Structural dynamics of neural plasticity in the supraoptic nucleus of the rat hypothalamus during dehydration and rehydration

Miyata, Seiji; Nakashima, Toshihiro; Kiyohara, Toshikazu

doi:10.1016/0361-9230(94)90057-4

Cited by 63 publications

(51 citation statements)

References 42 publications

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“…However, whereas approximately equal proportions of symmetric and asymmetric synaptic inputs were observed following GH trough periods, this ratio is shifted to 70:30 in favor of symmetric, i.e., inhibitory, inputs after prolonged exposure to high circulating GH, suggesting that a rewiring of the synaptic connectivity has taken place during the GH peak period. This finding is consistent with reports of various forms of synaptic reorganization in the hypothalamus in response to exogenous signals and endogenous rhythms such as changes in water balance (Miyata et al, 1994;Stern and Armstrong, 1998) or in circulating levels of estradiol (Garcia-Segura et al, 1986;Zsarnovszky et al, 2001;Parducz et al, 2003). Similarly, synaptic plasticity together with changes in the molecular machinery modulating synaptic efficacy may play a key role in the regulation of GH secretion at the level of the hypothalamus.…”

Section: Discussionsupporting

confidence: 92%

Subcellular Dynamics of Somatostatin Receptor Subtype 1 in the Rat Arcuate Nucleus: Receptor Localization and Synaptic Connectivity Vary in Parallel with the Ultradian Rhythm of Growth Hormone Secretion

Stroh¹,

Schouwenburg²,

Beaudet³

et al. 2009

Journal of Neuroscience

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Growth hormone (GH) secretion in male rats exhibits a 3.3 h ultradian rhythm generated by the reciprocal interaction of GH-releasing hormone (GHRH) and somatostatin (SRIF). SRIF receptor subtypes sst 1 and sst 2 are highly expressed in GHRH neurons of the hypothalamic arcuate nucleus (ARC). We previously demonstrated an ultradian oscillation in binding of SRIF analogs to the ARC in relation to GH peaks and troughs. Here we tested the hypothesis that these ultradian changes in SRIF binding are due to differential plasma membrane targeting of sst 1 receptors in ARC neurons using immunocytochemistry and electron microscopy. We found that 87% of sst 1 -positive ARC neurons also synthesized GHRH. Subcellularly, 80% of sst 1 receptors were located intracellularly and 20% at the plasma membrane regardless of GH status. However, whereas 30% of the cell-surface sst 1 receptors were located perisynaptically or subsynaptically following exposure to high GH secretion, this fraction was increased to 42% following a GH trough period ( p ϭ 0.05). Furthermore, the relative abundance of symmetric and asymmetric synapses on sst 1 -positive dendrites also varied significantly, depending on the GH cycle, from approximately equal numbers following GH troughs to 70:30 in favor of symmetric, i.e., inhibitory, inputs after GH peaks ( p Ͻ 0.02). These findings suggest that postsynaptic localization of sst 1 receptors and synaptic connectivity in the ARC undergo pronounced remodeling in parallel with the GH rhythm. Such synaptic plasticity may be an important mechanism by which sst 1 mediates SRIF's cyclical effects on ARC GHRH neurons to generate the ultradian rhythm of GH secretion.

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Section: Discussionsupporting

confidence: 92%

Subcellular Dynamics of Somatostatin Receptor Subtype 1 in the Rat Arcuate Nucleus: Receptor Localization and Synaptic Connectivity Vary in Parallel with the Ultradian Rhythm of Growth Hormone Secretion

Stroh¹,

Schouwenburg²,

Beaudet³

et al. 2009

Journal of Neuroscience

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“…First, loss of GlyR-dependent gliotransmission was also observed in explants prepared from lactating rats (data not shown), a completely distinct physiological state that also induces a profound retraction of astrocytic processes in this nucleus (Theodosis and Poulain, 1984). Second, the time course of recovery of GlyR tone was concurrent with the slow reestablishment of glial coverage after rehydration and not with the more rapid recovery of physiological parameters such as blood osmolality (Miyata et al, 1994). Third, loss of gliotransmission was not associated with a decline in SON taurine content, hypotonicity-induced taurine release (Fig.…”

Section: Glyr Tone Reflects Vrac-dependent Gliotransmissionmentioning

confidence: 86%

“…Electron microscopy has shown that the retraction of astrocyte processes induced by salt-loading recovers progressively when animals are allowed to rehydrate over a 2 week period (Miyata et al, 1994). Therefore, if the loss of GlyR tone in SL rats is caused specifically by a loss of spatial proximity between as astrocytic processes and neuronal membranes, then the recovery of GlyR tone after rehydration should follow a similar time course.…”

Section: Taurinergic Gliotransmission Is Spatially Confinedmentioning

confidence: 99%

Taurine Release by Astrocytes Modulates Osmosensitive Glycine Receptor Tone and Excitability in the Adult Supraoptic Nucleus

2012

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Cells can release the free amino acid taurine through volume-regulated anion channels (VRACs), and it has been hypothesized that taurine released from glial cells is capable of inhibiting action potential (AP) firing by activating neuronal glycine receptors (GlyRs) (Hussy et al., 1997). Although an inhibitory GlyR tone is widely observed in the brain, it remains unknown whether this specifically reflects gliotransmission because most neurons also express VRACs and other endogenous molecules can activate GlyRs. We found that VRACs are absent in neurons of the rat supraoptic nucleus (SON), suggesting that glial cells are the exclusive source of taurine in this nucleus. Application of strychnine to rat hypothalamic explants caused a depolarization of SON neurons associated with a decrease of chloride conductance and could excite these cells in the absence of fast synaptic transmission. This inhibitory GlyR tone was eliminated by pharmacological blockade of VRACs, by cellular taurine depletion, by metabolic inactivation of glia with fluorocitrate, and after retraction of astrocytic processes that intercalate neuronal somata and dendrites. Finally, GlyR tone varied inversely with extracellular fluid tonicity to mediate the osmotic control of AP firing by SON neurons. These findings establish taurine as a physiological gliotransmitter and show that gliotransmission is a spatially constrained process that can be modulated by the morphological rearrangement of astrocytes.

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“…Other strong possibilities include an increase in extracellular K+ (Canady et al, 1990) or increased osmolality. Thus far, our data suggest that proliferation continues for at least several days following rehydration, a time when plasma osmolarity returns to nearly normal levels (Miyata et al, 1994), and vasopressin remains depleted (Young, 1968).…”

Section: Possible Mitogensmentioning

confidence: 61%

“…As noted earlier, rehydration of rats after 10 days of 2% saline treatment results in nearly complete recovery of plasma osmolarity within 24 h (Miyata et al, 1994). Hence, the regulatory mechanisms of this neurosecretory system appear functionally normal under this regimen.…”

Section: Saline Substitution As a Stimulusmentioning

confidence: 79%

Dehydration‐induced proliferation of identified pituicytes in fully adult rats

Murugaiyan

Salm

1995

Glia

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The mitotic activity astrocytes in the adult central nervous system (CNS) is of interest due to their roles in gliosis and tumorigenesis, and their potential in aiding recovery of function following injury or disease. The posterior pituitary offers a potentially powerful model to study proliferation in vivo, since its resident astrocytes, called pituicytes, have been reported to divide concurrently with hormone release from the neurosecretory terminals there. our aim in this study was to confirm and characterize this proliferative response during dehydration and rehydration in fully adult animals using contemporary techniques. Adult male rats were given 2% saline in substitution for water for 0-9 days. Proliferation of pituicytes was quantified in tissue sections triple-labeled with the proliferation marker, 5-bromodeoxyuridine (BrdU), the astrocyte marker glial fibrillary acidic protein (GFAP), and the DNA marker 4,6,diamidino-2-phenylindole, HCL(DAPI). A robust proliferative response began within three days of dehydration and continued at a constant rate thereafter. In animals allowed to rehydrate, this response continued. After 9 days of dehydration, approximately 35% of pituicytes had participated in mitosis. While cell density remained constant across conditions, a reversible increase in posterior pituitary area was seen, suggesting that some cell death also occurs simultaneously. A significant proportion of non-pituicytes also underwent similar changes. These results indicate that pituicytes in the adult posterior pituitary retain characteristics necessary for reentering the cell cycle in response to local factors present during neurosecretory activity. We hypothesize that this proliferative response is directly related to the morphological changes previously reported for these cells under activating conditions.

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Structural dynamics of neural plasticity in the supraoptic nucleus of the rat hypothalamus during dehydration and rehydration

Cited by 63 publications

References 42 publications

Subcellular Dynamics of Somatostatin Receptor Subtype 1 in the Rat Arcuate Nucleus: Receptor Localization and Synaptic Connectivity Vary in Parallel with the Ultradian Rhythm of Growth Hormone Secretion

Subcellular Dynamics of Somatostatin Receptor Subtype 1 in the Rat Arcuate Nucleus: Receptor Localization and Synaptic Connectivity Vary in Parallel with the Ultradian Rhythm of Growth Hormone Secretion

Taurine Release by Astrocytes Modulates Osmosensitive Glycine Receptor Tone and Excitability in the Adult Supraoptic Nucleus

Dehydration‐induced proliferation of identified pituicytes in fully adult rats

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