Regulation and Mechanism of L-Type Calcium Channel Activation via V1a Vasopressin Receptor Activation in Cultured Cortical Neurons

Son, Michael C.; Brinton, Roberta Dı́az

doi:10.1006/nlme.2001.4020

Cited by 17 publications

(7 citation statements)

References 46 publications

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“…Additionally, U73122 significantly inhibited both AVP-induced inward current and the increase in [Ca 2ϩ ] i . An involvement of PLC␤ downstream of V1aR is also found in cultured cortical neurons (Son and Brinton, 2001). These results suggest that the calcium influx from the extracellular solution is the main source of the CCK-8S-induced response, whereas both calcium influx and calcium release from intracellular calcium stores are involved in the AVP-induced response.…”

Section: Discussionmentioning

confidence: 92%

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Tsunematsu¹,

Fu²,

Yamanaka³

et al. 2008

J. Neurosci.

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Water homeostasis is a critical challenge to survival for land mammals. Mice display increased locomotor activity when dehydrated, a behavior that improves the likelihood of locating new sources of water and simultaneously places additional demands on compromised hydration levels. The neurophysiology underlying this well known behavior has not been previously elucidated. We report that the anti-diuretic hormone arginine-vasopressin (AVP) is involved in this response. AVP and oxytocin directly induced depolarization and an inward current in orexin/hypocretin neurons. AVP-induced activation of orexin neurons was inhibited by a V1a receptor (V1aR)-selective antagonist and was not observed in V1aR knock-out mice, suggesting an involvement of V1aR. Subsequently activation of phospholipase C␤ triggers an increase in intracellular calcium by both calcium influx through nonselective cation channels and calcium release from calcium stores in orexin neurons. Intracerebroventricular injection of AVP or water deprivation increased locomotor activity in wild-type mice, but not in transgenic mice lacking orexin neurons. V1aR knock-out mice were less active than wild-type mice. These results suggest that the activation of orexin neurons by AVP or oxytocin has an important role in the regulation of spontaneous locomotor activity in mice. This system appears to play a key role in water deprivation-induced hyperlocomotor activity, a response to dehydration that increases the chance of locating water in nature.

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Section: Discussionmentioning

confidence: 92%

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Tsunematsu¹,

Fu²,

Yamanaka³

et al. 2008

J. Neurosci.

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“…On the other hand, released AVP can bind to V1aRs expressed on CRH neurons. V1aRs are also coupled to stimulatory G-proteins (59, 60) and their activation enhances AC activity and increases cAMP and intracellular 2+ Ca (61, 62) within CRH neurons projecting to the LS where CRH is released and acts on CRHR2s (63, 64) to escalate aggression (65, 66). Thus, AH-AVP microinfusion can increase CRH levels and may reduce 5-HT inputs to the AH by stimulating GABA-ergic projections synapsing onto 5-HT neurons in the DR-AH pathway.…”

Section: Discussionmentioning

confidence: 99%

Neurochemical Mediation of Affiliation and Aggression Associated With Pair-Bonding

Gobrogge

Jia

Liu

et al. 2017

Biological Psychiatry

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Background The neuropeptides vasopressin (AVP) and corticotrophin-releasing hormone (CRH) facilitate while serotonin (5-HT) inhibits aggression. How the brain is wired to coordinate interactions between these functionally opposed neurotransmitters to control behavioral states is poorly understood. Methods Pair-bonded male prairie voles (Microtus ochrogaster) were infused with a retrograde tracer, fluorogold, and tested for affiliation and aggression toward a female partner or novel female. Subsequent immunocytochemical experiments examined neuronal activation using FOS and neuro-chemical/-receptor profiles on brain areas involved in the behaviors. Finally, a series of behavioral pharmacological and real-time in-vivo brain microdialysis experiments were performed on male prairie voles displaying affiliation or aggression. Results We localized a subpopulation of excitatory AVP neurons in the anterior hypothalamic nucleus (AH) that may gate CRH output from the amygdala to the AH and then the lateral septum to modulate aggression associated with mate guarding. Conversely, we identified a subset of inhibitory 5-HT-ergic projection neurons in the dorsal raphe nucleus to the AH that mediates the spatio-temporal release of neuropeptides and their interactions in modulating aggression and affiliation. Conclusions Together, this study establishes the medial extended amygdala as a major neural substrate regulating the switch between positive and negative affective states wherein several neurochemicals converge and interact to coordinate divergent social behaviors.

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“…The binding of calcium ions to CaM leads to conformational changes and activation of CaM; activated CaM regulates calcium transport and facilitates L‐type calcium channels . While inhibiting calcium influx, nifedipine inhibits CaM‐mediated signal transduction and L‐type calcium channel facilitation . The inhibition ultimately led to the inhibition of excess cellular calcium.…”

Section: Discussionmentioning

confidence: 99%

Early administration of nifedipine protects against angiotensin II‐induced cardiomyocyte hypertrophy through regulating CaMKII–SERCA2a pathway and apoptosis in rat cardiomyocytes

Luo

Zhang

2016

Cell Biochemistry & Function

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The calcium channel blocker (CCB), nifedipine, is a more effective treatment for early- than late-stage cardiac hypertrophy. We investigated the effects of early- and late-stage nifedipine administration on calcium homeostasis, CaMKII (Ca(2+) /calmodulin-dependent protein kinase II) activity and apoptosis of cardiomyocytes under hypertrophic stimulation with angiotensin II (AngII). Primary rat cardiomyocytes were divided into five treatment groups: AK, AngII plus the CaMKII inhibitor, KN-93; AN-1 (early-stage), AngII plus nifedipine × 48 h; AN-2 (late-stage), AngII × 48 h, then AngII plus nifedipine × 48 h; C, untreated; and A, AngII × 48 h. The t1/2β [time required for intracellular Ca(2+) concentration ([Ca(2+) ]i) to decline to one half of the peak value] decreased; however, CaMKII and SERCA2a (sarcoplasmic reticulum Ca(2+) -ATPase 2a) activities increased in the AN-1 group compared with the AK group. In the AN-2 group compared with the AN-1 group, CaMKII activity, t1/2α [time required for [Ca(2+) ]i to increase from the bottom to one half of peak value], t1/2β, and apoptosis increased. These results indicate that the timing of CCB administration affects the calcium concentration and apoptosis of hypertrophic cardiomyocytes through the CaMKII-SERCA2a signalling pathway, thereby influencing the drug's protective activity against cardiomyocyte hypertrophy.

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Regulation and Mechanism of L-Type Calcium Channel Activation via V1a Vasopressin Receptor Activation in Cultured Cortical Neurons

Cited by 17 publications

References 46 publications

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Neurochemical Mediation of Affiliation and Aggression Associated With Pair-Bonding

Early administration of nifedipine protects against angiotensin II‐induced cardiomyocyte hypertrophy through regulating CaMKII–SERCA2a pathway and apoptosis in rat cardiomyocytes

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