Effects of Body Temperature on Neural Activity in the Hippocampus: Regulation of Resting Membrane Potentials by Transient Receptor Potential Vanilloid 4

Shibasaki, Kazuo; Suzuki, Makoto; Mizuno, Atsuko; Tominaga, Makoto

doi:10.1523/jneurosci.4284-06.2007

Cited by 266 publications

(214 citation statements)

References 45 publications

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“…Indeed, it has been previously reported [10] that 4α-PDD (a TRPV4 agonist) activates currents in hippocampal neurons in primary cultures. Therefore, we compared the effects of this agonist between primary hippocampal cultures and slices.…”

Section: Resultsmentioning

confidence: 99%

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Cellular Mechanisms of Desynchronizing Effects of Hypothermia in an In Vitro Epilepsy Model

et al. 2012

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Hypothermia can terminate epileptiform discharges in vitro and in vivo epilepsy models. Hypothermia is becoming a standard treatment for brain injury in infants with perinatal hypoxic ischemic encephalopathy, and it is gaining ground as a potential treatment in patients with drug resistant epilepsy. However, the exact mechanism of action of cooling the brain tissue is unclear. We have studied the 4-aminopyridine model of epilepsy in mice using single-and dual-patch clamp and perforated multielectrode array recordings from the hippocampus and cortex. Cooling consistently terminated 4-aminopyridine induced epileptiform-like discharges in hippocampal neurons and increased input resistance that was not mimicked by transient receptor potential channel antagonists. Dual-patch clamp recordings showed significant synchrony between distant CA1 and CA3 pyramidal neurons, but less so between the pyramidal neurons and interneurons. In CA1 and CA3 neurons, hypothermia blocked rhythmic action potential discharges and disrupted their synchrony; however, in interneurons, hypothermia blocked rhythmic discharges without abolishing action potentials. In parallel, multi-electrode array recordings showed that synchronized discharges were disrupted by hypothermia, whereas multi-unit activity was unaffected. The differential effect of cooling on transmitting or secreting γ-aminobutyric acid interneurons might disrupt normal network synchrony, aborting the epileptiform discharges. Moreover, the persistence of action potential firing in interneurons would have additional antiepileptic effects through tonic γ-aminobutyric acid release.

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Section: Resultsmentioning

confidence: 99%

“…In addition, presence of temperature sensitive ion channels in the neurons may mediate the effects of cooling. In hippocampal cultures, the presence of transient receptor potential channel V (TRPV)-4 that is activated at temperatures within the physiological range (>27°-34°C) has been reported [10].…”

Section: Introductionmentioning

confidence: 99%

Cellular Mechanisms of Desynchronizing Effects of Hypothermia in an In Vitro Epilepsy Model

et al. 2012

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“…The specificity of two anti-TRPV4 antibodies is described elsewhere (32,33). ␤-Catenin and mouse TRPV4 cDNA were generously provided by Dr. M. Takeichi and Dr. M. Caterina, respectively.…”

Section: Methodsmentioning

confidence: 99%

The TRPV4 Channel Contributes to Intercellular Junction Formation in Keratinocytes

Sokabe

Fukumi-Tominaga

Yonemura³

et al. 2010

Journal of Biological Chemistry

168

151

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Transient receptor potential vanilloid 4 (TRPV4) channel is a physiological sensor for hypo-osmolarity, mechanical deformation, and warm temperature. The channel activation leads to various cellular effects involving Ca 2؉ dynamics. We found that TRPV4 interacts with ␤-catenin, a crucial component linking adherens junctions and the actin cytoskeleton, thereby enhancing cell-cell junction development and formation of the tight barrier between skin keratinocytes. TRPV4-deficient mice displayed impairment of the intercellular junction-dependent barrier function in the skin. In TRPV4-deficient keratinocytes, extracellular Ca 2؉ -induced actin rearrangement and stratification were delayed following significant reduction in cytosolic Ca 2؉ increase and small GTPase Rho activation. TRPV4 protein located where the cell-cell junctions are formed, and the channel deficiency caused abnormal cell-cell junction structures, resulting in higher intercellular permeability in vitro. Our results suggest a novel role for TRPV4 in the development and maturation of cell-cell junctions in epithelia of the skin. Transient receptor potential vanilloid 4 (TRPV4),3 a member of the TRP superfamily of cation channels, is a Ca 2ϩ -permeable channel expressed in both neuronal and non-neuronal cells. Channel activation allows cation influx into cells, leading to various Ca 2ϩ -dependent processes (1, 2). TRPV4 can be activated by a variety of chemical and physical stimuli such as synthetic phorbol ester 4␣-phorbol 12,13-didecanoate (4␣-PDD) (3), a botanical agent (bisandrographolide A) (4), anandamide metabolites including arachidonic acid and epoxyeicosatrienoic acids (5), hypo-osmotic stimulation (6, 7), shear stress (8), mechanical stretch (9), and moderate warmth (27-35°C) (7, 10). Therefore, the TRPV4 channel functions as a multimodal transducer in various tissues and cells.Keratinocytes in the skin epidermis express TRPV4 (10, 11), and it has been proposed that the channel is involved in the detection of warm temperature (12). Skin keratinocytes express another warm temperature-sensitive TRP channel, TRPV3 (activated by temperature above 32°C), which is also implicated in temperature sensation in mice (13). Because both TRPV3 and TRPV4 are expressed in keratinocytes and are activated by a similar range of temperatures, these channels likely have distinct functions in the skin. Consistent with this idea, a recent report provided evidence that TRPV3, rather than TRPV4, mainly participates in transmission of warm temperature information from keratinocytes to adjacent nerve endings through ATP release (14). It has also been reported that mutation of TRPV3 is linked to defective hair growth and dermatitis in rodents (15, 16), although the involvement of TRPV4 has not been confirmed.The skin constitutes an interface between the external environment and the body, serving as a hydrophobic barrier essential for protection against infection from the outside and dehydration from the inside. The skin barrier function is achieved by keratinocytes in...

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“…This endocannabinoid-induced plasticity could also be triggered by other TRP channels. Indeed Wanabe et al (2003) showed that anandamine could activate TRPV4 via epoxyeicosatrienoic acid and TRPV4 is known to be expressed in hippocampus (Shibasaki et al, 2007). Another possibility is that TRPV1 triggers LTD via a nonconducting function (Kaczmarek, 2006) or via a capsaicin-resistant TRPV1.…”

Section: Review Of Cavanaugh Et Almentioning

confidence: 99%

The Expression Pattern of TRPV1 in Brain

Menigoz¹,

Boudes²

2011

J. Neurosci.

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Effects of Body Temperature on Neural Activity in the Hippocampus: Regulation of Resting Membrane Potentials by Transient Receptor Potential Vanilloid 4

Cited by 266 publications

References 45 publications

Cellular Mechanisms of Desynchronizing Effects of Hypothermia in an In Vitro Epilepsy Model

Cellular Mechanisms of Desynchronizing Effects of Hypothermia in an In Vitro Epilepsy Model

The TRPV4 Channel Contributes to Intercellular Junction Formation in Keratinocytes

The Expression Pattern of TRPV1 in Brain

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