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Dominique Richard - One of the best experts on this subject based on the ideXlab platform.
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axonal projections from the organum vasculosum lamina terminalis to the supraoptic nucleus functional analysis and Presynaptic Modulation
Clinical and Experimental Pharmacology and Physiology, 2001Co-Authors: Charles W. Bourque, Dominique RichardAbstract:SUMMARY 1. The rat organum vasculosum lamina terminalis (OVLT) contains GABA- and glutamate-releasing neurons that project directly to magnocellular neurosecretory cells (MNC) in the supraoptic nucleus. 2. Changes in osmolality over the OVLT in hypothalamic explants cause proportional changes in firing in MNC through corresponding changes in the frequency of spontaneous glutamatergic excitatory post-synaptic potentials without affecting GABAergic inhibitory post-synaptic potentials. 3. Exogenously applied atrial natriuretic peptide inhibits the osmotic control of MNC by causing a decrease in the amount of glutamate released provoked by action potentials originating from OVLT neurons.
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Circumventricular Organs: Gateways to the Brain Axonal Projections From The Organum Vasculosum Lamina Terminalis To The Supraoptic Nucleus: Functional Analysis And Presynaptic Modulation
Clinical and Experimental Pharmacology and Physiology, 2001Co-Authors: Charles W. Bourque, Dominique RichardAbstract:SUMMARY 1. The rat organum vasculosum lamina terminalis (OVLT) contains GABA- and glutamate-releasing neurons that project directly to magnocellular neurosecretory cells (MNC) in the supraoptic nucleus. 2. Changes in osmolality over the OVLT in hypothalamic explants cause proportional changes in firing in MNC through corresponding changes in the frequency of spontaneous glutamatergic excitatory post-synaptic potentials without affecting GABAergic inhibitory post-synaptic potentials. 3. Exogenously applied atrial natriuretic peptide inhibits the osmotic control of MNC by causing a decrease in the amount of glutamate released provoked by action potentials originating from OVLT neurons.
Suguru Kobayashi - One of the best experts on this subject based on the ideXlab platform.
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organization of the procerebrum in terrestrial pulmonates helix limax reconsidered cell mass layer synaptology and its serotonergic input system
Brain Structure & Function, 2013Co-Authors: Karoly Elekes, Izabella Battonyai, Suguru KobayashiAbstract:The synaptology of the cell body layer of the olfactory center, procerebrum, was investigated in two prominent terrestrial pulmonate gastropod species, Helix pomatia and Limax valentianus. In addition, the analysis of the 5-HT-immunoreactive innervation, including ultrastructural level, was performed at high resolution in H. pomatia. A highly complex system of synaptic and non-synaptic connections was found in the procerebrum of both species connected to local neuropil areas of different size. The procerebral (globuli) cell perikarya were richly innervated by varicosities meanwhile the axon profiles also established contacts with each other. Synaptic configurations including convergence, divergence and Presynaptic Modulation were also revealed. The frequent occurrence of unspecialized but close axo-somatic and axo-axonic membrane contacts referring to the modulatory forms of transmitter release were also accompanied by membrane configurations indicative of active exocytosis. In H. pomatia, the cell mass layer was shown to receive a rich 5-HT-immunoreactive innervation, forming a dense network around the cell bodies. At ultrastructural level, 5-HT-immunoreactive varicosities contacted both cell bodies and different unlabeled axon profiles. Our results suggest that the local neuropil regions in the cell body layer are site of local circuits, which may play a decisive role in olfactory integrative processes bound to the procerebrum. The pattern and form of the 5-HT-immunoreactive innervation of extrinsic origin suggest an overall modulatory role in the cell body layer. The results may serve a basis for considering the role of local intercellular events, connected to microcircuits, within the procerebrum cell body layer involved in oscillation activities.
Eduard Khaziev - One of the best experts on this subject based on the ideXlab platform.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei VerkhratskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurones in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fibre. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analogue carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei Verkhratsky, Evgeny NikolskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurons in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fiber. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analog carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.
E A Bukharaeva - One of the best experts on this subject based on the ideXlab platform.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei VerkhratskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurones in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fibre. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analogue carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei Verkhratsky, Evgeny NikolskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurons in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fiber. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analog carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.
D V Samigullin - One of the best experts on this subject based on the ideXlab platform.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei VerkhratskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurones in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fibre. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analogue carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.
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acetylcholine induced inhibition of Presynaptic calcium signals and transmitter release in the frog neuromuscular junction
Frontiers in Physiology, 2016Co-Authors: Eduard Khaziev, D V Samigullin, N V Zhilyakov, N F Fatikhov, E A Bukharaeva, Alexei Verkhratsky, Evgeny NikolskyAbstract:Acetylcholine (ACh), released from axonal terminals of motor neurons in neuromuscular junctions regulates the efficacy of neurotransmission through activation of Presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated Presynaptic regulation could reflect either direct action on exocytotic machinery or Modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fiber. Activation of Presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analog carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in Presynaptic Modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of Presynaptic Modulation in frog neuromuscular junction.