Parasympathetic Ganglia

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Allen C. Myers - One of the best experts on this subject based on the ideXlab platform.

  • Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway Parasympathetic Ganglia.
    American journal of physiology. Lung cellular and molecular physiology, 2006
    Co-Authors: Mehdi S. Hazari, Jenny H. Pan, Allen C. Myers
    Abstract:

    Elevated levels of nerve growth factor (NGF) and NGF-mediated neural plasticity may have a role in airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). Although NGF is known to affect sensory and sympathetic nerves, especially during development, little is known regarding its effect on Parasympathetic nerves, especially on adult neurons. The purpose of this study was to analyze the acute and chronic effects of NGF on the electrophysiological and anatomical properties of neurons in airway Parasympathetic Ganglia from adult guinea pigs. Using single cell recording, direct application of NGF caused a lasting decrease in the cumulative action potential afterhyperpolarization (AHP) and increased the amplitude of vagus nerve-stimulated nicotinic fast excitatory postsynaptic potentials. Neuronal responsiveness to nicotinic receptor stimulation was increased by NGF, which was blocked by the tyrosine kinase inhibitor, K-252a, implicating neurotrophin-specific (Trk) receptors. Neurotrophin-3 and brain-derived neurotrophic factor had no effect on the synaptic potentials, AHP, or nicotinic response; inhibition of cyclooxygenase with indomethacin inhibited the effect of NGF on the cumulative AHP. Forty-eight hours after in vivo application of NGF to the trachealis muscle caused an increase in dendritic length on innervating neurons. These results are the first to demonstrate that NGF increases the excitability of lower airway Parasympathetic neurons, primarily through enhanced synaptic efficacy and changes to intrinsic neuron properties. NGF also had dramatic effects on the growth of dendrites in vivo. Such effects may indicate a new role for NGF in the regulation of Parasympathetic tone in the diseased or inflamed lower airways.

  • Endogenous neurokinins facilitate synaptic transmission in guinea pig airway Parasympathetic Ganglia.
    American journal of physiology. Regulatory integrative and comparative physiology, 2002
    Co-Authors: Brendan J. Canning, Sandra M. Reynolds, Linus U. Anukwu, Radhika Kajekar, Allen C. Myers
    Abstract:

    Neurokinin-containing nerve fibers were localized to guinea pig airway Parasympathetic Ganglia in control tissues but not in tissues pretreated with capsaicin. The purpose of the present study was ...

  • The Integrative Membrane Properties of Human Bronchial Parasympathetic Ganglia Neurons
    American Journal of Respiratory and Critical Care Medicine, 2001
    Co-Authors: Radhika Kajekar, Holly Rohde, Allen C. Myers
    Abstract:

    Parasympathetic Ganglia neurons in the lower airway of laboratory animals have membrane properties associated with integration of signals from the central nervous system. In this study, intracellular recordings were made from Parasympathetic Ganglia located on bronchi from human lungs in order to determine the level of integration provided by human neurons. Ganglion neurons were characterized as either tonic or phasic: tonic neurons responded with repetitive action potentials sustained throughout a depolarizing current step whereas phasic neurons generated one action potential and accommodated. Phasic neurons could be further differentiated as having either short or long duration after hyperpolarizing potentials following single action potentials. In phasic neurons, stimulation of preganglionic nerves elicited one or two populations of nicotinic fast excitatory postsynaptic potentials (fEPSPs) that were graded in amplitude, subthreshold for action potential generation, and decreased in amplitude during higher frequency stimulation. In tonic neurons, single preganglionic stimuli evoked two to five populations of fEPSPs, one to three of which were at threshold for action potential generation. Dye injection into the neurons revealed multiple, branching dendrites. These results provide evidence that human bronchial ganglion neurons have unique membrane properties and anatomical characteristics associated with integrating presynaptic stimuli. Changes in these properties may thus affect output from these Ganglia and, consequently, autonomic tone in the lower airways.

  • Anatomical characteristics of tonic and phasic postganglionic neurons in guinea pig bronchial Parasympathetic Ganglia.
    The Journal of comparative neurology, 2000
    Co-Authors: Allen C. Myers
    Abstract:

    Anatomical characteristics of principal Parasympathetic Ganglia neurons on the guinea pig primary bronchus were analyzed, and the procedure for localizing the Ganglia without the aid of staining for in vitro physiological studies is described. The neurons were tightly packed within a perineural sheath, and the cell bodies formed a homogeneous population based on size and shape. By using intracellular electrophysiological recordings, unstained neurons within these Ganglia were characterized with suprathreshold depolarizing stimuli as having either accommodating action potential patterns (phasic neurons) or repetitive action potential patterns (tonic neurons). After determining whether a cell was tonic or phasic, it was injected with either horseradish peroxidase or Neurobiotin for characterization of its dendrites. There were no differences between tonic and phasic neurons, and both exhibited the following: (1) dendrites were multiple and branching; (2) all processes (axon and dendrites) arose from a circumscribed area on the somatic surface; (3) the initial direction of the processes was usually toward the center of the ganglion, creating a very dense intraganglionic neuropil; (4) tapering processes (presumed dendrites) extended beyond the border of the perineural sheath; and (5) many processes terminated with bouton-like swellings near the somatic surfaces of neighboring neurons within the same ganglion. Electron microscopic examination of dendritic and cell body membranes revealed that greater than 90% of the synapses occurred on dendrites. Based on immunohistochemical staining, all neurons were calbindin negative. These results indicate a relatively homogeneous population of neurons in bronchial Parasympathetic Ganglia displaying dendritic characteristics compatible with complex integrative properties.

  • Muscarinic receptor regulation of synaptic transmission in airway Parasympathetic Ganglia.
    American Journal of Physiology-Lung Cellular and Molecular Physiology, 1996
    Co-Authors: Allen C. Myers, Bradley J. Undem
    Abstract:

    Muscarinic receptor regulation of synaptic transmission in guinea pig bronchial Parasympathetic Ganglia was evaluated with the use of intracellular recording of the intrinsic ganglion neurons. Methacholine (1 microM) decreased the amplitude of vagus nerve-stimulated fast excitatory postsynaptic potentials (fEPSP) by 33 and 46% (at 0.8 and 8.0 Hz, respectively) but had no effect on the amplitude of the depolarizations evoked by a bath-applied nicotinic receptor agonist. Methoctramine (1 microM) inhibited methacholine9s effect on fEPSP but alone did not influence the magnitude of the fEPSP evoked by vagus nerve stimulation. Methacholine (10 microM) depolarized a subpopulation of neurons (approximately 4 mV), which was blocked by pirenzepine (0.1 microM). In other neurons, either no effect or a small (1-5 mV) hyperpolarization was noted. Cholinergic contractions of bronchial smooth muscle elicited by electrical field stimulation were potentiated by methoctramine to the same extent as those evoked by vagus nerve (preganglionic) stimulation. The data indicate that M2 receptor activation can lead to inhibition of presynaptic acetylcholine release and consequently a significant inhibition of synaptic transmission in bronchial Parasympathetic Ganglia. The physiological role of this neuromodulatory effect appears limited, however, when studied in the in vitro setting.

Toshihiko Nishimura - One of the best experts on this subject based on the ideXlab platform.

  • Effects of adenosine on cholinergic transmission in mammalian vesical Parasympathetic Ganglia.
    The Tokai journal of experimental and clinical medicine, 1997
    Co-Authors: Toshihiko Nishimura
    Abstract:

    Intracellular recordings were made from mammalian vesical Parasympathetic Ganglia. A fast excitatory postsynaptic potential (EPSP) was abolished by hexamethonium (200 microM) in rabbit and feline Ganglia. A slow inhibitory postsynaptic potential (IPSP) and a following slow EPSP were abolished by atropine (1 microM) in the feline Ganglia. Bath application of adenosine (300 microM) depressed the amplitude of nicotinic fast EPSP by 48 +/- 4% in the rabbit Ganglia. The action of adenosine was dose-dependent. An antagonist of A1-purinoceptors, 8-cyclopentyltheophylline (1-10 microM), inhibited the adenosine-induced depression but not the amplitude of fast EPSP. Adenosine (2-3 mM) did not significantly affect either the muscarinic slow IPSP, or the slow EPSP, in the feline Ganglia. Adenosine also caused a hyperpolarization (1-5 mV) in 40% of the rabbit neurons and 66% of the feline neurons. However a purinergic IPSP was not recorded from either species. These data suggest diverse actions of adenosine in modulating cholinergic transmission in rabbit and feline vesical Ganglia.

  • Purinergic cation channels in neurons of rabbit vesical Parasympathetic Ganglia.
    Neuroscience letters, 1996
    Co-Authors: Toshihiko Nishimura, Takayuki Tokimasa
    Abstract:

    Abstract Membrane current was recorded from neurons in rabbit vesical Parasympathetic Ganglia, utilizing single electrode voltage clamp techniques. ATP (0.1–1 mM) caused an inward current (IATp) associated with an increased conductance at a holding potential of −50 mV. ADP (0.1–1 mM) and 5′-O-3-thiotriphosphate (0.1–0.6 mM) but not AMP (0.3–2 mM) and adenosine (0.1–2 mM) mimicked the actions of ATP. The IATp reversed its polarity at −12.1 ± 1.4 mV. The amplitude of the IATp was depressed in low sodium solutions and in nominally calcium-free solutions but not in low chloride solutions. Suramin (10–100 μM) and reactive blue 2 (10–100 μM), P2-antagonists, reversibly depressed the IATp. In contrast, hexamethonium (100 μM) did not affect the IATp. These data suggest that ATP activates cation channels through P2X receptor subtypes in rabbit Parasympathetic neurons.

  • Activation of calcium-dependent chloride channels causes post-tetanic depolarization in rabbit Parasympathetic neurons
    Journal of the autonomic nervous system, 1995
    Co-Authors: Toshihiko Nishimura
    Abstract:

    Abstract Intracellular recordings were made from neurons in rabbit and feline vesical Parasympathetic Ganglia in vitro. In response to cathodal current injection (0.1–1 nA for 2–20 ms) the majority of rabbit neurons (229 out of 250) exhibited a single action potential that was followed by a fast and slow after-hyperpolarization (sAHP neuron). The remainder of the cells exhibited an action potential followed by only a fast after-hyperpolarization (fAHP neuron). fAHP neurons did not exhibit anomalous rectification and a spontaneous rhythmic hyperpolarization, which were common membrane properties in sAHP neurons. In response to a train of cathodal current pulses (5–20 Hz for 0.1–10 s), fAHP neurons exhibited action potentials followed by a post-tetanic depolarization (PTD). The PTD was associated with a decrease in membrane input resistance. The amplitude and duration of the PTD were a function of the number of action potentials in the train. The amplitude of the PTD was increased by membrane hyperpolarization and its estimated reversal potential was approximately −30 mV. Low-chloride solution and intracellular injection of chloride ions augmented the amplitude and duration of the PTD, whereas low-sodium, high-potassium and low-potassium solutions did not affect them. Tetraethylammonium (5–10 mM) and barium (0.5–1 mM) increased the amplitude and duration of the PTD. Nominal calcium-free solutions and ω-conotoxin (500 nM) abolished the PTD. The data suggest that activation of chloride channels by calcium influx through ω-conotoxin-sensitive calcium channels mediates the PTD. Repetitive stimulation of the pelvic nerve evoked a train of orthodromic action potentials followed by the PTD of fAHP neurons. (+)-Tubocurarine (10 μM) and hexamethonium (200 μM), but not atropine (1 μM), abolished orthodromic action potentials and the PTD, whereas these cholinergic antagonists did not depress the PTD evoked by direct action potentials. In summary, the data suggest that the PTD may function as a slow synaptic potential in fAHP neurons. This appears likely because neither slow excitatory nor inhibitory postsynaptic potentials are present in neurons of rabbit vesical Parasympathetic Ganglia. In contrast, slow inhibitory and excitatory postsynaptic potentials were recorded from neurons in feline vesical Parasympathetic Ganglia.

Takayuki Tokimasa - One of the best experts on this subject based on the ideXlab platform.

  • Purinergic cation channels in neurons of rabbit vesical Parasympathetic Ganglia.
    Neuroscience letters, 1996
    Co-Authors: Toshihiko Nishimura, Takayuki Tokimasa
    Abstract:

    Abstract Membrane current was recorded from neurons in rabbit vesical Parasympathetic Ganglia, utilizing single electrode voltage clamp techniques. ATP (0.1–1 mM) caused an inward current (IATp) associated with an increased conductance at a holding potential of −50 mV. ADP (0.1–1 mM) and 5′-O-3-thiotriphosphate (0.1–0.6 mM) but not AMP (0.3–2 mM) and adenosine (0.1–2 mM) mimicked the actions of ATP. The IATp reversed its polarity at −12.1 ± 1.4 mV. The amplitude of the IATp was depressed in low sodium solutions and in nominally calcium-free solutions but not in low chloride solutions. Suramin (10–100 μM) and reactive blue 2 (10–100 μM), P2-antagonists, reversibly depressed the IATp. In contrast, hexamethonium (100 μM) did not affect the IATp. These data suggest that ATP activates cation channels through P2X receptor subtypes in rabbit Parasympathetic neurons.

Norio Akaike - One of the best experts on this subject based on the ideXlab platform.

  • α1-Adrenoceptor-activated cation currents in neurones acutely isolated from rat cardiac Parasympathetic Ganglia
    The Journal of Physiology, 2003
    Co-Authors: Hitoshi Ishibashi, Mari Umezu, Il-sung Jang, Yushi Ito, Norio Akaike
    Abstract:

    The noradrenaline (NA)-induced cation current was investigated in neurones freshly isolated from rat cardiac Parasympathetic Ganglia using the nystatin-perforated patch recording configuration. Under current-clamp conditions, NA depolarized the membrane, eliciting repetitive action potentials. NA evoked an inward cation current under voltage-clamp conditions at a holding potential of -60 mV. The NA-induced current was inhibited by extracellular Ca2+ or Mg2+, with a half-maximal concentration of 13 microM for Ca2+ and 1.2 mM for Mg2+. Cirazoline mimicked the NA response, and prazosin and WB-4101 inhibited the NA-induced current, suggesting the contribution of an alpha1-adrenoceptor. The NA-induced current was inhibited by U73122, a phospholipase C (PLC) inhibitor. The membrane-permeable IP3 receptor blocker xestospongin-C also blocked the NA-induced current. Furthermore, pretreatment with thapsigargin and BAPTA-AM could inhibit the NA response while KN-62, phorbol 12-myristate 13-acetate (PMA) and staurosporine had no effect. These results suggest that NA activates the extracellular Ca2+- and Mg2+-sensitive cation channels via alpha 1-adrenoceptors in neurones freshly isolated from rat cardiac Parasympathetic Ganglia. This activation mechanism also involves phosphoinositide breakdown, release of Ca2+ from intracellular Ca2+ stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in rat cardiac Ganglia.

  • Alpha 1-adrenoceptor-activated cation currents in neurones acutely isolated from rat cardiac Parasympathetic Ganglia.
    The Journal of physiology, 2003
    Co-Authors: Hitoshi Ishibashi, Mari Umezu, Il-sung Jang, Yushi Ito, Norio Akaike
    Abstract:

    The noradrenaline (NA)-induced cation current was investigated in neurones freshly isolated from rat cardiac Parasympathetic Ganglia using the nystatin-perforated patch recording configuration. Under current-clamp conditions, NA depolarized the membrane, eliciting repetitive action potentials. NA evoked an inward cation current under voltage-clamp conditions at a holding potential of -60 mV. The NA-induced current was inhibited by extracellular Ca2+ or Mg2+, with a half-maximal concentration of 13 microM for Ca2+ and 1.2 mM for Mg2+. Cirazoline mimicked the NA response, and prazosin and WB-4101 inhibited the NA-induced current, suggesting the contribution of an alpha1-adrenoceptor. The NA-induced current was inhibited by U73122, a phospholipase C (PLC) inhibitor. The membrane-permeable IP3 receptor blocker xestospongin-C also blocked the NA-induced current. Furthermore, pretreatment with thapsigargin and BAPTA-AM could inhibit the NA response while KN-62, phorbol 12-myristate 13-acetate (PMA) and staurosporine had no effect. These results suggest that NA activates the extracellular Ca2+- and Mg2+-sensitive cation channels via alpha 1-adrenoceptors in neurones freshly isolated from rat cardiac Parasympathetic Ganglia. This activation mechanism also involves phosphoinositide breakdown, release of Ca2+ from intracellular Ca2+ stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in rat cardiac Ganglia.

Christer Owman - One of the best experts on this subject based on the ideXlab platform.