Differential osmoresponsiveness of periventricular neurons in duck hypothalamus

Kazuyuki Kanosue, H. Schmid, E. Simon

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14 Citations (Scopus)

Abstract

Single-unit responses to osmotic stimulation were recorded extracellularly in slice preparations from the duck's hypothalamus in the periventricular layer (pl), magnocellular center (mc), and deep periventricular neuropil of the paraventricular nucleus (PVN). The pl neurons were located in the dorsorostral third ventricular region of maximum osmoresponsiveness determined in vivo. Hypertonic stimulation (+20 to +35 mosmol/kgH2O) by excess NaCl in the incubation medium excited 25 and inhibited 4 out of 48 pl neurons. Hypotonic (-10 to -20 mosmol/kgH2O) stimulation inhibited 9 out of 10 neurons activated by hypertonic stimulation. Hypertonic activation of pl neurons was maintained in seven out of nine neurons when NaCl was replaced by LiCl, but replacing NaCl by sucrose was ineffective in each of 10 neurons. Synaptic blockade (Ca2+-free/high-Mg2+ medium) did not abolish hypertonic activation in 8 out of 11 pl neurons. Among 30 mc neurons, 2 were activated and 1 inhibited by hypertonic stimulation with NaCl (+20 to +35 mosmol/kgH2O), and among 24 neurons in the periventricular neuropil, 2 were activated and 4 inhibited. The function of osmoresponsive pl neurons as specific receptors would be consistent with their morphological characteristics and with the location and functional properties of the duck's third ventricular osmoresponsiveness in vivo.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number4 27-4
Publication statusPublished - 1990
Externally publishedYes

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Ducks
Hypothalamus
Neurons
Neuropil
Paraventricular Hypothalamic Nucleus
Sucrose

Keywords

  • avian osmoregulation
  • brain stem cytoarchitecture
  • hypothalamic slice
  • osmoreceptive neurons

ASJC Scopus subject areas

  • Physiology

Cite this

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abstract = "Single-unit responses to osmotic stimulation were recorded extracellularly in slice preparations from the duck's hypothalamus in the periventricular layer (pl), magnocellular center (mc), and deep periventricular neuropil of the paraventricular nucleus (PVN). The pl neurons were located in the dorsorostral third ventricular region of maximum osmoresponsiveness determined in vivo. Hypertonic stimulation (+20 to +35 mosmol/kgH2O) by excess NaCl in the incubation medium excited 25 and inhibited 4 out of 48 pl neurons. Hypotonic (-10 to -20 mosmol/kgH2O) stimulation inhibited 9 out of 10 neurons activated by hypertonic stimulation. Hypertonic activation of pl neurons was maintained in seven out of nine neurons when NaCl was replaced by LiCl, but replacing NaCl by sucrose was ineffective in each of 10 neurons. Synaptic blockade (Ca2+-free/high-Mg2+ medium) did not abolish hypertonic activation in 8 out of 11 pl neurons. Among 30 mc neurons, 2 were activated and 1 inhibited by hypertonic stimulation with NaCl (+20 to +35 mosmol/kgH2O), and among 24 neurons in the periventricular neuropil, 2 were activated and 4 inhibited. The function of osmoresponsive pl neurons as specific receptors would be consistent with their morphological characteristics and with the location and functional properties of the duck's third ventricular osmoresponsiveness in vivo.",
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AU - Kanosue, Kazuyuki

AU - Schmid, H.

AU - Simon, E.

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N2 - Single-unit responses to osmotic stimulation were recorded extracellularly in slice preparations from the duck's hypothalamus in the periventricular layer (pl), magnocellular center (mc), and deep periventricular neuropil of the paraventricular nucleus (PVN). The pl neurons were located in the dorsorostral third ventricular region of maximum osmoresponsiveness determined in vivo. Hypertonic stimulation (+20 to +35 mosmol/kgH2O) by excess NaCl in the incubation medium excited 25 and inhibited 4 out of 48 pl neurons. Hypotonic (-10 to -20 mosmol/kgH2O) stimulation inhibited 9 out of 10 neurons activated by hypertonic stimulation. Hypertonic activation of pl neurons was maintained in seven out of nine neurons when NaCl was replaced by LiCl, but replacing NaCl by sucrose was ineffective in each of 10 neurons. Synaptic blockade (Ca2+-free/high-Mg2+ medium) did not abolish hypertonic activation in 8 out of 11 pl neurons. Among 30 mc neurons, 2 were activated and 1 inhibited by hypertonic stimulation with NaCl (+20 to +35 mosmol/kgH2O), and among 24 neurons in the periventricular neuropil, 2 were activated and 4 inhibited. The function of osmoresponsive pl neurons as specific receptors would be consistent with their morphological characteristics and with the location and functional properties of the duck's third ventricular osmoresponsiveness in vivo.

AB - Single-unit responses to osmotic stimulation were recorded extracellularly in slice preparations from the duck's hypothalamus in the periventricular layer (pl), magnocellular center (mc), and deep periventricular neuropil of the paraventricular nucleus (PVN). The pl neurons were located in the dorsorostral third ventricular region of maximum osmoresponsiveness determined in vivo. Hypertonic stimulation (+20 to +35 mosmol/kgH2O) by excess NaCl in the incubation medium excited 25 and inhibited 4 out of 48 pl neurons. Hypotonic (-10 to -20 mosmol/kgH2O) stimulation inhibited 9 out of 10 neurons activated by hypertonic stimulation. Hypertonic activation of pl neurons was maintained in seven out of nine neurons when NaCl was replaced by LiCl, but replacing NaCl by sucrose was ineffective in each of 10 neurons. Synaptic blockade (Ca2+-free/high-Mg2+ medium) did not abolish hypertonic activation in 8 out of 11 pl neurons. Among 30 mc neurons, 2 were activated and 1 inhibited by hypertonic stimulation with NaCl (+20 to +35 mosmol/kgH2O), and among 24 neurons in the periventricular neuropil, 2 were activated and 4 inhibited. The function of osmoresponsive pl neurons as specific receptors would be consistent with their morphological characteristics and with the location and functional properties of the duck's third ventricular osmoresponsiveness in vivo.

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