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Biomedical subjects

M Sasa

Publications and source records attributed to M Sasa.

At least 199 records · Page 11Linked to original sources
PubMed1986

Beta-receptor involvement in locus coeruleus-induced inhibition of spinal trigeminal nucleus neurons: microiontophoretic and HRP studies.

Microiontophoretic and HRP studies were performed on cats anesthetized with alpha-chloralose to determine whether or not the locus coeruleus (LC)- and noradrenaline (NA)-induced inhibition of relay neurons in the subnucleus oralis of the spinal trigeminal nucleus (STN) is mediated by beta-adrenergic receptors. The inhibition of orthodromic spike generation upon intracranial trigeminal nerve stimulation by LC conditioning stimulation and microiontophoretically applied NA (100-200 nA) was antagonized during microiontophoretic application of sotalol, a beta-adrenergic antagonist, but not affected by phentolamine, an alpha-adrenergic antagonist. When HRP at doses of 300-500 nA was applied for 5-15 min to the immediate vicinity of the STN relay or interneuron, which was electrophysiologically identified by stimulating the ipsilateral trigeminal nerve and contralateral medial lemniscus, the injection site was localized to an area 0.3 mm in diameter and HRP-reactive cells were found in the ipsilateral LC, dorsal raphe nucleus and periaqueductal gray ventral to the aqueduct. These results strongly suggest that NA released from the nerve terminals of LC cells inhibits transmission in the STN relay neuron via beta-adrenergic receptors.

Animals↗
PubMed1986

Excitation by dopamine D-2 receptor agonists, bromocriptine and LY 171555, in caudate nucleus neurons activated by nigral stimulation.

Electrophysiological studies using cats anesthetized with alpha-chloralose were carried out to determine whether or not the dopamine D-2 receptor mediates the excitation of the caudate nucleus (CN) neurons activated by stimulation of the substantia nigra (SN). Microiontophoretic application of domperidone (D-2 antagonist) produced a significant inhibition of spikes elicited by SN stimulation in 20 of 27 CN neurons. When bromocriptine and LY 171555 (D-2 agonists) were iontophoretically applied to the CN neurons in which the SN-induced spikes were inhibited by domperidone, an increase in spontaneous firing rate was observed in 18 of 20 neurons and all of 10 neurons tested, respectively. However, no alterations of firing occurred with bromocriptine or LY 171555 in any 7 neurons in which the SN-induced spikes were not affected by domperidone. The increase in firing rate by the D-2 agonists was apparently antagonized during simultaneous application of domperidone and haloperidol, but not affected during application of SCH 23390 (D-1 antagonist). These results strongly suggest that the spike generation of the CN neurons upon SN stimulation is mediated by the dopamine D-2 receptor.

Animals↗
PubMed1986

Effects of eperisone applied by microiontophoresis on neurons in the medial and lateral vestibular nuclei.

Electrophysiological studies were performed to elucidate the mechanism underlying the antivertigo action of eperisone, an antispastic drug, using cats anesthetized with alpha-chloralose. Iontophoretic application of eperisone up to 100 nA produced a dose-dependent inhibition of spike generation upon vestibular nerve stimulation in monosynaptic and polysynaptic neurons of the medial vestibular nucleus (MVN). The inhibition of neurons in the MVN was more prominent than that in the lateral vestibular nucleus. In addition, iontophoretically applied eperisone in doses of 50-100 nA inhibited the orthodromic spike elicited by vestibular nerve stimulation in the MVN monosynaptic neurons projecting to the abducens nucleus (ascending neuron), without affecting that in the MVN neurons projecting to the spinal cord (descending neuron). An inhibition of antidromic spike elicited by abducens nucleus stimulation in the MVN monosynaptic ascending neurons was observed in some cases during application of eperisone. These results suggest that eperisone predominantly inhibits synaptic transmission of the MVN ascending neurons.

Animals↗
PubMed1986

Activation of lateral vestibular nucleus neurons by iontophoretically applied phencyclidine.

Microiontophoretic studies were performed to elucidate the effects of phencyclidine (PCP) on neuronal activity in the lateral vestibular nucleus (LVN) of cats anesthetized with alpha-chloralose. Spikes elicited in the monosynaptic LVN neurons by vestibular nerve stimulation were not affected by iontophoretic application of PCP up to 100 nA, but they were blocked by atropine (30-50 nA). A dose-dependent increase in spontaneous firing during application of PCP was obtained in 11 of 15 monosynaptic neurons, in all of which firing was increased by iontophoretically applied acetylcholine (ACh). Simultaneous application of atropine completely inhibited the PCP- and ACh-induced increase in the firing without affecting the glutamate-induced firing. These results indicate that PCP acts on the LVN monosynaptic neurons receiving input from the vestibular nerve in a similar manner to ACh.

Acetylcholine↗
PubMed1986

Skin test and radioallergosorbent test with extracts of larval and adult midges of Tokunagayusurika akamusi Tokunaga (Diptera: Chironomidae) in asthmatic patients of the metropolitan area of Tokyo.

Prick test and radioallergosorbent test to extracts of larval and adult midges, Tokunagayusurika akamusi (Tokunaga) were done in randomly selected asthmatic patients in the metropolitan area of Tokyo, Japan. Thirty-eight percent of 303 asthmatic patients were prick-test positive to either larval or adult midges, and 32.4% of 105 asthmatic patients were positive to either extracts by RAST, while only one out of 20 normal individuals was positive to RAST. These positive rates in the asthmatic patients were the second to the positive rates of prick test and RAST using mite antigen. Antigens from midges seem to be the second important allergens in the metropolitan area of Tokyo.

Asthma↗
PubMed1985

Dopamine D-2 receptor-mediated excitation of caudate nucleus neurons from the substantia nigra.

Microiontophoretic studies using cats anesthetized with alpha-chloralose were performed to elucidate whether the excitatory response of caudate nucleus (CN) neurons upon stimulation of the pars compacta of the substantia nigra (SN) is mediated by the dopamine D-1 or D-2 receptor. There were rare convergent inputs from the SN and motor cortex (MC) in the CN neurons. Iontophoretic application of haloperidol and domperidone (dopamine D-2 receptor antagonist) produced dose-dependent inhibition of spikes elicited by SN stimulation in 25 of 42 and 50 of 82 CN neurons, respectively, however, no alterations of spikes elicited by MC stimulation occurred in any 11 neurons tested. Iontophoretically applied SCH 23390 (D-1 antagonist) did not inhibit the SN-induced spikes in any CN neurons, of which spikes were inhibited by domperidone. These results suggest that the SN-induced spikes are mediated by dopamine, which acts on postsynaptic D-2 receptors.

Animals↗
PubMed1985

Commissural and ipsilateral internuclear connection of vestibular nuclear complex of the cat.

Commissural and ipsilateral intrinsic connections of the vestibular nuclear complex of cats were investigated using retrograde transport of horseradish peroxidase (HRP). HRP was microiontophoretically injected into limited areas (0.2-0.5 mm in diameter) of the respective vestibular nuclei. In the commissural connections, major fibers were observed between the bilateral superior vestibular nuclei (SVN) and between the bilateral descending vestibular nuclei (DVN); a moderate number of fibers was found from the medial vestibular nucleus (MVN) to the contralateral MVN, SVN and lateral vestibular nucleus (LVN) and from the DVN to the contralateral LVN. Minor commissural connections were detected between the bilateral LVN. The ipsilateral internuclear connections of the vestibular nuclear complex were: (1) from the LVN, MVN and DVN to the SVN, (2) from the MVN and DVN to the LVN and (3) from the MVN to the DVN. Minor ipsilateral intrinsic connections were found from the SVN to the MVN.

Animals↗
PubMed1985

Inhibition from locus coeruleus of nucleus accumbens neurons activated by hippocampal stimulation.

Electrophysiological studies using rats were performed to examine the influence of locus coeruleus (LC) on nucleus accumbens (Acc) neurons. Spike generation by hippocampal stimulation was inhibited by both LC conditioning stimulation and iontophoretic application of noradrenaline, but spikes elicited by stimulation of parafascicular nucleus of thalamus were rarely affected by LC conditioning stimulation or noradrenaline. The LC-induced inhibition was antagonized by iontophoretic sotalol, but not by phentolamine, suggesting that noradrenaline derived from the LC inhibits the Acc neurons receiving input from the hippocampus, probably acting on a beta-adrenergic receptor.

Animals↗
PubMed1985

A noradrenaline-induced inhibition from locus coeruleus of nucleus accumbens neuron receiving input from hippocampus.

Electrophysiological studies using rats anesthetized with chloral hydrate were performed to determine whether or not noradrenaline originating in the locus coeruleus (LC) produces a beta-receptor-mediated inhibition of the nucleus accumbens (Acc) neurons receiving input from the hippocampus (HPC). When conditioning stimuli were applied to the LC preceding a test stimulus to the HPC, an inhibition of spike generation with HPC stimulation was observed during 20-100 msec of the conditioning-test time interval. This inhibition was observed when the stimulating electrode was located in the LC or its immediate vicinity. The spike generation upon HPC stimulation was also inhibited by iontophoretic application of noradrenaline, and the inhibition was antagonized by iontophoretically applied sotalol, a beta-adrenergic blocker, but not by phentolamine, an alpha-adrenergic blocker. These results suggest that noradrenaline derived from the LC produces a beta-receptor-mediated inhibition of the Acc neurons receiving input from the HPC.

Animals↗
PubMed1985

Effects of adenosine triphosphate on neuron activities in the lateral and medial vestibular nuclei.

Electrophysiological studies were carried out to elucidate the effects of adenosine triphosphate (ATP) on the vestibular nuclei of cats anesthetized with alpha-chloralose. Intravenous (i.v.) administration of ATP in doses of 0.5-2.0 mg/kg produced an enhancement of spike generation with vestibular nerve stimulation and spontaneous firing in both monosynaptic and polysynaptic neurons in the lateral vestibular nucleus (LVN) as well as in the medial vestibular nucleus (MVN). These effects of ATP, however, were not dose-dependent. In contrast, iontophoretic application of ATP up to 200 nA had only negligible effect on spike generation of mono- and polysynaptic neurons in the LVN and those in the MVN upon vestibular nerve stimulation. The results suggest that the enhancement of neuron activities in the vestibular nuclei following i.v. injection of ATP is due to the indirect effect probably resulting from an increase in blood flow in the brain, but not to a direct, excitatory effect of the drug on the neurons themselves.

Action Potentials↗
PubMed1984

Serotonin-mediated inhibition from dorsal raphe nucleus of neurons in dorsal lateral geniculate and thalamic reticular nuclei.

Electrophysiological studies using rats anesthetized with chloral hydrate were performed to determine whether or not serotonin originating in the dorsal raphe nucleus (DR) acts as an inhibitory transmitter or neuromodulator on neurons of the dorsal lateral geniculate nucleus (LGN) and neurons located in the thalamic reticular nucleus (TRN) immediately rostral to the dorsal LGN. In the LGN, conditioning stimuli applied to the DR preceding test stimulus to the optic tract and visual cortex inhibited orthodromic and antidromic spikes in about one-third of the relay neurons and in more than half of the intrageniculate interneurons. Conditioning stimulation of the DR also produced an inhibition of the spikes elicited by stimulation of the optic tract and visual cortex of at least three-quarters of the TRN neurons. Iontophoretic application of serotonin (25 nA) inhibited the orthodromic spikes of the LGN relay neuron and TRN neuron. A close correlation was observed between the effects of DR conditioning stimulation and iontophoretic serotonin in the same neurons. The inhibition with DR conditioning stimulation and iontophoretically applied serotonin was antagonized during iontophoretic application of methysergide (15-40 nA), a serotonin antagonist. These results strongly suggest that serotonin derived from the DR acts on the LGN and TRN neurons as an inhibitory transmitter or neuromodulator to inhibit transmission in these nuclei.

Animals↗
PubMed1984

Effects of ethanol applied by electrosmosis on neurons in the lateral and medial vestibular nuclei.

Electrophysiological studies were performed to elucidate the effects of ethanol on neuron activities in the lateral vestibular nucleus (LVN) and medial vestibular nucleus (MVN) of cats using an electrosmotic and microiontophoretic method. The LVN and MVN neurons were classified into two types according to the firing pattern and latency of the first spike with vestibular nerve stimulation: monosynaptic and polysynaptic neurons. Electrosmotic application of ethanol up to 200 nA produced a dose-dependent inhibition of spikes of the LVN monosynaptic neurons with vestibular nerve stimulation and iontophoretically applied glutamate, but no significant alterations of the spikes of the LVN polysynaptic neurons. Acetylcholine-induced firing in the LVN monosynaptic neurons was also inhibited by ethanol. In the MVN, spike generation of the monosynaptic and polysynaptic neurons with vestibular nerve stimulation and iontophoretically applied glutamate remained unaltered with ethanol up to 200 nA. These results indicate that ethanol predominantly inhibits synaptic transmission of the LVN monosynaptic neurons, probably by acting on the postsynaptic cell bodies.

Acetylcholine↗
PubMed1984

Internuclear fiber connections of vestibular nuclear complex. A horseradish peroxidase study.

Internuclear fiber connections among the superior (SVN), lateral (LVN), medial (MVN) and descending (DVN) vestibular nuclei were examined in cats using retrograde transport of horseradish peroxidase (HRP). HRP was microiontophoretically applied in the respective vestibular nucleus at doses of 300-500 nA for 5-10 min, and with the treatment the HRP injection site was limited to 0.2-0.5 mm in diameter within the nucleus. Major commissural connections were found between the bilateral SVN and between the bilateral DVN. Minor commissural connections were observed from MVN to SVN, LVN and MVN, from DVN to LVN, and from LVN to the contralateral LVN. In the ipsilateral vestibular nuclei, fiber connections were found from LVN to SVN, from MVN to SVN, LVN and DVN, and from DVN to SVN and LVN.

Animals↗
PubMed1984

Experimental vestibular pharmacology: a minireview with special reference to neuroactive substances and antivertigo drugs.

Neurotransmitters and neuromodulators involved in the function of vestibular nuclei were reviewed with special reference to drugs used for treatment of motion sickness and vertigo. Biochemical, histochemical and electrophysiological studies have demonstrated that acetylcholine is a transmitter candidate from the afferent vestibular nerve to the lateral vestibular nucleus (LVN), because acetylcholine satisfies most criteria for a chemical transmitter in the central nervous system. It is unlikely, however, that monoamines such as noradrenaline, dopamine and serotonin are transmitters in the vestibular neurons, since cell bodies and nerve terminals containing the monoamines have not been detected yet in the vestibular nuclei. Although histamine and H1-receptor blockers inhibit neuron activities in the vestibular nuclei, it is unclear at present whether histaminergic system is directly related to the function of vestibular neurons. It has been established that GABA is an inhibitory transmitter from the cerebellar Purkinje cells to the LVN neurons. Diazepam is considered to enhance the GABA effect on the LVN, thereby modifying the vestibular neuronal firing. Enkephalin-containing cell bodies and nerve terminals are found in the medial vestibular nucleus, and a few substance P-containing neurons have been observed in the vestibular nuclei. However, the functional role of these peptides on the vestibular system remains to be determined. Unlike histamine H1-receptor blockers, vasodilators such as cinnarizine, ifenprodil and adenosine triphosphate, which are effective in treatment of vertigo, produce an enhancement of responsiveness of neuron activities in the vestibular nuclei, probably as a result of an increase in blood flow in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Electrophysiological and HRP studies on feedback loop between inferior olivary nucleus and lateral vestibular nucleus in the cat.

The role of input from the inferior olivary nucleus (IO) of decerebellate cats were studied on the lateral vestibular nucleus (LVN) neurons which were monosynaptically activated by vestibular nerve stimulation. Out of 168 monosynaptic neurons, test stimuli to the contralateral IO elicited a monosynaptic spike in 43 neurons and an antidromic spike in 9 neurons. Conditioning stimulus applied to the IO preceding vestibular nerve stimulation produced an inhibition of spike generation in 22 other LVN neurons upon the nerve stimulation. When horseradish peroxidase (HRP) was iontophoretically applied into the immediate vicinity of the LVN monosynaptic neurons, HRP-reactive cells were found in the dorsal cap and beta-nucleus of the contralateral IO. These results suggest that the LVN neurons monosynaptically activated by vestibular nerve stimulation receive both excitation and inhibition from the IO.

Action Potentials↗