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

Wang, Yufeng; Hatton, Glenn I.

doi:10.1523/jneurosci.4119-07.2007

Cited by 48 publications

(89 citation statements)

References 47 publications

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“…In previous work, we found that suckling changed astrocytic morphology (Wang and Hatton, 2007b), which is usually associated with GFAP plastic changes (Weinstein et al, 1991). Thus, we further observed effects of intracerebroventricular application of L-AAA and fluorocitrate on GFAP expression in the SON.…”

Section: Rapid Changes In Gfap Plasticity During Sucklingsupporting

confidence: 73%

“…In observing effects of suckling on GFAP expression, immunocytochemistry was performed as described previously (Hatton et al, 1987;Wang and Hatton, 2007b) with minor modification. In brief, hypothalamic slices containing the SON were permeated with 0.3% Triton X-100 for 30 min, and nonspecific binding sites to antibodies were blocked by incubation of the sections in 0.3% gelatin for 30 min.…”

Section: Methodsmentioning

confidence: 99%

“…OT is a critical mediator of suckling-evoked MER (Wakerley et al, 1994) and can cause acute retraction of astrocytic processes (Wang and Hatton, 2007b). Thus, it is likely that OT also mediates suckling-elicited GFAP reduction.…”

Section: Suckling-reduced Gfap By Direct Action Of Ot On Astrocytesmentioning

confidence: 99%

“…In spinal cord white matter, the overlap between AQP4 and GFAP is almost complete (Vitellaro-Zuccarello et al, 2005), suggesting that AQP4 is a binding partner of GFAP. Actin is a dynamic astrocytic cytoskeletal element (Wang and Hatton, 2007b). Astrocytic process elongation and branching are related to redistribution of both GFAP and actin filaments (Boran and Garcia, 2007).…”

Section: Suckling-evoked Gfap Reexpansion By Transiently Increasing Ementioning

confidence: 99%

“…However, this experiment presents neither GFAP involvement nor acute effects of astrocytic plasticity in the modulation of OT neuronal activity. Recently, we have determined that brief suckling can also cause apposition of magnocellular neurons in the supraoptic nucleus (SON), likely resulting from retraction of astrocytic processes (Wang and Hatton, 2007b). It remains unknown whether or not this type of acute astrocytic plasticity has a causal relationship with OT neuronal activity.…”

Section: Introductionmentioning

confidence: 99%

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Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Wang¹,

Hatton²

2009

J. Neurosci.

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123

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Astroglial-neuronal interactions are important in brain functions. However, roles of glial fibrillary acidic protein (GFAP) in this interaction remain unclear in acute physiological processes. We explored this issue using the supraoptic nucleus (SON) in lactating rats. At first, we identified the essential role of astrocytes in the milk-ejection reflex (MER) by disabling astrocytic functions via intracerebroventricular application of L-aminoadipic acid (L-AAA). L-AAA blocked the MER and reduced GFAP levels in the SON. In brain slices, L-AAA suppressed oxytocin (OT) neuronal activity and EPSCs. Suckling reduced GFAP in immunocytochemical images and in Western blots, reductions that were partially reversed after the MER. OT, the dominant hormone mediating the MER, reduced GFAP expression in brain slices. Tetanus toxin suppressed EPSCs but did not influence OT-reduced GFAP. Protease inhibitors did not influence OT-reduced GFAP images but blocked the degradation of GFAP molecules. In the presence of OT, transient 12 mM K ϩ exposure, simulating effects of synchronized bursts before the MER, reversed OT-reduced GFAP expression. Consistently, suckling first reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K ϩ channels. Moreover, GFAP molecules were associated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine racemase. GFAP-aquaporin 4 association decreased during initial suckling and increased after the MER, whereas opposite changes occurred between GFAP and actin. MER also decreased the association between GFAP and glutamine synthetase. These results indicate that suckling elicits dynamic glial neuronal interactions in the SON; GFAP plasticity dynamically reflects OT neuronal activity.

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Section: Rapid Changes In Gfap Plasticity During Sucklingsupporting

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Section: Suckling-reduced Gfap By Direct Action Of Ot On Astrocytesmentioning

confidence: 99%

Section: Suckling-evoked Gfap Reexpansion By Transiently Increasing Ementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Wang¹,

Hatton²

2009

J. Neurosci.

Self Cite

123

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EphA7 regulates spiral ganglion innervation of cochlear hair cells

Kim

Ibrahim

Wang

et al. 2015

Developmental Neurobiology

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During the development of periphery auditory circuitry, spiral ganglion neurons (SGNs) form a spatially precise pattern of innervation of cochlear hair cells (HCs), which is an essential structural foundation for central auditory processing. However, molecular mechanisms underlying the developmental formation of this precise innervation pattern remain not well understood. Here, we specifically examined the involvement of Eph family members in cochlear development. By performing RNA-sequencing for different types of cochlear cell, in situ hybridization and immunohistochemistry, we found that EphA7 was strongly expressed in a large subset of SGNs. In EphA7 deletion mice, there was a reduction in the number of inner radial bundles originating from SGNs and projecting to HCs as well as in the number of ribbon synapses on inner hair cells (IHCs), as compared with wild-type or heterozygous mutant mice, attributable to fewer type I afferent fibers. The overall activity of the auditory nerve in EphA7 deletion mice was also reduced, although there was no significant change in the hearing intensity threshold. In vitro analysis further suggested that the reduced innervation of HCs by SGNs could be attributed to a role of EphA7 in regulating outgrowth of SGN neurites, as knocking down EphA7 in SGNs resulted in diminished SGN fibers. In addition, suppressing the activity of ERK1/2, a potential downstream target of EphA7 signaling, either with specific inhibitors in cultured explants or by knocking out Prkg1, also resulted in reduced SGN fibers. Together, our results suggest that EphA7 plays an important role in the developmental formation of cochlear innervation pattern through controlling SGN fiber ontogeny. Such regulation may contribute to the salience level of auditory signals presented to the central auditory system.

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Contribution of sodium channels to lamellipodial protrusion and Rac1 and ERK1/2 activation in ATP‐stimulated microglia

Persson

Estacion

Ahn

et al. 2014

Glia

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Microglia are motile resident immune cells of the central nervous system (CNS) that continuously explore their territories for threats to tissue homeostasis. Following CNS insult (e.g., cellular injury, infection, or ischemia), microglia respond to signals such as ATP, transform into an activated state, and migrate towards the threat. Directed migration is a complex and highly-coordinated process involving multiple intersecting cellular pathways, including signal transduction, membrane adhesion and retraction, cellular polarization, and rearrangement of cytoskeletal elements. We previously demonstrated that the activity of sodium channels contributes to ATP-induced migration of microglia. Here we show that TTX-sensitive sodium channels, specifically NaV 1.6, participate in an initial event in the migratory process, i.e., the formation in ATP-stimulated microglia of polymerized actin-rich membrane protrusions, lamellipodia, containing accumulations of Rac1 and phosphorylated ERK1/2. We also examined Ca(2+) transients in microglia and found that blockade of sodium channels with TTX produced a downward shift in the level of [Ca(2+) ]i during the delayed, slower recovery of [Ca(2+) ]i following ATP stimulation. These observations demonstrate a modulatory role of sodium channels on Ca(2+) transients in microglia that are likely to affect down-stream signaling cascades. Consistent with these observations, we demonstrate that ATP-induced microglial migration is mediated via Rac1 and ERK1/2, but not p38α/β and JNK, dependent pathways, and that activation of both Rac1 and ERK1/2 is modulated by sodium channel activity. Our results provide evidence for a direct link between sodium channel activity and modulation of Rac1 and ERK1/2 activation in ATP-stimulated microglia, possibly by regulating Ca(2+) transients.

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

Cited by 48 publications

References 47 publications

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

EphA7 regulates spiral ganglion innervation of cochlear hair cells

Contribution of sodium channels to lamellipodial protrusion and Rac1 and ERK1/2 activation in ATP‐stimulated microglia

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