Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma membrane Cl- channels perform a variety of functions, including control of excitability in neurons and muscle, cell volume regulation and transepithelial transport. Structurally, three classes of Cl- channels have been identified: ligand-gated, postsynaptic Cl- channels (e.g. GABA and glycine receptors); the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels (which belong to the traffic ATPase superfamily); and the CLC family of Cl- channels. Recent developments of note include further characterization of the expanding CLC Cl- channel family, advances in understanding the regulation of the CFTR Cl- channel and its emergent role as a regulator of other channels, clarification of issues related to swelling-activated Cl- channels, and the discovery that several co-transporter molecules are now known to induce Cl- currents in Xenopus oocytes.
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PMID:Chloride channels: a molecular perspective. 879 80

Elliptical cells (E-P) are present at the perilymphatic interface lumen (PIL) of the lagena. The E-P cells often separate from the tegmentum vasculosum (TV) and have touching processes that form a monolayer between the K+ rich perilymph and the Na+ rich endolymph, similar to the mammalian Reissner's membrane. We examined the TV of chicks (Gallus domesticus) and quantitated the expression of anti-S100 alphaalphabetabeta and S100 beta. There was a 30% increase of S100 beta saturation in the light cells facing the PIL when compared to other TV light cells. We show that: (1) the dimer anti- S100 alphaalphabetabeta and the monomer anti-S100 beta are expressed preferentially in the light cells and the E-P cells of TV; (2) expression of S100 beta is higher in light cells facing the PIL than in adjacent cells; (3) the expression of the dimer S100 alphaalphabetabeta and monomer S100 beta overlaps in most inner ear cell types, including the cells of the TV, most S100 alphaalphabetabeta positive cells express S 100 beta, but S100 beta positive cells do not always express S100 alphaalphabetabeta; and (4) the S100 beta expression in light cells, the abundant Na+-K+ ATPase on dark cells of the TV, and previously demonstrated co-localization of S100 beta/GABA in sensory cells suggest that S100 beta could have, in the inner ear, a dual neurotrophic-ionic modulating function.
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PMID:Elliptical-P cells in the avian perilymphatic interface of the Tegmentum vasculosum. 881 99

We compared the effect of GABA and the serotonin receptor agonist (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT) on compound action potential amplitudes, latency, and conduction velocity in the spinal cord isolated from young (eight to 13-day-old) Long-Evans hooded rats. Supramaximally activated conducting action potentials and extracellular K+ activity were recorded with microelectrodes from the cuneatus-gracilis fasciculi and corticospinal tract. In the cuneatus-gracilis fasciculi, 8-OH-DPAT (10(-4) M) significantly reduced response amplitudes by 26.1 +/- 10.3% (mean +/- S.D., P < 0.0001, paired t-test, n = 27) and increased latencies by 20.3 +/- 7.9% (P < 0.0001). GABA (10(-4) M) reduced/amplitudes by 31.7 +/- 15.0% (P < 0.0001, n = 28) and increased latencies by 6.1 +/- 5.4% (P < 0.0001). However, neither GABA nor 8-OH-DPAT significantly altered conduction velocities, suggesting that the latency shifts are due to changes in activation time and not conduction velocity. In cortical spinal tract, 8-OH-DPAT (10(-4) M) depressed response amplitudes by 18.9 +/- 9.6% (P < 0.05, n = 5), increased latencies by 23.3 +/- 7.2% (P < 0.0001), but reduced conduction velocities by 19.9 +/- 10.2%. GABA (10(-4) M) reduced amplitudes by 16.4 +/- 7.5% (P < 0.01, n = 5), increased latencies by 5.3 +/- 2.3% (P < 0.05), and did not change conduction velocities. Bicuculline or picrotoxin blocked the GABA effects but did not affect the 8-OH-DPAT effects on both tracts. The potassium channel blocker tetraethylammonium did not alter the 8-OH-DPAT effects. The Na+/K(+)-ATPase inhibitor ouabain (10(-6) M) markedly enhanced the depressive GABA effects from 27.9 +/- 12.0% to 49.4 +/- 24.5% (P < 0.01, n = 9), but had no effect on 8-OH-DPAT-mediated effects. These results suggest that GABA and serotonin agonists depress axonal excitability through different and independent mechanisms.
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PMID:Independent depressive mechanisms of GABA and (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide on young rat spinal axons. 895 85

The expression and function of large-conductance Ca2+ -activated K+ (BK) channels in the GT1-7 line of immortalized gonadotropin-releasing hormone (GnRH) neurons was investigated. Ionic currents were recorded using the patch-clamp technique, cytoplasmic free Ca2+ concentration ([Ca2+]i) was monitored using the fluorescent indicator, fura-2, and GnRH secretion was measured by radioimmunoassay. In cell-attached and inside-out patch-clamp recordings, K+ channels with a single-channel conductance of approximately 200 pS were detected. Depolarizing the patch increased the unitary current size and the open probability. In perforated-patch recordings, depolarizing pulses (50 ms) to potentials of -10 to +60 mV from a holding potential of -90 mV elicited outward current with early transient and sustained components. The transient current peaked 2-10 ms after the beginning of each pulse and increased in a voltage-dependent manner. This current was: (1) unaffected by the small-conductance Ca2+ -activated K+ channel blocker, apamin (100 nM); (2) reduced by the BK channel blocker, charybdotoxin (5 nM); (3) abolished by the Ca2+ channel blocker, CdCl2 (25 mu M), and (4) prolonged by the endoplasmic reticulum Ca2+ -ATPase inhibitor, thapsigargin (1 mu M). Based on the single-channel and whole-cell conductances, the number of channels per patch, the patch area, and the surface area of the cell, each GT1-7 cell contains 30-60 BK channels. The functional role of BK channels in GT1-7 cells was evaluated by measuring the effect of charybdotoxin (100 nM) on basal [Ca2+]i and GnRH secretion, as well as on the [Ca2+]i and GnRH secretory responses to gamma-aminobutyric acid (GABA, 100 mu M), an excitatory neurotransmitter in this system. Charybdotoxin had no effect on basal [Ca2+]i or GnRH secretion, or on the GABA-evoked [Ca2+]i and GnRH secretory responses. These results indicate that GT1-7 cells express BK channels; however, the physiological role of BK channels in GT1-7 cells remains elusive.
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PMID:Immortalized GnRH neurons express large-conductance calcium-activated potassium channels. 905 74

1. The common inhibitory motoneurone 1 (CI1) in the mesothoracic ganglion of the locust was photoinactivated using a helium-cadmium laser or a mercury lamp as light source. Treated animals showed no signs of abnormal locomotory behaviour over periods of up to 40 days. 2. Photoinactivation of part of the neurone in the ganglion, i.e. the soma and the primary neurite, is sufficient to cause irreversible degeneration of all the peripheral extensions of the neurone. Three weeks after photoinactivation, all GABA immunoreactivity had disappeared from the axon branches of the photoinactivated neurone and from their terminals on one of the target muscles investigated, the anterior coxa rotator M92, and inhibitory postsynaptic potentials could no longer be elicited through stimulation. This was taken as proof of functional denervation of the muscle with regard to its inhibitory input. By this time, the axon of CI1 in nerve N3C1, which supplies M92, had also disappeared. 3. Animals treated during the fourth or fifth instars showed a permanent loss of the photoinactivated mesothoracic CI1 neurone after moulting into adulthood. 4. Denervation of M92 in the middle legs of instars and adults by axotomy of N3 always led to rapid functional reinnervation of the muscle. The first sign of reinnervation (excitatory neuromuscular activity upon mechanical stimulation of the tarsi) was detected electrophysiologically as early as 8 days after severing the motor nerve. 5. The elimination of CI1 by photoinactivation for a period of up to 40 days did not influence parameters of the target muscle, such as size, number of fibres and phenotypes of fibres defined histochemically according to their myofibrillar ATPase isoforms, irrespective of whether the operation was performed in instars or adults. Similarly, the short period of denervation following axotomy before reinnervation took place did not affect the fibre type composition of the muscle.
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PMID:Photoinactivation of an identified motoneurone in the locust Locusta migratoria. 911 2

The temperature dependence of transmitter release associated with axonal conduction, evoked by ligand-gated mechanism and by reversed operation of plasma membrane transporter was studied in superfused slice preparation. When the temperature was reduced from 37-17 degrees C the release of [3H]noradrenaline ([3H]NA) and [3H]dopamine ([3H]DA) in response to field stimulation was significantly enhanced in slice preparations of the hippocampus and main olfactory bulbs. The release of [3H]dopamine evoked by a ligand-gated mechanism (nicotine receptor stimulation) was potentiated at low temperature (12 degrees C). In contrast, when transmitter release was evoked by ouabain, a drug inhibiting Na+/K+-activated ATPase and thereby increasing [Na+]i the release of [3H]GABA was enhanced. This release was very sensitive to cooling (Q10=3.5 between 37 degrees C and 27 degrees C), indicating that the release was induced by a reversed operation of the transporter. The excessive release of [3H]NA from the hippocampal slice in response to oxygen and glucose deprivation (simulation of ischemia) was also inhibited in a temperature-dependent manner. Because at low temperatures (17-12 degrees C) only one type of release mechanism (exocytosis) is operational and carrier-mediated uptake and release is inhibited, this temperature condition provides a method to study the mode of action of different drugs (e.g. amphetamine) and the effect(s) of certain conditions (e.g. ischemia) on the mechanisms of transmitter release, specifically whether they exert their transmitter releasing effect through an exocytotic process or through the reversed operation of plasma membrane transporter. This finding also suggests that it would be important to re-examine mechanistic conclusions based on results from electrophysiological, neurochemical and pharmacological studies that have been carried out at room temperature (approximately 20 degrees C). In particular because transmitter release associated with the action potential, diffusion, receptor kinetics, active transport in both directions (uptake and release) and the probability of transmitter release are all temperature dependent, it would seem important to carry out experiments involving these processes at physiological temperature (37 degrees C).
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PMID:Different temperature dependence of carrier-mediated (cytoplasmic) and stimulus-evoked (exocytotic) release of transmitter: a simple method to separate the two types of release. 984 Feb 27

Adaptive effects of delta-sleep inducing peptide (DSIP, 12 microgram/100 g body weight, single intraperitoneal injection) and piracetam (3 mg/100 g body weight, daily intraperitoneal injection for 3 days) are manifested via differential changes in neurotransmitter amino acids (GABA, glutamate, aspartate), modulation of transport ATPase activity, and decreased accumulation of lipid peroxidation products (conjugated dienes, malonic dialdehyde, Schiff bases) in various fractions of neuronal membranes (myelin, synaptic and mitochondrial membranes) in the sensomotor cortex of rat brain. Under hyperbaric oxygenation (0.3 MPa for 2 h), the combination of DSIP and piracetam enhanced the protective effect of each compound.
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PMID:Metabolic features of the adaptive effect of delta-sleep inducing peptide and piracetam under hyperoxic conditions. 1039 80

In this study the temperature dependence of [3H]GABA release from brain slices evoked by electrical field stimulation and the Na+/K+ ATPase inhibitor ouabain was investigated. [3H]GABA has been taken up and released from hippocampal slices at rest and in response to electrical field stimulation (20 V, 10 Hz, 3 msec, 180 pulses) at 37 degrees C. When the bath temperature was cooled to 7 degrees C, during the sample collection period, the tissue uptake and the resting outflow of [3H]GABA were not significantly changed. In contrast, the stimulation-induced tritium outflow increased both in absolute amount (Bq/g) and in fractional release and the S2/S1 ratio was also higher at 7 degrees C. Perfusion of the slices with tetrodotoxin (TTX, 1 microM) inhibited stimulation-induced [3H]GABA efflux indicating that exocytotic release of vesicular origin is maintained under these conditions. 15 min perfusion with ouabain (10-20 microM) induced massive tritium release both in hippocampal and in striatal slices. However, the fraction of [3H]GABA outflow evoked by ouabain was much higher in the hippocampus than in the striatum. Sequential lowering the bath temperature from 37 degrees C to 17 degrees C completely abolished ouabain-induced [3H]GABA release in both brain regions, indicating that it is a temperature-dependent, carrier-mediated process. When the same experiments were repeated under Ca2+ free conditions, cooling the bath temperature to 17 degrees C, although substantially decreased the release but failed to completely abolish the tritium outflow evoked by ouabain, a significant part was maintained. Our results show that vesicular (field stimulation-evoked) and carrier-mediated (ouabain-induced) release of GABA is differentially affected by low temperature: while vesicular release is unaffected, carrier-mediated release is abolished at low bath temperature. Therefore, lowering the temperature offers a reliable tool to separate these two kinds of release and makes possible to study exclusively the pure neuronal release of GABA of vesicular origin.
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PMID:Separation of carrier mediated and vesicular release of GABA from rat brain slices. 1039 69

Streptosotocin-induced diabetes in rats is accompanied by the development of diabetic complications such as neuropathies. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation. Aldose reductase inhibitors (AL-1576, sorbinil) administration leads to partial restoration of serotonin and GABA release, while picamilon restored only GABA release. It was shown that Na+,K(+)-ATPase activities decreased in synaptosomes, synaptic membranes and sciatic nerve of diabetic rats compared to control. Administration of AL-1576 normalized Na+, K(+)-ATPase activity, while sorbinil and picamilon less effectively. Sorbitol level are increased in streptozotocin-diabetic rats as compared to control. The picamilon and aldose reductase inhibitors administration to diabetic rats is accompanied by the partial reduction of brain sorbitol level. The findings confirm the important role of picamilon and aldose reductase inhibitors in the prevention and treatment of diabetic neuropathy.
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PMID:[Correction of diabetic neuropathies using aldose reductase inhibitors and pikamilon]. 1059 42

Rett syndrome (RTT) is an X-linked dominant neurodevelopmental disorder that affects females. Exclusion mapping studies using a new family with maternal inheritance of RTT defined Xq28 as the candidate region for the RTT gene. Six candidate genes were selected for mutation analysis based on their established expression patterns and known functions in the CNS. These are: Glutamate receptor subunit 3 (GLUR3), GABA receptor subunit alpha 3 (GABRA3), GABA receptor subunit e1 (GABRE1), Vacuolar ATPase subunit 1 (VATPS1, XAP3), the human homologue of plexin 3-SEX (XAP6) and the Synaptobrevin-like protein (SYBL1). Major rearrangements involving these genes were excluded by Southern analysis. No disease-causing mutations were found, but several single-nucleotide polymorphisms (SNPs) were detected. These SNPs will be useful in future linkage analysis and whole-genome association studies for other diseases. The genomic characterization of GLUR3 and GABRA3 will allow mutational analysis of these genes as candidates for other X-linked neurological disorders mapping to Xq25-Xq26 and Xq28.
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PMID:Candidate gene analysis in Rett syndrome and the identification of 21 SNPs in Xq. 1060 20


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