Hypertonicity Sensing in Organum Vasculosum Lamina Terminalis Neurons: A Mechanical Process Involving<i>TRPV1</i>But Not<i>TRPV4</i>

Ciura, Sorana; Liedtke, Wolfgang; Bourque, Charles W.

doi:10.1523/jneurosci.1420-11.2011

Cited by 115 publications

(112 citation statements)

References 46 publications

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“…These signals influence OVLT to act on the MNCs in either an inhibitory or excitatory fashion, in addition to the OVLT's osmosensing regulation. Similar to MNC osmosensing, the neurons of the OVLT are mechanically regulated, with hypertonic cell shrinkage leading to increased firing [30]. This osmomechanical regulation is mediated via TRPV1 channels which are non selective cation channels.…”

Section: Osmolal Regulationmentioning

confidence: 99%

“…This osmomechanical regulation is mediated via TRPV1 channels which are non selective cation channels. The TRPV channels are mechanically activated due to cell shrinkage [30]. Other influences on ADH secretion include sleep cycle, and thermal regulation.…”

Section: Osmolal Regulationmentioning

confidence: 99%

“…This increase in ADH output is anticipatory of future water losses due to panting, sweating and the like, and occurs before any changes in osmolality occur. This thermally regulated ADH output is also assumed to be mediated via a heat sensitive variant of the TRPV1 channel [30].…”

Section: Osmolal Regulationmentioning

confidence: 99%

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Diabetes Insipidus: A Review

Shapiro¹

2013

J Diabetes Metab

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Section: Osmolal Regulationmentioning

confidence: 99%

Section: Osmolal Regulationmentioning

confidence: 99%

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Diabetes Insipidus: A Review

Shapiro¹

2013

J Diabetes Metab

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“…ANG II acts on angiotensin type I receptors (AT 1 -R), which are present in neurons and which by activating two different intracellular pathways have been proposed to lead to either water or sodium intake (31,(75)(76)(77)86). Hyperosmolarity activates nonselective cation channels (e.g., transient receptor potential vanilloid-related channels) and hypernatremia activates Na x channels (25,26,84,118,119).The NTS contains the first synapse in the central nervous system (CNS) that receives input from systemic visceral receptors. Signals that arise from peripheral high-and lowpressure baroreceptors (23, 30) can inhibit thirst and sodium appetite when blood volume is expanded or blood pressure is high and facilitate thirst and salt intake when pressure and volume are low (79,112,128,129).…”

mentioning

confidence: 99%

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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.-In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review. sodium intake; angiotensin; electrolyte balance; thirst ANIMALS CONSTANTLY LOSE WATER and electrolytes to the external environment, but specific autonomic, hormonal, and behavioral mechanisms operate continuously to adjust and restore body fluid-electrolyte balance. The rate of loss from the kidneys is primarily controlled by neural and hormonal actions, but loss may also occur passively through the largely uncontrolled processes of respiration (evaporation), perspiration, transpiration, and salivation. These later modes of loss are referred to as insensible loss because they cannot be easily measured. Severe loss of both sodium and water may also occur in disorders associated with emesis and diarrhea. However, despite such ongoing challenges, the osmolarity and volume of body fluids are maintained within reasonably narrow limits, thus allowing normal metabolic and cardiovascular functions. Although renal mechanisms can slow water and sodium loss, the restoration of fluid homeostasis is only made possible by the mobilization of behaviors that result in the ingestion of water and sodium (usually NaCl). The behavioral responses of seeking out and consuming water and salty substances involve the motivational states of thirst and salt appetite. Salt appetite is also frequently referred to as sodium appetit...

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“…Subsequent studies have shown that TRPV1 2/2 mice show altered mechanical hypersensitivity in colonic afferents (Jones et al, 2005;De Schepper et al, 2008), bladder afferents (Daly et al, 2007), urothelial cells (Birder et al, 2001;Birder et al, 2002), osmosensory neurons (Ciura et al, 2011) and muscle (Ro et al, 2009). Mechanical activation of TRPV1, through either direct or indirect mechanisms, might be involved in the mechanics of Ca 2+ influx during the migration of epidermal keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Epidermal keratinocyte polarity and motility require Ca2+ influx through TRPV1

Graham

Huang

Robinson

et al. 2013

Journal of Cell Science

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Summary Ca2+ has long been known to play an important role in cellular polarity and guidance. We studied the role of Ca 2+ signaling during random and directed cell migration to better understand whether Ca 2+ directs cell motility from the leading edge and which ion channels are involved in this function by using primary zebrafish keratinocytes. Rapid line-scan and time-lapse imaging of intracellular Ca 2+ (Ca 2+ i ) during migration and automated image alignment enabled us to characterize and map the spatiotemporal changes in Ca 2+ i . We show that asymmetric distributions of lamellipodial Ca 2+ sparks are encoded in frequency, not amplitude, and that they correlate with cellular rotation during migration. Directed migration during galvanotaxis increases the frequency of Ca 2+ sparks over the entire lamellipod; however, these events do not give rise to asymmetric Ca 2+ i signals that correlate with turning. We demonstrate that Ca 2+ -permeable channels within these cells are mechanically activated and include several transient receptor potential family members, including TRPV1. Last, we demonstrate that cell motility and Ca 2+ i activity are affected by pharmacological agents that target TRPV1, indicating a novel role for this channel during cell migration.

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Hypertonicity Sensing in Organum Vasculosum Lamina Terminalis Neurons: A Mechanical Process InvolvingTRPV1But NotTRPV4

Cited by 115 publications

References 46 publications

Diabetes Insipidus: A Review

Diabetes Insipidus: A Review

Role of the lateral parabrachial nucleus in the control of sodium appetite

Epidermal keratinocyte polarity and motility require Ca2+ influx through TRPV1

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