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Yasuteru Shiroshita - One of the best experts on this subject based on the ideXlab platform.

  • the tachykinin NK1 Receptor Antagonist gr205171 abolishes the retching activity of neurons comprising the central pattern generator for vomiting in dogs
    Neuroscience Research, 1999
    Co-Authors: Hiroyuki Fukuda, Emi Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Abstract Tachykinin NK1 Receptor Antagonists are known to act centrally and to have broad-spectrum antiemetic effects, but their precise site of action has not yet been defined. To identify this site, the effects of the NK1 Receptor Antagonist GR205171 on the activities of neurons comprising the central pattern generator (CPG) for vomiting were observed in decerebrate paralyzed dogs. A non-respiratory neuron in each of nine dogs was considered to be a CPG neuron based on its response to abdominal vagal stimulation, its location in the CPG area in the reticular formation dorsomedial to the retrofacial nucleus, its firing patterns in prodromal and retching phases and its response to apomorphine. In response to vagal stimulation at 3–10 Hz, the firing of these neurons transiently increased at the onset of stimulation (fast component), gradually increased again (slow component), and finally developed into rhythmic bursts synchronous with retching bursts of the phrenic and abdominal muscle nerves. GR205171 (25–50 μg/kg, i.v.) abolished the slow component and retching bursts in the neurons, and the retching activities of both nerves, but did not change the fast component. The responses of these neurons to repetitive pulse–train vagal stimulation exhibited a vigorous ‘wind-up’ and finally developed into retching bursts. Both the ‘wind-up’ phenomenon and retching bursts disappeared after the application of GR205171. These results suggest that the site of the antiemetic action of NK1 Receptor Antagonists is located in the CPG or in the pathway connecting the solitary nucleus to the CPG.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs
    Brain Research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg−1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml−1, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs.
    Brain research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05-0.7 mg kg-1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml-1, 30 microliters) into the 4th ventricle abolished retching, with latencies in excess of 120 min These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

Hiroyuki Fukuda - One of the best experts on this subject based on the ideXlab platform.

  • the tachykinin NK1 Receptor Antagonist gr205171 abolishes the retching activity of neurons comprising the central pattern generator for vomiting in dogs
    Neuroscience Research, 1999
    Co-Authors: Hiroyuki Fukuda, Emi Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Abstract Tachykinin NK1 Receptor Antagonists are known to act centrally and to have broad-spectrum antiemetic effects, but their precise site of action has not yet been defined. To identify this site, the effects of the NK1 Receptor Antagonist GR205171 on the activities of neurons comprising the central pattern generator (CPG) for vomiting were observed in decerebrate paralyzed dogs. A non-respiratory neuron in each of nine dogs was considered to be a CPG neuron based on its response to abdominal vagal stimulation, its location in the CPG area in the reticular formation dorsomedial to the retrofacial nucleus, its firing patterns in prodromal and retching phases and its response to apomorphine. In response to vagal stimulation at 3–10 Hz, the firing of these neurons transiently increased at the onset of stimulation (fast component), gradually increased again (slow component), and finally developed into rhythmic bursts synchronous with retching bursts of the phrenic and abdominal muscle nerves. GR205171 (25–50 μg/kg, i.v.) abolished the slow component and retching bursts in the neurons, and the retching activities of both nerves, but did not change the fast component. The responses of these neurons to repetitive pulse–train vagal stimulation exhibited a vigorous ‘wind-up’ and finally developed into retching bursts. Both the ‘wind-up’ phenomenon and retching bursts disappeared after the application of GR205171. These results suggest that the site of the antiemetic action of NK1 Receptor Antagonists is located in the CPG or in the pathway connecting the solitary nucleus to the CPG.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs
    Brain Research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg−1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml−1, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs.
    Brain research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05-0.7 mg kg-1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml-1, 30 microliters) into the 4th ventricle abolished retching, with latencies in excess of 120 min These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

Sandra E. File - One of the best experts on this subject based on the ideXlab platform.

  • Anxiolytic actions of the substance P (NK1) Receptor Antagonist L-760735 and the 5-HT1A agonist 8-OH-DPAT in the social interaction test in gerbils
    Brain research, 2001
    Co-Authors: Survjit Cheeta, Nadia M. J. Rupniak, Sonia Tucci, J Sandhu, A.r Williams, Sandra E. File
    Abstract:

    The gerbil social interaction test has previously detected anxiolytic effects of nicotine and diazepam. In the present study, the high affinity substance P (NK1) Receptor Antagonist L-760735 (3 mg/kg) significantly increased the time spent in social interaction, whereas its low affinity analogue L-781773 (3 mg/kg) was without effect. Diazepam (0.1 mg/kg) and the 5-HT1A Receptor agonist 8-OH-DPAT (0.003 and 0.01 mg/kg) also increased social interaction, whereas an acute dose of the selective serotonin re-uptake inhibitor fluoxetine (10 mg/kg) decreased the time spent in social interaction. Diazepam (0.1 mg/kg) significantly increased locomotor activity, but this effect was independent of the increase in social interaction. The other drugs tested were without effect on locomotor activity. The present findings suggest that the gerbil social interaction may well provide a useful assay for detecting both anxiolytic and anxiogenic compounds, and suggests that the high affinity NK1 Receptor Antagonist L-760735 may prove to be useful as an anxiolytic therapy.

  • NKP608, an NK1 Receptor Antagonist, has an anxiolytic action in the social interaction test in rats
    Psychopharmacology, 2000
    Co-Authors: Sandra E. File
    Abstract:

    Rationale: Evidence is starting to accumulate that NK1 Receptor Antagonists might have anxiolytic effects in animal tests and in patients. Objective: To examine the effects of NKP608, a substance P Antagonist acting at NK1 Receptors, in various conditions of the social interaction test of anxiety and to determine its effects after 3 and 6 weeks of treatment. Methods: Rats were tested after vehicle, 0.01 or 0.1 mg/kg PO in three conditions of the social interaction test that varied in the level of anxiety generated. Thus pairs of rats were tested in an arena with which they were unfamiliar that was lit by high (HU) or low (LU) light and in the condition that generated the lowest level of anxiety, i.e. an arena with which they were familiar, lit by low light (LF). They were also tested after 3 and 6 weeks of treatment with 0.03 mg/kg and after 24 h withdrawal from these chronic treatments. Results: NKP608 had significant anxiolytic effects at 0.01, 0.03 and 0.1 mg/kg PO in the HU and LU test conditions, but was without effect in the LF condition, except for an increased incidence of bite attacks at 0.1 mg/kg. The anxiolytic effect of 0.03 mg/kg remained after 3 weeks of chronic treatment and there was no anxiogenic effect after 24 h of drug withdrawal. Following 6 weeks of chronic treatment (0.03 mg/kg per day), tolerance had developed, but no anxiogenic withdrawal effect was seen 24 h after the last dose. Conclusions: These results provide further evidence that substance P may play a role in mediating states of anxiety and suggest that the selective NK1 Receptor Antagonist NKP608 may prove a useful anxiolytic compound.

Tomoshige Koga - One of the best experts on this subject based on the ideXlab platform.

  • the tachykinin NK1 Receptor Antagonist gr205171 abolishes the retching activity of neurons comprising the central pattern generator for vomiting in dogs
    Neuroscience Research, 1999
    Co-Authors: Hiroyuki Fukuda, Emi Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Abstract Tachykinin NK1 Receptor Antagonists are known to act centrally and to have broad-spectrum antiemetic effects, but their precise site of action has not yet been defined. To identify this site, the effects of the NK1 Receptor Antagonist GR205171 on the activities of neurons comprising the central pattern generator (CPG) for vomiting were observed in decerebrate paralyzed dogs. A non-respiratory neuron in each of nine dogs was considered to be a CPG neuron based on its response to abdominal vagal stimulation, its location in the CPG area in the reticular formation dorsomedial to the retrofacial nucleus, its firing patterns in prodromal and retching phases and its response to apomorphine. In response to vagal stimulation at 3–10 Hz, the firing of these neurons transiently increased at the onset of stimulation (fast component), gradually increased again (slow component), and finally developed into rhythmic bursts synchronous with retching bursts of the phrenic and abdominal muscle nerves. GR205171 (25–50 μg/kg, i.v.) abolished the slow component and retching bursts in the neurons, and the retching activities of both nerves, but did not change the fast component. The responses of these neurons to repetitive pulse–train vagal stimulation exhibited a vigorous ‘wind-up’ and finally developed into retching bursts. Both the ‘wind-up’ phenomenon and retching bursts disappeared after the application of GR205171. These results suggest that the site of the antiemetic action of NK1 Receptor Antagonists is located in the CPG or in the pathway connecting the solitary nucleus to the CPG.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs
    Brain Research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg−1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml−1, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs.
    Brain research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05-0.7 mg kg-1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml-1, 30 microliters) into the 4th ventricle abolished retching, with latencies in excess of 120 min These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

N Furukawa - One of the best experts on this subject based on the ideXlab platform.

  • the tachykinin NK1 Receptor Antagonist gr205171 abolishes the retching activity of neurons comprising the central pattern generator for vomiting in dogs
    Neuroscience Research, 1999
    Co-Authors: Hiroyuki Fukuda, Emi Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Abstract Tachykinin NK1 Receptor Antagonists are known to act centrally and to have broad-spectrum antiemetic effects, but their precise site of action has not yet been defined. To identify this site, the effects of the NK1 Receptor Antagonist GR205171 on the activities of neurons comprising the central pattern generator (CPG) for vomiting were observed in decerebrate paralyzed dogs. A non-respiratory neuron in each of nine dogs was considered to be a CPG neuron based on its response to abdominal vagal stimulation, its location in the CPG area in the reticular formation dorsomedial to the retrofacial nucleus, its firing patterns in prodromal and retching phases and its response to apomorphine. In response to vagal stimulation at 3–10 Hz, the firing of these neurons transiently increased at the onset of stimulation (fast component), gradually increased again (slow component), and finally developed into rhythmic bursts synchronous with retching bursts of the phrenic and abdominal muscle nerves. GR205171 (25–50 μg/kg, i.v.) abolished the slow component and retching bursts in the neurons, and the retching activities of both nerves, but did not change the fast component. The responses of these neurons to repetitive pulse–train vagal stimulation exhibited a vigorous ‘wind-up’ and finally developed into retching bursts. Both the ‘wind-up’ phenomenon and retching bursts disappeared after the application of GR205171. These results suggest that the site of the antiemetic action of NK1 Receptor Antagonists is located in the CPG or in the pathway connecting the solitary nucleus to the CPG.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs
    Brain Research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg−1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml−1, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.

  • The tachykinin NK1 Receptor Antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs.
    Brain research, 1998
    Co-Authors: Hiroyuki Fukuda, E. Nakamura, N Furukawa, Tomoshige Koga, Yasuteru Shiroshita
    Abstract:

    Tachykinin NK1 Receptor Antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 Receptor Antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05-0.7 mg kg-1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml-1, 30 microliters) into the 4th ventricle abolished retching, with latencies in excess of 120 min These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.