Voltage‐dependent calcium channels of dog basilar artery

Nikitina, Elena; Zhang, Zhen Du; Kawashima, Ayako; Jahromi, Babak S.; Bouryi, V. A.; Takahashi, Masato; Xie, An; Macdonald, R. Loch

doi:10.1113/jphysiol.2006.126128

Cited by 48 publications

(62 citation statements)

References 66 publications

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“…For Ca v 2.3 (R-type) Ca 2+ channels it is established that their expression and current density is increased in rabbit cerebral artery myocytes [43,44]. Similar results were found for two out of three T-type (transiently and low voltage-activated Ca 2+ channels), named Ca v 3.1 and Ca v 3.3 [42]. The retina as an organotypical neuronal network expresses several voltage-gated calcium channels (Ca v 1.2, Ca v 1.3, and Ca v 1.4), and R-type calcium channel Ca v 2.3.…”

Section: Voltage-gated Ion Channels Of the Retina May Be Involved In Sahsupporting

confidence: 69%

“…Much is known about the beneficial effects of dihydropyridine L-type calcium (Ca 2+ ) channel antagonists that are routinely recommended in clinical practice for the prevention and treatment of DCI [34]. When applied in a rather high local concentration, side effects on additional voltage-gated Ca 2+ channels may be assumed, which are rather up-than downregulated in experimentally induced SAH in dogs [42]. For Ca v 2.3 (R-type) Ca 2+ channels it is established that their expression and current density is increased in rabbit cerebral artery myocytes [43,44].…”

mentioning

confidence: 99%

“…The retina as an organotypical neuronal network expresses several voltage-gated calcium channels (Ca v 1.2, Ca v 1.3, and Ca v 1.4), and R-type calcium channel Ca v 2.3. The retina also contains T-type calcium channels, which were also considered to be involved in the mechanism of experimentally induced aSAH, too [42,45]. …”

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confidence: 99%

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Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Albanna¹,

Lüke²,

Alpdogan³

et al. 2018

New Front Ophthalmol

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Purpose: The isolated and superfused retina from vertebrates is routinely used for neurophysiological measurements of basic retinal signal generation and transduction. Such an ex vivo isolated neural network moreover represents a useful model system for the investigation of drugs and toxins and may also be helpful to elucidate molecular mechanisms of CNS diseases. The present overview aims to bring observations to the reader's attention, which, in part, have been made more than 50 years ago and were sparsely followed up upon in subsequent research, but may support the idea that the isolated bovine retina represents a useful system to investigate the physiology and pathophysiology of energy supply to neuronal tissue. Material and methods:Parallel recording of ERGs and pyridine nucleotide oxidation in the isolated and superfused vertebrate retina. The review will focus on topics, which discuss the connection between retinal electrophysiology and underlying energy metabolism.Results: Previous and present reports about (i) transretinal signaling cascades, (ii) the involvement of the pharmacoresistant Cav2.3 / R-type calcium channel in transretinal signaling and (iii) data about the retinal oxygen demands and concentration in different layers are collected, which elucidate that the retina may be used as a cerebral surrogate model in different research areas. Retinal tolerance to ischemia is several times larger than the tolerance in the remaining brain. Conclusions:The retinal energy supply through retinal vessels is regulated and controlled by neurovascular coupling. Classical retinal recording techniques and special retinal abilities in electrical-vascular coupling will be set in perspective with novel recording techniques, currently brought into clinical application for the detection of impaired neurovascular coupling after aneurysmal subarachnoid hemorrhage in the brain. The present review elucidates that important pathophysiological aspects related to the upregulation of pharmacoresistant Cav2.3 / R-type calcium channels during SAH may be investigated in the isolated vertebrate retina. Ischemic tolerance in the vertebrate retinaThe oxygen consumption of the vertebrate retina on a per gram basis has been described as higher than that of the brain [1,2]. Oxygen cannot be "stored" in tissue so that a constant and adequate supply must be guaranteed to preserve function. Metabolic dysfunction regarding to impaired vascular supply is directly reflected by retinal oxygen saturation which can be detected noninvasively by dual wavelength fundus photography [3]. Normally, the oxygen saturation in retinal vessels differs along vascular segments and is higher in the macular region than retinal periphery [4]. Many retinal diseases are caused by a dysfunction of the vascular network. Interestingly, the venous oxygen saturation in diabetic retinopathy was higher in venules draining the macular surroundings than retinal periphery that reflect specific metabolic conditions [5,6].Since a relatively unobstructed light path...

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Section: Voltage-gated Ion Channels Of the Retina May Be Involved In Sahsupporting

confidence: 69%

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confidence: 99%

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Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Albanna¹,

Lüke²,

Alpdogan³

et al. 2018

New Front Ophthalmol

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“…The former mimics physiological conditions while the latter was designed to accentuate charge flow through open channels (Perez-Reyes, 2003;Nikitina et al, 2007;Li et al, 2010;Harraz and Welsh, 2013). Stepping from 290 mV to voltages ranging from 250 to +40 mV (10 mV intervals, 300 ms each), we observed a voltage-dependent change in whole-cell current density.…”

Section: Resultsmentioning

confidence: 91%

Protein kinase a regulation of T-type Ca2+ channels in rat cerebral arterial smooth muscle

Harraz

Welsh

2013

Journal of Cell Science

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Summary Recent investigations have identified that T-type Ca2+ channels (Ca V 3.x) are expressed in rat cerebral arterial smooth muscle. In the study reported here, we isolated the T-type conductance, differentiated the current into the Ca V 3.1/Ca V 3.2 subtypes and determined whether they are subject to protein kinase regulation. Using patch clamp electrophysiology, whole-cell Ba 2+ current was monitored and initially subdivided into nifedipine-sensitive and -insensitive components. The latter conductance was abolished by T-type Ca 2+ channel blockers and was faster with leftward shifted activation/inactivation properties, reminiscent of a T-type channel. Approximately 60% of this T-type conductance was blocked by 50 mM Ni 2+ , a concentration that selectively interferes with Ca V 3.2 channels. Subsequent work revealed that the whole-cell T-type conductance was subject to protein kinase A (PKA) modulation. Specifically, positive PKA modulators (db-cAMP, forskolin, isoproterenol) suppressed T-type currents and evoked a hyperpolarized shift in steady-state inactivation. Blocking PKA (with KT5720) masked this suppression without altering the basal T-type conductance. A similar effect was observed with stHt31, a peptide inhibitor of A-kinase anchoring proteins. A final set of experiments revealed that PKA-induced suppression targeted the Ca V 3.2 subtype. In summary, this study revealed that a T-type Ca 2+ channel conductance can be isolated in arterial smooth muscle, and differentiated into Ca V 3.1 and Ca V 3.2 components. It also showed that vasodilatory signaling cascades inhibit this conductance by targeting Ca V 3.2. Such targeting would impact Ca 2+ dynamics and consequent tone regulation in the cerebral circulation.

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“…Total RNA and protein were extracted with TRIzol (Gibco BRL, Life Technologies, Rockville, MD, USA) from individual basilar arteries denuded of endothelium as we described before (Aihara et al, 2004;Nikitina et al, 2007;Xie et al, 2007). RNase-free DNase (Promega, Madison, WI, USA) was used to eliminate contamination with genomic DNA.…”

Section: Quantitative Real-time Mrna Analysis and Western Blottingmentioning

confidence: 99%

Voltage-Gated K⁺ Channel Dysfunction in Myocytes from a Dog Model of Subarachnoid Hemorrhage

Jahromi

Aihara

et al. 2007

J Cereb Blood Flow Metab

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Delayed cerebral vasospasm after subarachnoid hemorrhage is primarily due to sustained contraction of arterial smooth muscle cells. Its pathogenesis remains unclear. The degree of arterial constriction is regulated by membrane potential that in turn is determined predominately by K+ conductance (GK). Here, we identified the main voltage-gated K+ (Kv) channels contributing to outward delayed rectifier currents in dog basilar artery smooth muscle as Kv2 class through a combination of electrophysiological and pharmacological methods. Kv2 current density was nearly halved in vasospastic myocytes after subarachnoid hemorrhage (SAH) in dogs, and Kv2.1 and Kv2.2 were downregulated in vasospastic myocytes when examined by quantitative mRNA, Western blotting, and immunohistochemistry. Vasospastic myocytes were depolarized and had a smaller contribution of GK toward maintenance of their membrane potential. Pharmacological block of Kv current in control myocytes mimicked the depolarization observed in vasospastic arteries. The degree of membrane depolarization was found to be compatible with the amount of vasoconstriction observed after SAH. We conclude that Kv2 dysfunction after SAH contributes to the pathogenesis of delayed cerebral vasospasm. This may confer a novel target for treatment of delayed cerebral vasospasm.

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Voltage‐dependent calcium channels of dog basilar artery

Cited by 48 publications

References 66 publications

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Protein kinase a regulation of T-type Ca2+ channels in rat cerebral arterial smooth muscle

Voltage-Gated K⁺ Channel Dysfunction in Myocytes from a Dog Model of Subarachnoid Hemorrhage

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Voltage‐dependent calcium channels of dog basilar artery

Cited by 48 publications

References 66 publications

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Protein kinase a regulation of T-type Ca2+ channels in rat cerebral arterial smooth muscle

Voltage-Gated K+ Channel Dysfunction in Myocytes from a Dog Model of Subarachnoid Hemorrhage

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Voltage-Gated K⁺ Channel Dysfunction in Myocytes from a Dog Model of Subarachnoid Hemorrhage