Emerging concepts of structure-function dynamics in adult brain: The hypothalamo-neurohypophysial system

Hatton, Glenn I.

doi:10.1016/0301-0082(90)90017-b

Cited by 430 publications

(273 citation statements)

References 432 publications

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“…Disruption of F-actin in astrocytes by bath application of actin-disrupting agents may contribute to glial retraction and their burst-evoking actions. Astrocytic retraction during lactation has been proposed as a mechanism underlying bursts in OT neurons (Hatton, 1990;Hatton, 2004); the present results extend the relevance of this mechanism to periods of suckling.…”

Section: Actin Reorganization and Ot-evoked Burstssupporting

confidence: 84%

Interaction of Extracellular Signal-Regulated Protein Kinase 1/2 with Actin Cytoskeleton in Supraoptic Oxytocin Neurons and Astrocytes: Role in Burst Firing

Wang¹,

Hatton²

2007

J. Neurosci.

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Neuronal firing patterns determine the manner of neurosecretion, the underlying mechanisms of which are poorly understood. Using supraoptic nuclei in brain slices from lactating rats, we examined the involvement of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and filamentous actin (F-actin) in burst generation by oxytocin (OT) neurons. Blocking phosphorylation of ERK1/2 (pERK1/2) decreased miniature EPSCs and blocked OT-evoked bursts, as did intracellularly loading an antibody against pERK1/2. OT (10 pM) increased cytosolic pERK1/2 close to the cell membrane within the first 5 min, subsiding by 30 min, whereas OT elicited pERK1/2 nuclear translocation in closely associated supraoptic astrocytes. The increased pERK1/2 was tightly correlated with spatiotemporal actin dynamics. In OT neurons, OT initially increased F-actin, particularly at membrane subcortical areas, and then decreased it after 30 min. Both polymerization and depolymerization of actin cytoskeleton were associated with bursts, but only polymerization facilitated OTevoked bursts. Blocking ERK1/2 activation blocked OT-evoked actin polymerization, whereas depolymerizing F-actin increased pERK1/2 expression. These changes were further identified in vivo. In intact animals, suckling increased ERK1/2 activation in the cytosol and membrane subcortical area F-actin formation in OT neurons, whereas it increased F-actin concentration in astrocytic somata. Coimmunoprecipitation showed that suckling increased molecular interactions between pERK1/2 and actin. Finally, two different blockers of ERK1/2 kinase injected intracerebroventricularly reduced suckling-evoked milk ejections. This is the first demonstration that OT mediation of suckling-evoked bursts/milk ejections is via interactions between pERK1/2 and actin cytoskeleton.

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Section: Actin Reorganization and Ot-evoked Burstssupporting

confidence: 84%

Interaction of Extracellular Signal-Regulated Protein Kinase 1/2 with Actin Cytoskeleton in Supraoptic Oxytocin Neurons and Astrocytes: Role in Burst Firing

Wang¹,

Hatton²

2007

J. Neurosci.

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“…The hypothalamic-neurohypophyseal system (HNS) (Cunningham and Sawchenko, 1991, Johnson et al, 1993, Kato et al, 1995 is constituted by magnocellular neurons located in the PVN and hypothalamic supraoptic nucleus (SON) sending their axons to the posterior pituitary, where AVP is released into the general circulation to control antidiuresis and vasoconstriction/glycogen metabolism. There is growing evidence that the HNS provides as a second neuronal-humoral system that is activated during stress (Hatton, 1990, Engelmann et al, 1998.…”

Section: Introductionmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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“…These two peptide hormones are, after axonal transport and storage, released from nerve endings in the posterior pituitary into the systemic circulation to control fluid balance and smooth muscle contractility (Hatton 1990). Apart from vasopressin and oxytocin, magnocellular neurons of the PVN and SON synthesize and store several other chemical messengers.…”

Section: Introductionmentioning

confidence: 99%

“…Local interactions at the pituitary level and effects on peripheral tissues, via their systemic release, are current possibilities (Brownstein & Mezey 1986, Hatton 1990, Villar et al 1990, Meister 1993. In this regard, PRLs were found to be released from neurohypophyseal endings in response to high potassium and the 14 kDa variant was found in the circulation (Torner et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Changes in the expression of neurohypophyseal prolactins during the estrous cycle and after estrogen treatment

Torner¹,

Nava²,

Dueñas³

et al. 1999

Journal of Endocrinology

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Estrogens are recognized regulators of the expression of neurohypophyseal hormones and of anterior pituitary prolactin (PRL). Here we have investigated whether the levels of PRL mRNA and of 23 and 14 kDa PRL variants present in the hypothalamo-neurohypophyseal system change during the estrous cycle or in response to estrogen treatment. The reverse transcription polymerase chain reaction (RT-PCR) was performed to examine PRL mRNA expression in isolated paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei. In both nuclei PRL mRNA levels appeared higher in cycling females than in male rats, with the highest level occurring at estrus. This increase may involve estrogen action, since estrogen administration to ovariectomized rats was associated with apparently higher PRL mRNA levels in both the PVN and SON. Expression of the PRL gene at these sites may occur via both transcriptional factor Pit-1-dependent and -independent mechanisms. RT-PCR detected the mRNA for Pit-1 in the PVN but only at estrus. The concentration of the 23 kDa immunoreactive PRL determined in the neurohypophysis was significantly higher during estrus and after estrogen treatment. However, no difference was detected in the levels of the neurohypophyseal 14 kDa PRL-like fragment along the estrous cycle nor after estrogen administration. This lack of parallelism between neurohypophyseal PRLs could relate to an estrogen-induced inhibition of the proteolysis of 23 kDa PRL at this site, since estrogen treatment reduced the activity of neurohypophyseal proteolytic enzymes able to cleave PRL. Altogether our results are consistent with estrogens having a stimulatory effect on PRL gene expression in the hypothalamo-neurohypophyseal system and a concomitant inhibitory action on PRL proteolysis at this site.

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Emerging concepts of structure-function dynamics in adult brain: The hypothalamo-neurohypophysial system

Cited by 430 publications

References 432 publications

Interaction of Extracellular Signal-Regulated Protein Kinase 1/2 with Actin Cytoskeleton in Supraoptic Oxytocin Neurons and Astrocytes: Role in Burst Firing

Interaction of Extracellular Signal-Regulated Protein Kinase 1/2 with Actin Cytoskeleton in Supraoptic Oxytocin Neurons and Astrocytes: Role in Burst Firing

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Changes in the expression of neurohypophyseal prolactins during the estrous cycle and after estrogen treatment

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