c-fos may code for a common transcription factor within the hypothalamic neural circuits involved in osmoregulation

Hamamura, Mitsuko; Nunez, Derek J.; Leng, Gareth; Emson, Piers C.; Kiyama, Hiroshi

doi:10.1016/0006-8993(92)90448-i

Cited by 106 publications

(31 citation statements)

References 24 publications

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“…For example, neurotransmitter receptors are involved in the relay of osmotic information to VP and OT neurons. Osmotic stimulation of VP and OT release is dependent on glutamatergic transmission from neurons in organum vasculosum of the lamina terminalis (Russell et al, 1989;Hamamura et al, 1992). Previous experiments using HNS explants demonstrated that the glutamate receptor agonist NMDA evokes VP secretion, whereas its antagonists significantly inhibit osmotically stimulated VP release (Swenson et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Osmotic Regulation of Estrogen Receptor-β in Rat Vasopressin and Oxytocin Neurons

2003

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Section: Discussionmentioning

confidence: 99%

Osmotic Regulation of Estrogen Receptor-β in Rat Vasopressin and Oxytocin Neurons

2003

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“…Indeed, there is evidence that intraperitoneal injec tion of HS causes rapid morphological changes in the SON [40], Likewise, central infusion of OT produces changes in glial arrangement, that is, a retraction in glial processes and an uncovering of synaptic elements [7], It is surprising that TTX administered into the SON reduced basal plasma VP levels and completely abolished the response to a systemic osmotic stimulus. Intraperito neal HS would be expected to increase neurosecretion from both SON [41.42] and PVN [42] neurons. It is possi ble that the neurotoxin may diffuse to PVN axons cours ing near the border of the SON, thus affecting neural activity [43], There is no information on the diffusion gra dient of TTX from the SON microdialysis probe.…”

Section: Discussionmentioning

confidence: 99%

Effects of Tetrodotoxin on Osmotically Stimulated Central and Peripheral Vasopressin and Oxytocin Release

Ludwig

Callahan

Morris³

1995

Neuroendocrinology

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Tetrodotoxin (TTX) was used to (1) distinguish between axonal and dendritic/ somatic release of vasopressin (VP) and oxytocin (OT) within the supraoptic nucleus (SON) and (2) to determine whether neuronal inputs trigger intranuclear peptide release in the response to osmotic stimulation. Microdialysis was used to administer TTX (10^-6 M or 10^–4M) bilaterally into the SON with simultaneous monitoring of central and peripheral peptide release and mean arterial pressure in urethane-anesthetized male rats. Osmotic stimuli were given via the microdialysis probe (1 M NaCl-artificial CSF) or injected intraperitoneally (3.5 M NaCl; 600 µl/100 g b.w.) SON perfusion with TTX did not alter basal intranuclear VP or OT release or the intranuclear peptide response to direct NaCl stimulation of the SON. However, TTX treatment abolished the effect of peripheral osmotic stimulation on central peptide release. Basal plasma peptide levels were significantly reduced by TTX, e.g. decreases of 94.8 and 75.8% for VP and OT, respectively. TTX also blocked the peripheral endocrine and cardiovascular reponses to both modes of osmotic stimulation. The TTX insensitivity of directly stimulated intranuclear release suggests non-synaptic peptide release from dendrites and/or cell bodies. The ability of TTX to abolish the central peptide response to systemic osmotic stimulation demonstrates that intranuclear release is a part of a cascade produced by osmotic activation of multisynaptic pathways.

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“…c-fos expression has been well described as a marker of neuronal activation in both adult and fetal brain nuclei (6). McDonald et al (7) recently showed that FOS-ir was evident in the SFO, OVLT, and MnPO, as well as in the PVN and SON of the near-term fetal forebrain in response to maternal hypertonicity.…”

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confidence: 99%

Plasma Osmolality Dipsogenic Thresholds and c-fos Expression in the Near-Term Ovine Fetus

Nijland

Ross

2001

Pediatr Res

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In ovine and human pregnancy, fetal swallowing contributes importantly to amniotic fluid homeostasis. Fetal dipsogenic responsiveness to short-term plasma hyperosmolality develops in late gestation, although fetal swallowing is not stimulated in response to long-term plasma osmolality increases (2 to 3%), which typically stimulate adult drinking behavior. To explore the near-term fetal plasma osmolality threshold for swallowing stimulation, we examined the effects of i.v. hypertonic saline-induced subacute increases in plasma hypertonicity on fetal swallowing behavior. Central sites of activation were examined by c-fos expression in putative dipsogenic nuclei. The results demonstrate that subacute 2 to 3% plasma osmolality increases do not stimulate near-term ovine fetal swallowing. However, fetal swallowing activity significantly increased (3 times) after plasma osmolality increased Ͼ6% above basal values. Consistent with a specific dipsogenic response, i.v. hypertonic saline induced c-fos expression in the anterior third ventricle region, a putative dipsogenic center, as well as in the fetal hindbrain. The stimulation of fetal swallowing under conditions of higher osmotic stimulation and the correlation with forebrain c-fos expression indicates that near-term fetal osmoregulation mechanisms are functional, although not completely mature. Intravascular osmolality and body fluid homeostasis are maintained primarily by coordination of thirst-mediated drinking behavior and neuroendocrine-mediated renal fluid regulatory mechanisms. During in utero development, fetal swallowing contributes importantly to amniotic fluid volume homeostasis. Previous studies in this laboratory have demonstrated that near-term ovine fetal swallowing is stimulated by intravenous, intracarotid, and intracerebroventricular hyperosmolality (1-4), consistent with the activation of central osmoreceptors in regions responsive to both vascular and cerebrospinal fluid tonicity. Despite intact fetal osmotic-dipsogenic responsiveness, fetal swallowing is not stimulated in response to plasma osmolality increases (2 to 3%), which typically stimulate adult drinking behavior. For example, despite continually elevated plasma osmolality (10 -14 mosmol/kg) in response to short-term i.v. hypertonic saline injection, fetal swallowing activity is only stimulated for a maximum of 5 min (1). Furthermore, long-term increases in plasma osmolality of 10 mosmol/kg do not alter fetal swallowed volume (5). These responses suggest either a reduced population of fetal osmoreceptor cells, reduced sensitivity of osmoreceptors, or altered secondary neural mechanisms, in comparison to the adult. c-fos expression has been well described as a marker of neuronal activation in both adult and fetal brain nuclei (6). McDonald et al. (7) recently showed that FOS-ir was evident in the SFO, OVLT, and MnPO, as well as in the PVN and SON of the near-term fetal forebrain in response to maternal hypertonicity. These results are comparable to physiological and c-fos responses observe...

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c-fos may code for a common transcription factor within the hypothalamic neural circuits involved in osmoregulation

Cited by 106 publications

References 24 publications

Osmotic Regulation of Estrogen Receptor-β in Rat Vasopressin and Oxytocin Neurons

Osmotic Regulation of Estrogen Receptor-β in Rat Vasopressin and Oxytocin Neurons

Effects of Tetrodotoxin on Osmotically Stimulated Central and Peripheral Vasopressin and Oxytocin Release

Plasma Osmolality Dipsogenic Thresholds and c-fos Expression in the Near-Term Ovine Fetus

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