The Experts below are selected from a list of 1710 Experts worldwide ranked by ideXlab platform
David J. Adams - One of the best experts on this subject based on the ideXlab platform.
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ω conotoxin cvid inhibits a pharmacologically distinct voltage sensitive calcium channel associated with transmitter release from Preganglionic Nerve terminals
Journal of Biological Chemistry, 2003Co-Authors: David J. Adams, Amanda Smith, Christina I Schroeder, Takahiro Yasuda, Richard J LewisAbstract:Abstract Neurotransmitter release from Preganglionic parasympathetic neurons is resistant to inhibition by selective antagonists of L-, N-, P/Q-, R-, and T-type calcium channels. In this study, the effects of different ω-conotoxins from genusConus were investigated on current flow-through cloned voltage-sensitive calcium channels expressed in Xenopusoocytes and Nerve-evoked transmitter release from the intact Preganglionic cholinergic Nerves innervating the rat submandibular ganglia. Our results indicate that ω-conotoxin CVID from Conus catus inhibits a pharmacologically distinct voltage-sensitive calcium channel involved in neurotransmitter release, whereas ω-conotoxin MVIIA had no effect. ω-Conotoxin CVID and MVIIA inhibited depolarization-activated Ba2+ currents recorded from oocytes expressing N-type but not L- or R-type calcium channels. High affinity inhibition of the CVID-sensitive calcium channel was enhanced when position 10 of the ω-conotoxin was occupied by the smaller residue lysine as found in CVID instead of an arginine as found in MVIIA. Given that relatively small differences in the sequence of the N-type calcium channel α1B subunit can influence ω-conotoxin access (Feng, Z. P., Hamid, J., Doering, C., Bosey, G. M., Snutch, T. P., and Zamponi, G. W. (2001)J. Biol. Chem. 276, 15728–15735), it is likely that the calcium channel in Preganglionic Nerve terminals targeted by CVID is a N-type (Cav2.2) calcium channel variant.
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Calcium channels controlling acetylcholine release from Preganglionic Nerve terminals in rat autonomic ganglia.
Neuroscience, 1999Co-Authors: Amanda Smith, Leonid Motin, Nickolas A. Lavidis, David J. AdamsAbstract:Little is known about the nature of the calcium channels controlling neurotransmitter release from Preganglionic parasympathetic Nerve fibres. In the present study, the effects of selective calcium channel antagonists and amiloride were investigated on ganglionic neurotransmission. Conventional intracellular recording and focal extracellular recording techniques were used in rat submandibular and pelvic ganglia, respectively. Excitatory postsynaptic potentials and excitatory postsynaptic currents preceded by Nerve terminal impulses were recorded as a measure of acetylcholine release from parasympathetic and sympathetic Preganglionic fibres following Nerve stimulation. The calcium channel antagonists omega-conotoxin GVIA (N type), nifedipine and nimodipine (L type), omega-conotoxin MVIIC and omega-agatoxin IVA (P/Q type), and Ni2+ (R type) had no functional inhibitory effects on synaptic transmission in both submandibular and pelvic ganglia. The potassium-sparing diuretic, amiloride, and its analogue, dimethyl amiloride, produced a reversible and concentration-dependent inhibition of excitatory postsynaptic potential amplitude in the rat submandibular ganglion. The amplitude and frequency of spontaneous excitatory postsynaptic potentials and the sensitivity of the postsynaptic membrane to acetylcholine were unaffected by amiloride. In the rat pelvic ganglion, amiloride produced a concentration-dependent inhibition of excitatory postsynaptic currents without causing any detectable effects on the amplitude or configuration of the Nerve terminal impulse. These results indicate that neurotransmitter release from Preganglionic parasympathetic and sympathetic Nerve terminals is resistant to inhibition by specific calcium channel antagonists of N-, L-, P/Q- and R-type calcium channels. Amiloride acts presynaptically to inhibit evoked transmitter release, but does not prevent action potential propagation in the Nerve terminals, suggesting that amiloride may block the pharmacologically distinct calcium channel type(s) on rat Preganglionic Nerve terminals. (C) 1999 IBRO. Published by Elsevier Science Ltd.
Richard J Lewis - One of the best experts on this subject based on the ideXlab platform.
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ω conotoxin cvid inhibits a pharmacologically distinct voltage sensitive calcium channel associated with transmitter release from Preganglionic Nerve terminals
Journal of Biological Chemistry, 2003Co-Authors: David J. Adams, Amanda Smith, Christina I Schroeder, Takahiro Yasuda, Richard J LewisAbstract:Abstract Neurotransmitter release from Preganglionic parasympathetic neurons is resistant to inhibition by selective antagonists of L-, N-, P/Q-, R-, and T-type calcium channels. In this study, the effects of different ω-conotoxins from genusConus were investigated on current flow-through cloned voltage-sensitive calcium channels expressed in Xenopusoocytes and Nerve-evoked transmitter release from the intact Preganglionic cholinergic Nerves innervating the rat submandibular ganglia. Our results indicate that ω-conotoxin CVID from Conus catus inhibits a pharmacologically distinct voltage-sensitive calcium channel involved in neurotransmitter release, whereas ω-conotoxin MVIIA had no effect. ω-Conotoxin CVID and MVIIA inhibited depolarization-activated Ba2+ currents recorded from oocytes expressing N-type but not L- or R-type calcium channels. High affinity inhibition of the CVID-sensitive calcium channel was enhanced when position 10 of the ω-conotoxin was occupied by the smaller residue lysine as found in CVID instead of an arginine as found in MVIIA. Given that relatively small differences in the sequence of the N-type calcium channel α1B subunit can influence ω-conotoxin access (Feng, Z. P., Hamid, J., Doering, C., Bosey, G. M., Snutch, T. P., and Zamponi, G. W. (2001)J. Biol. Chem. 276, 15728–15735), it is likely that the calcium channel in Preganglionic Nerve terminals targeted by CVID is a N-type (Cav2.2) calcium channel variant.
Amanda Smith - One of the best experts on this subject based on the ideXlab platform.
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ω conotoxin cvid inhibits a pharmacologically distinct voltage sensitive calcium channel associated with transmitter release from Preganglionic Nerve terminals
Journal of Biological Chemistry, 2003Co-Authors: David J. Adams, Amanda Smith, Christina I Schroeder, Takahiro Yasuda, Richard J LewisAbstract:Abstract Neurotransmitter release from Preganglionic parasympathetic neurons is resistant to inhibition by selective antagonists of L-, N-, P/Q-, R-, and T-type calcium channels. In this study, the effects of different ω-conotoxins from genusConus were investigated on current flow-through cloned voltage-sensitive calcium channels expressed in Xenopusoocytes and Nerve-evoked transmitter release from the intact Preganglionic cholinergic Nerves innervating the rat submandibular ganglia. Our results indicate that ω-conotoxin CVID from Conus catus inhibits a pharmacologically distinct voltage-sensitive calcium channel involved in neurotransmitter release, whereas ω-conotoxin MVIIA had no effect. ω-Conotoxin CVID and MVIIA inhibited depolarization-activated Ba2+ currents recorded from oocytes expressing N-type but not L- or R-type calcium channels. High affinity inhibition of the CVID-sensitive calcium channel was enhanced when position 10 of the ω-conotoxin was occupied by the smaller residue lysine as found in CVID instead of an arginine as found in MVIIA. Given that relatively small differences in the sequence of the N-type calcium channel α1B subunit can influence ω-conotoxin access (Feng, Z. P., Hamid, J., Doering, C., Bosey, G. M., Snutch, T. P., and Zamponi, G. W. (2001)J. Biol. Chem. 276, 15728–15735), it is likely that the calcium channel in Preganglionic Nerve terminals targeted by CVID is a N-type (Cav2.2) calcium channel variant.
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Calcium channels controlling acetylcholine release from Preganglionic Nerve terminals in rat autonomic ganglia.
Neuroscience, 1999Co-Authors: Amanda Smith, Leonid Motin, Nickolas A. Lavidis, David J. AdamsAbstract:Little is known about the nature of the calcium channels controlling neurotransmitter release from Preganglionic parasympathetic Nerve fibres. In the present study, the effects of selective calcium channel antagonists and amiloride were investigated on ganglionic neurotransmission. Conventional intracellular recording and focal extracellular recording techniques were used in rat submandibular and pelvic ganglia, respectively. Excitatory postsynaptic potentials and excitatory postsynaptic currents preceded by Nerve terminal impulses were recorded as a measure of acetylcholine release from parasympathetic and sympathetic Preganglionic fibres following Nerve stimulation. The calcium channel antagonists omega-conotoxin GVIA (N type), nifedipine and nimodipine (L type), omega-conotoxin MVIIC and omega-agatoxin IVA (P/Q type), and Ni2+ (R type) had no functional inhibitory effects on synaptic transmission in both submandibular and pelvic ganglia. The potassium-sparing diuretic, amiloride, and its analogue, dimethyl amiloride, produced a reversible and concentration-dependent inhibition of excitatory postsynaptic potential amplitude in the rat submandibular ganglion. The amplitude and frequency of spontaneous excitatory postsynaptic potentials and the sensitivity of the postsynaptic membrane to acetylcholine were unaffected by amiloride. In the rat pelvic ganglion, amiloride produced a concentration-dependent inhibition of excitatory postsynaptic currents without causing any detectable effects on the amplitude or configuration of the Nerve terminal impulse. These results indicate that neurotransmitter release from Preganglionic parasympathetic and sympathetic Nerve terminals is resistant to inhibition by specific calcium channel antagonists of N-, L-, P/Q- and R-type calcium channels. Amiloride acts presynaptically to inhibit evoked transmitter release, but does not prevent action potential propagation in the Nerve terminals, suggesting that amiloride may block the pharmacologically distinct calcium channel type(s) on rat Preganglionic Nerve terminals. (C) 1999 IBRO. Published by Elsevier Science Ltd.
M R Bennett - One of the best experts on this subject based on the ideXlab platform.
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calcium in sympathetic boutons of rat superior cervical ganglion during facilitation augmentation and potentiation
Journal of The Autonomic Nervous System, 1998Co-Authors: Yong Qi Lin, Keith L Brain, M R BennettAbstract:The sympathetic Preganglionic Nerve terminals of the rat superior cervical ganglion were loaded with the calcium indicator oregon green 488 BAPTA-1 to measure the change in calcium concentration in the terminal boutons, (Δ[Ca2+]b) following short (1 or 5 impulses) and long (200 impulses) trains at 30 Hz. The Δ[Ca2+]b after a single action potential or a short train declined in two phases: a fast phase with a time constant of 530±30 ms and a moderate phase with a time constant of 4.0±0.2 s. The Δ[Ca2+]b following a long train eventually declined with a time constant of 127±34 s (slow phase). The addition of either ω-agatoxin TK (100 nM), ω-conotoxin GVIA (100 nM) or nifedipine (20 μM) to block P-type, N-type or L-type calcium channels respectively showed that the rise in Δ[Ca2+]b in boutons was predominantly mediated by an influx of calcium through P-type (53±7%) and N-type (46±4%) calcium channels. Experiments with caffeine, ryanodine and thapsigargin indicate that intracellular caffeine-sensitive calcium stores have a small but statistically significant effect on the fast and moderate phases. The mitochondrial uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 2 μM) significantly decreased the amplitude of the slow phase of Δ[Ca2+]b relaxation, and sped its time course, suggesting that mitochondria normally dump calcium during this phase. Adenosine reduced the amplitude of Δ[Ca2+]b in response to single action potentials by 30±6%, suggesting that adenosine-mediated autoinhibition in these boutons reduces Ca2+ influx. Spontaneous increases in Δ[Ca2+]b demonstrated Ca2+ coupling between adjacent boutons. The Δ[Ca2+]b kinetics are compared with F2 facilitation, augmentation and post-tetanicpotentiation.
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adenosine modulation of potassium currents in Preganglionic Nerve terminals of avian ciliary ganglia
Neuroscience Letters, 1992Co-Authors: M R BennettAbstract:Abstract Potassium currents in calyciform Nerve terminals of the avian ciliary ganglion were analyzed using a single microelectrode voltage clamp. The modulatory affects of adenosine on these currents was also determined. Intracellular CsCl (1 M) blocked the steady-state outward current, indicating that it is mostly carried by K + . Tetraethylammonium (TEA, 10 mM) blocked over 40% of the outward current at a command potential of 30 mV. If Ca 2+ influx was blocked by CoCl 2 (5 mM), the steady-state outward current was reduced by over 16% in the Nerve terminals suggesting that about one fifth of the outward current passes through calcium-activated potassium channels I K(Ca) . Adenosine (50 mM) decreased the outward steady-state current over a wide range of command potentials in most terminals studied but failed to decrease this current in the presence of CoCl 2 (5 mM). It is concluded that adenosine blocks I K(Ca) in Nerve terminals.
Paola Paggi - One of the best experts on this subject based on the ideXlab platform.
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nicotinic acetylcholine receptor subtypes in the rat sympathetic ganglion pharmacological characterization subcellular distribution and effect of pre and postganglionic Nerve crush
Journal of Neuropathology and Experimental Neurology, 2004Co-Authors: Arianna Del Signore, M. Moretti, C. Gotti, Angela Rizzo, Paola PaggiAbstract:Nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission in autonomic ganglia, which innervate and control the activity of most visceral organs. By combining ultrastructural, immunocytochemical, and pharmacological analyses, we characterized the nAChR subtypes in the rat superior cervical ganglion (SCG) and the effect of pre- and postganglionic Nerve crush on their number in the ganglion and their distribution at the intraganglionic synapses. Binding with radioactive nicotinic ligands, immunoprecipitation, and immunolocalization experiments revealed the presence of different nAChR subtypes: those containing the alpha3 subunit associated with beta4 and/or beta2 subunits that bind 3H-Epibatidine with high affinity, and those containing the alpha7 subunit that bind 125I-alphaBungarotoxin. After postganglionic Nerve crush, the number of nicotinic receptors and immunopositive intraganglionic synapses for each nAChR subunit strongly decreased. Both the number of nAChRs and immunoreactivity recovered 26 days after injury, when regenerating postganglionic fibers had reinnervated the peripheral target organs, as shown by the restoration of tyrosine hydroxylase immunoreactivity in the iris. This observation and the lack of any effect of Preganglionic Nerve crush on the number of nicotinic receptors suggest that the peripheral targets affect the organization of intraganglionic synapses in adult SCG.