Q000502:physiology*; D013997:Time Factors
D012965:Sodium Chloride; D008012:Lidocaine