Key role of calcium signaling in synaptic transmission

Kostyuk, P. G.

doi:10.1007/s11062-007-0034-5

Cited by 8 publications

(7 citation statements)

References 11 publications

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“…Several neurochemical mechanisms may account for the function of P2X4Rs in brain and behavioral functions, as well as its potential implication in neurodevelopmental and autism-related alterations. P2X4Rs have substantial calcium permeability (Egan and Khakh, 2004;North, 2002;Soto et al, 1996); thus, the lack of P2X4Rs is likely to result to alterations of calcium homeostasis, which may in turn lead to alterations in synaptic transmission and higher vulnerability to abnormalities of neural plasticity (Kostyuk, 2007). P2X4Rs have been shown to exert complex modulatory effects on the function and/or composition of other receptors, including NMDA (Baxter et al, 2011) and AMPA (Andries et al, 2007) receptors.…”

Section: Discussionmentioning

confidence: 99%

Sociocommunicative and Sensorimotor Impairments in Male P2X4-Deficient Mice

Wyatt

Godar

Khoja

et al. 2013

Neuropsychopharmacol

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Purinergic P2X receptors are a family of ligand-gated ion channels gated by extracellular adenosine 5'-triphosphate (ATP). Of the seven P2X subtypes, P2X4 receptors (P2X4Rs) are richly expressed in the brain, yet their role in behavioral organization remains poorly understood. In this study, we examined the behavioral responses of P2X4R heterozygous (HZ) and knockout (KO) mice in a variety of testing paradigms designed to assess complementary aspects of sensory functions, emotional reactivity, and cognitive organization. P2X4R deficiency did not induce significant alterations of locomotor activity and anxiety-related indices in the novel open field and elevated plus-maze tests. Conversely, P2X4R KO mice displayed marked deficits in acoustic startle reflex amplitude, as well as significant sensorimotor gating impairments, as assessed by the prepulse inhibition of the startle. In addition, P2X4R KO mice displayed enhanced tactile sensitivity, as signified by a lower latency in the sticky-tape removal test. Moreover, both P2X4R HZ and KO mice showed significant reductions in social interaction and maternal separation-induced ultrasonic vocalizations in pups. Notably, brain regions of P2X4R KO mice exhibited significant brain-regional alterations in the subunit composition of glutamate ionotropic receptors. These results collectively document that P2X4-deficient mice exhibit a spectrum of phenotypic abnormalities partially akin to those observed in other murine models of autism-spectrum disorder. In conclusion, our findings highlight a putative role of P2X4Rs in the regulation of perceptual and sociocommunicative functions and point to these receptors as putative targets for disturbances associated with neurodevelopmental disorders.

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Section: Discussionmentioning

confidence: 99%

Sociocommunicative and Sensorimotor Impairments in Male P2X4-Deficient Mice

Wyatt

Godar

Khoja

et al. 2013

Neuropsychopharmacol

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“…Analogous currents were observed in acutely isolated neurons of the spinal dorsal horn. It was demonstrated that not only Ca 2+ ions but also other ions can pass through the corresponding channels, and this induces the pain syndrome [25,26]. As was noted, application of capsaicin to differentiated afferent units causes modulation of voltage-dependent calcium currents just in small-sized DRG neurons [21].…”

Section: Role Of Transmembrane Calcium Currents In Transmission Of Nomentioning

confidence: 89%

“…To elucidate the direct role of Ca 2+ in intracellular processes related to generation of nociceptive signals and their transmission within the CNS, a number of studies of transmembrane calcium currents in primary afferent and central relay neurons of the nociceptive system were carried out [25].…”

Section: Role Of Transmembrane Calcium Currents In Transmission Of Nomentioning

confidence: 99%

Peculiarities of Ion Channels and Modulation of Their Functions in Neurons Belonging to the Nociceptive System

Kostyuk

2009

Neurophysiology

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This review deals with the questions related to the composition of ion channels in the membranes of neurons belonging to the nociceptive system; special attention is focused on channels belonging to the TRP family. The factors (in particular, genetically determined) influencing the activity of these channels are discussed. The roles of certain enzymes (protein kinases, phospholipases, etc.) in modulation of the functioning of channel structures typical of nociceptive neurons are reviewed. The roles of calcium transmembrane currents and the state of cellular calcium-controlling compartments in transmission of nociceptive signals are also discussed. Special attention is paid to long-lasting modulatory changes in the activity of different ion channels responsible for the development of stable shifts of sensitive abilities of the nociceptive system (hyperalgesia, hypoalgesia, and allodynia) typical of certain neurological disorders.From a general biological aspect, processes responsible for reception of pain influences and central processing of the corresponding information are the most important components of functioning of the sensory systems in vertebrates (including humans) and some other animal groups. Pain perception allows the organism to avoid the action of stimuli dangerous for normal vital functions and to keep the organism's integrity. Dysfunctions of the nociceptive system can result in disastrous consequences for the organism. Such disorders appear and develop in numerous diseases and accompany these diseases; at the same time, such disorders can play the role of crucial independent pathogenetic factors in the development of one pathology or another.The system of nociception is a part of the total somatosensory system. Similarly to other subdivisions of the somatosensory system, primary afferent neurons and central relay neurons that transmit nociceptive information to the higher CNS "floors" are its input elements. Nociceptors per se, primary sensory structures of certain groups of segmental afferent neurons and afferent neurons of some nuclei of the craniocerebral nerves, constitute primary links in the nociceptive system. Nociceptors differ from other receptor structures of the somatosensory system in their relatively high thresholds for excitation; the generator potential and initiation of impulse activity in these nociceptors are developed only upon the action of stimuli (mechanical, thermal, and chemical) that possess rather high energy and endanger the integrity of the organism and its tissues. This explains, in general, the low modal specificity of nociceptors. Classification of such receptor structures by their modality (mechanonociceptors, thermonociceptors, etc.) is an independent aspect; in our review, we will deal with this aspect only to a limited extent.

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“…ITSN1 is an important player in synaptic vesicle cycling [6]. It is widely accepted that the majority of molecular events associated with the synaptic vesicle trafficking are triggered by changes in Ca 2+ concentration and subsequent activation of the Ca 2+ -dependent proteins, particularly kinases and phosphatases [7]. In this work we tested the hypothesis that ITSN1 may undergo the Ca 2+ /calmodulin-dependent phosphorylation.…”

mentioning

confidence: 97%

Ca/calmodulin-dependent phosphorylation of endocytic scaffold ITSN1

et al. 2014

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ITSN1 is an endocytic scaffold protein with a prominent function in synaptic transmission. It is known that Ca 2+ signaling is crucial for the regulation of synaptic proteins functioning. Aim. Checking the possibility of Ca 2+ /calmodulin-dependent phosphorylation of ITSN1. Methods. Affinity chromatography, in vitro kinase reaction, Western blotting, gel staining with fluorescent stains. Results. We show that the fraction of calmodulin-binding proteins is able to phosphorylate the recombinant fragments encoding the coiled-coil region and the SH3 domain-containing region of ITSN1 in the presence of Ca 2+ ions and calmodulin. Conclusions. The coiledcoil region and the SH3 domain-containing region of ITSN1 undergo Ca 2+ /calmodulin-dependent phosphorylation in vitro, suggesting a possible regulation of ITSN1 by Ca signaling.

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Key role of calcium signaling in synaptic transmission

Cited by 8 publications

References 11 publications

Sociocommunicative and Sensorimotor Impairments in Male P2X4-Deficient Mice

Sociocommunicative and Sensorimotor Impairments in Male P2X4-Deficient Mice

Peculiarities of Ion Channels and Modulation of Their Functions in Neurons Belonging to the Nociceptive System

Ca/calmodulin-dependent phosphorylation of endocytic scaffold ITSN1

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