The Experts below are selected from a list of 30 Experts worldwide ranked by ideXlab platform

C K Atterwill - One of the best experts on this subject based on the ideXlab platform.

  • nerve growth factor ngf receptors on mast cells effects of the cholinergic neurotoxin Ethylcholine Mustard Aziridinium ion ecma
    Neurotoxicology, 1992
    Co-Authors: H B Johnston, C K Atterwill
    Abstract:

    The effects of nerve growth factor (NGF) on rat peritoneal mast cells were studied as a model for delineating the potential actions of the cholinergic neurotoxin ethyl choline Mustard Aziridinium (ECMA) on cholinergic neuronal NGF receptors. Both NGF and compound 48/80 (a polycationic secretagogue) were used to induce histamine release from a mixed population of rat peritoneal cells in vitro. NGF induced a dose-dependent release of up to 80% of the total cellular content (160% of endogenous release) in the presence of L-alpha-phosphatidyl serine (10 micrograms/ml) at concentrations of 0.1-10 micrograms/ml. Compound 40/80 also elicited comparable release of histamine over a concentration range of 1-10 micrograms/ml. ECMA had no effect on endogenous histamine release and was also shown to partially block the NGF induced histamine release at a concentration of 6 microM and 12.5 microM, and significantly at 50 microM (50 microM blocking up to 60% of the release). ECMA did not affect the 48/80 induced release. However, preincubation of the cells with ECMA (2 hr 37 degrees C) followed by replacement with fresh medium did not affect NGF induced histamine release. This suggests that although ECMA can alkylate NGF it probably does not inactivate the receptor in this peripheral model. Ouabain (1-10 mM) decreased histamine release by 25% supporting the proposed links between NGF receptor mediated events in neurones and the sodium pump.

Takeshi Kubo - One of the best experts on this subject based on the ideXlab platform.

  • role of cholinergic mossy fibers in medial vestibular and prepositus hypoglossal nuclei in vestibular compensation
    Neuroscience, 2001
    Co-Authors: Munehisa Fukushima, Noriaki Takeda, Tadashi Kitahara, Takanori Saika, A Uno, Takeshi Kubo
    Abstract:

    Several lines of evidence have suggested that acetylcholine is a possible neurotransmitter/neuromodulator involved in vestibular compensation. Further, the central vestibular system, oculo- and spino-motor neurons and peripheral vestibular efferents contain abundant cholinergic neurons. However, details of cholinergic effective sites during vestibular compensation remain to be clarified. In the present study, we selectively damaged rat vestibulo-floccular and vestibulo-uvulonodular cholinergic mossy fibers using Ethylcholine Mustard Aziridinium ions. In these treated animals, unilateral labyrinthectomy caused more severe vestibulo-ocular deficits especially during the initial stage. From these findings we suggest that vestibulo-floccular and vestibulo-uvulonodular cholinergic mossy fibers contribute to the restoration of a balance between intervestibular nuclear activities for the induction of vestibular compensation during the initial stage.

Masamichi Satoh - One of the best experts on this subject based on the ideXlab platform.

  • roles of endogenous cholinergic neurons in the induction of long term potentiation at hippocampal mossy fiber synapses
    Neuroscience Research, 1994
    Co-Authors: Takehiko Maeda, Shuji Kaneko, Masamichi Satoh
    Abstract:

    To evaluate the functional role of endogenous acetylcholine (ACh) in the induction of long-term potentiation (LTP) at mossy fiber-CA3 synapses, the influence of cholinergic hypofunction on it was investigated. Administration of a cholinergic neurotoxin, Ethylcholine Mustard Aziridinium ion (AF64A; 5 nmol, i.c.v.), to guinea pigs one week prior to preparing slices resulted in a significant decrease in the magnitude of LTP, associated with a significant decrease in cholineacetyltransferase (ChAT) activity and the number of ChAT immunoreactive cells in the hippocampal slices. Bath-application of a cholinesterase inhibitor, physostigmine at 0.1 μM and 10 μM, attenuated and augmented, respectively, the magnitude of LTP in slices prepared from vehicle-treated animals (naive slices), whereas that in slices prepared from AF64A-treated animals (lesioned slices) was not significantly affected by physostigmine at any concentration tested. The induction of LTP in naive slices was inhibited or facilitated by a muscarinic M1 antagonist pirenzepine (1 μM) and by an M2 antagonist AF-DX 116 (1 μM) alone, respectively, whereas that in lesioned slices was not significantly changed by either of them. Furthermore, bath-applied carbachol (CCh) at 0.01–10 μM augmented the magnitude of LTP in lesioned slices, whereas the induction of LTP in naive slices was inhibited and facilitated by CCh at 0.01–0.1 μM and 1–10 μM, respectively, as reported previously. Such an augmentation of LTP by CCh was reversed by pirenzepine, but not by AF-DX 116. These observations suggest that AF64A induces the defect in ACh release and the hypofunction of M2 receptors, but not of M1, at least during the induction of LTP at mossy fiber-CA3 synapses. Thus, it is conceivable that endogenous ACh plays a facilitatory and inhibitory role through muscarinic M1 and M2 receptors in the induction of LTP in the mossy fiber-CA3 pathway.

H B Johnston - One of the best experts on this subject based on the ideXlab platform.

  • nerve growth factor ngf receptors on mast cells effects of the cholinergic neurotoxin Ethylcholine Mustard Aziridinium ion ecma
    Neurotoxicology, 1992
    Co-Authors: H B Johnston, C K Atterwill
    Abstract:

    The effects of nerve growth factor (NGF) on rat peritoneal mast cells were studied as a model for delineating the potential actions of the cholinergic neurotoxin ethyl choline Mustard Aziridinium (ECMA) on cholinergic neuronal NGF receptors. Both NGF and compound 48/80 (a polycationic secretagogue) were used to induce histamine release from a mixed population of rat peritoneal cells in vitro. NGF induced a dose-dependent release of up to 80% of the total cellular content (160% of endogenous release) in the presence of L-alpha-phosphatidyl serine (10 micrograms/ml) at concentrations of 0.1-10 micrograms/ml. Compound 40/80 also elicited comparable release of histamine over a concentration range of 1-10 micrograms/ml. ECMA had no effect on endogenous histamine release and was also shown to partially block the NGF induced histamine release at a concentration of 6 microM and 12.5 microM, and significantly at 50 microM (50 microM blocking up to 60% of the release). ECMA did not affect the 48/80 induced release. However, preincubation of the cells with ECMA (2 hr 37 degrees C) followed by replacement with fresh medium did not affect NGF induced histamine release. This suggests that although ECMA can alkylate NGF it probably does not inactivate the receptor in this peripheral model. Ouabain (1-10 mM) decreased histamine release by 25% supporting the proposed links between NGF receptor mediated events in neurones and the sodium pump.

William A. Corrigall - One of the best experts on this subject based on the ideXlab platform.

  • The pedunculopontine tegmental nucleus and the role of cholinergic neurons in nicotine self-administration in the rat: a correlative neuroanatomical and behavioral study
    Neuroscience, 2000
    Co-Authors: A.j Lança, K. L. Adamson, Kathleen M. Coen, B. L. C. Chow, William A. Corrigall
    Abstract:

    The objective of this study was to determine whether the pedunculopontine tegmental nucleus plays a role in the maintenance of nicotine self-administration, and whether the ascending cholinergic projection from this nucleus to midbrain dopamine neurons in the ventral tegmental area might be involved. Studies were done with rats trained to self-administer nicotine intravenously. Self-administration was examined before and after the pedunculopontine tegmental nucleus was lesioned with the Ethylcholine Mustard Aziridinium ion, a selective cholinergic toxin. Lesions were assessed qualitatively and quantitatively in histological sections stained for either nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry to identify cholinergic neurons, or for Nissl. Self-administration was also tested after an acute manipulation in which microinfusions of the nicotinic cholinergic antagonist dihydro-beta-erythroidine were made into the pedunculopontine tegmentum. Infusions of neurotoxin into the pedunculopontine tegmentum reduced nicotine self-administration behaviour when tested weeks later. Toxin treatment reduced the number of cholinergic neurons in the tegmentum, while largely sparing the non-cholinergic population in this area. Lesions were limited to the pedunculopontine area and did not extend to the neighboring laterodorsal tegmental nucleus or to the substantia nigra. Acute manipulation of the pedunculopontine tegmental nucleus with microinfusions of dihydro-beta-erythroidine also produced an attenuation of nicotine self-administration. Collectively these data show that the pedunculopontine tegmental nucleus is part of the neuronal circuitry mediating nicotine self-administration, and that the population of cholinergic neurons is likely a critical element.