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Potassium Conductances (potassium + conductance)

Distribution by Scientific Domains
Life Sciences57%
Medical Sciences42%

Selected Abstracts

Presynaptic modulation of sensory neurons in the segmental ganglia of arthropods

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 4 2002
Alan Hugh David WatsonArticle first published online: 3 SEP 200
Abstract The afferent terminals of arthropod sensory neurones receive abundant input synapses, usually closely intermingled with the sites of synaptic output. The majority of the input synapses use the neurotransmitter GABA, but in some afferents there is a significant glutamatergic or histaminergic component. GABA and histamine shunt afferent action potentials by increasing chloride conductance. Though glutamate can also have this effect in the arthropod central nervous system, its action on afferent terminals appears to be mediated by increases in potassium conductance or by the action of metabotropic receptors. The action of the presynaptic synapses on the afferents are many and varied. Even on the same afferent, they may have several distinct roles that can involve both tonic and phasic patterns of primary afferent depolarisation. Despite the ubiquity and importance of their effects however, the populations of neurones from which the presynaptic synapses are made, remain largely unidentified. Microsc. Res. Tech. 58:262,271, 2002. © 2002 Wiley-Liss, Inc. [source]

Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic development

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2006
María Pilar de Castro
Abstract Voltage-dependent potassium channels consist of a pore-forming ,-subunit, which is modulated by additional ,-ancillary or regulatory subunits. Kcnq1 and Kcnh2 ,-channel subunits play pivotal roles in the developing and adult heart. However, Kcnq1 and Kcnh2 have a much wider expression profile than strictly confined to the myocardium, similar to their putative regulatory Kcne1-5 ,-subunits. At present, the distribution of distinct potassium channel subunits has been partially mapped in adult tissues, whereas almost no information is available during embryonic development. In this study, we report a detailed analysis of Kcnq1, Kcnh2, and Kcne3 protein expression during mouse embryogenesis. Our results demonstrate that Kcnq1 and Kcnh2 are widely distributed. Coexpression of both ,-subunits is observed in a wide variety of organs, such as heart and the skeletal muscle, whereas others display unique Kcnq1 or Knch2 expression. Interestingly, Kcne3 expression is also widely observed in distinct tissue layers during embryogenesis, supporting the notion that an exquisite balance of ,- and ,-subunit expression is required for modulating potassium conductance in distinct organs and tissue layers. © 2006 Wiley-Liss, Inc. [source]

Regulation of neuronal excitability in Drosophila by constitutively active CaMKII

DEVELOPMENTAL NEUROBIOLOGY, Issue 1 2002
Demian Park
Abstract The ability of calcium/calmodulin-dependent protein kinase II (CaMKII) to become calcium independent after autophosphorylation makes this enzyme a temporal marker of neuronal activity. Here we show that the calcium-independent form of CaMKII has unique effects on larval viability, locomotion, and neuronal excitability in Drosophila. Expression of constitutively active T287D, but not calcium-dependent T287A, mutant CaMKII in Drosophila neurons resulted in decreased viability, behavioral defects, and failure of action potential propagation. The actions of T287D may be mediated, at least in part, by increased potassium conductances. Expression of T287D CaMKII also stimulated an increase in the number of boutons at the larval neuromuscular junction, but did not affect the mechanics of release. This study defines a role for autophosphorylation of CaMKII in the regulation of multiple neuronal functions including the intrinsic properties of neurons. © 2002 Wiley Periodicals, Inc. J Neurobiol 52: 24,42, 2002 [source]

Astrocytes in the hippocampus of patients with temporal lobe epilepsy display changes in potassium conductances

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000
Stefan Hinterkeuser
Abstract Functional properties of astrocytes were investigated with the patch-clamp technique in acute hippocampal brain slices obtained from surgical specimens of patients suffering from pharmaco-resistant temporal lobe epilepsy (TLE). In patients with significant neuronal cell loss, i.e. Ammon's horn sclerosis, the glial current patterns resembled properties characteristic of immature astrocytes in the murine or rat hippocampus. Depolarizing voltage steps activated delayed rectifier and transient K+ currents as well as tetrodotoxin-sensitive Na+ currents in all astrocytes analysed in the sclerotic human tissue. Hyperpolarizing voltages elicited inward rectifier currents that inactivated at membrane potentials negative to -130 mV. Comparative recordings were performed in astrocytes from patients with lesion-associated TLE that lacked significant histopathological hippocampal alterations. These cells displayed stronger inward rectification. To obtain a quantitative measure, current densities were calculated and the ratio of inward to outward K+ conductances was determined. Both values were significantly smaller in astrocytes from the sclerotic group compared with lesion-associated TLE. During normal development of rodent brain, astroglial inward rectification gradually increases. It thus appears reasonable to suggest that astrocytes in human sclerotic tissue return to an immature current pattern. Reduced astroglial inward rectification in conjunction with seizure-induced shrinkage of the extracellular space may lead to impaired spatial K+ buffering. This will result in stronger and prolonged depolarization of glial cells and neurons in response to activity-dependent K+ release, and may thus contribute to seizure generation in this particular condition of human TLE. [source]

Endocannabinoids, a novel target in pain treatment

JOURNAL OF NEUROCHEMISTRY, Issue 2003
S. C. Azad
Cannabinoids display a variety of central effects including analgesia, control of spasticity and influence of emotional states. Activation of the brain-type cannabinoid receptor CB1 inhibits the adenylyl cyclase-protein kinase A-pathway and modulates calcium and potassium conductances. CB1 is widely distributed throughout the central nervous system. Among other brain regions, CB1 is highly expressed in the amygdala, which is important for the control of emotional behavior including anxiety and pain perception. In a recent investigation using auditory fear-conditioning tests, we showed that the endogenous cannabinoid system in the amygdala is crucially involved in the extinction of aversive memories. Using electrophysiological techniques, we also found that endogenous and exogenously applied cannabinoids play a major role in the modulation of both, synaptic transmission and plasticity in this brain region. Our behavioral and electrophysiological results indicate that the endogenous cannabinoid system may represent a novel target in the treatment of chronic pain. [source]

Morvan's syndrome: Clinical, laboratory, and in vitro electrophysiological studies

MUSCLE AND NERVE, Issue 2 2004
Wolfgang N. Löscher MD
Abstract Morvan's syndrome is a rare disorder characterized by neuromyotonia, hyperhidrosis, and central nervous system dysfunction. We report a patient with features of this syndrome, but who initially presented with breathing difficulties. Concentric needle electromyography showed an abundance of myokymic and neuromyotonic discharges. Exercise tests and repetitive nerve stimulation showed a decrement,increment response of compound muscle action potentials. Antibodies against voltage-gated potassium channels were not detected on repeated testing, but the presence of oligoclonal bands in the cerebrospinal fluid (CSF) suggested an autoimmune etiology. At follow-up over 3 years, no cancer was found. Electrophysiological in vitro studies of effects of patient serum and CSF on rat nerves provided no evidence of altered voltage-gated sodium or potassium conductances. We conclude that putative humoral factors do not block ion channels acutely but may cause channel dysfunction with chronic exposure. Muscle Nerve 30: 157,163, 2004 [source]

Modulation of sensory neuron potassium conductances by anandamide indicates roles for metabolites

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2008
R M Evans
Background and purpose: The endogenous cannabinoid anandamide (AEA) acts at cannabinoid (CB1) and vanilloid (TRPV1) receptors. AEA also shows antinociceptive properties; although the underlying mechanism for this is not fully understood, both CB1 and TRPV1 may be involved. Voltage-activated Ca2+ channels in rat-cultured dorsal root ganglion (DRG) neurons are modulated by AEA. However, AEA in different populations of neurons enhanced or attenuated KCl-evoked Ca2+ influx; these effects were linked with soma size. The aim of this study was to determine how AEA or its metabolites might produce these variable responses. Experimental approach: The whole cell patch-clamp technique and fura-2 Ca2+ imaging were used to characterize the actions of AEA on action potential firing and voltage-activated K+ currents and to determine whether AEA metabolism plays any role in its effects on cultured DRG neurons. Key results: AEA attenuated multiple action potential firing evoked by 300 ms depolarizing current commands in a subpopulation of DRG neurons. Application of 1 ,M AEA attenuated voltage-activated K+ currents and the recovery of KCl-evoked Ca2+ transients. The insensitivity of these responses to the CB1 receptor antagonist rimonabant (100 nM) and preincubation of DRG neurons with pertussis toxin suggested that these actions are not CB1 receptor-mediated. Preincubating DRG neurons with the fatty acid amide hydrolase (FAAH) inhibitor phenylmethylsulphonyl fluoride (PMSF) attenuated the inhibitory actions of AEA on K+ currents and Ca2+ influx. Conclusion and implications: These data suggest that the products of AEA metabolism by FAAH contribute to the attenuation of K+ conductances and altered excitability of cultured sensory neurons. British Journal of Pharmacology (2008) 154, 480,492; doi:10.1038/bjp.2008.93; published online 31 March 2008 [source]