1994 Fiscal Year Final Research Report Summary
Functional roles of co-transmitters in brainsten cholinergic neurons
| Project/Area Number |
05680725
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
神経・脳内生理学
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| Research Institution | Fukushima Medical College |
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Principal Investigator |
KAYAMA Yukihiko Fukushima Medical College, Dept.Physiol., Professor, 医学部, 教授 (30035224)
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| Co-Investigator(Kenkyū-buntansha) |
NINOMIYA Yaeko Fukushima Medical College, Dept.Physiol., Assistant, 医学部, 助手 (00136970)
KOYAMA Yoshimasa Fukushima Medical College, Dept.Physiol., Lecturer, 医学部, 講師 (80183812)
ITO Seisho Fukushima Medical College, Dept.Physiol., Associate Professor, 医学部, 助教授 (30004609)
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| Project Period (FY) |
1993 – 1994
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| Keywords | laterodorsal tegmental nucleus / acetylcholine / substance P / nitric oxide / co-transmitters / thalamus / cerebral blood flow / ascending activating system |
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| Research Abstract |
Cholinergic neurons gathering tightly in the laterodorsal tegmental nucleus (LDT) of the brainstem have nitric oxide (NO) and/or substance P (SP) as co-transmitters. The present study examined whether these co-transmitters released from axon terminals or varicosities, and what effects they gave to postsynaptic targets.
In the previous study we had shown that LDT stimulation produced excitation of thalamic relay neurons which received direct projection of the cholinergic neurons. We examined in urethane-anesthetized rats, using a laser-Doppler flow meter, how the same LDT stimulation affected cerebral blood flow in the thalamus, since the co-transmitters have strong action on the blood vessels. An increase of the blood flow was observed consistently starting within several seconds after the onset of LDT stimulation and continuing about 1 minute after the stimulation. The increase was reduced by administration of scopolamine, a muscarinic antagonist, but the treatment did not block it com
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pletely.
Whether NO concentration in the thalamus increased after the LDT stimulation was also examined in urethane-anesthetized rats, using electrochemical electrode sensitive specifically to NO (developed in Shionogi Research Laboratories) . The NO concentration increased transiently just after the stimulation only when the stimulating electrode was inserted in the LDT ; the stronger stimulation produced the stronger increase. The results show that NO is released from the axon terminals and/or varicosities by the excitation of LDT neurons.
Postsynaptic actions of the co-transmitters were examined in in vitro slice preparations of the rat thalamus. Most thalamic neurons were depolarized by application of acetylcholine (ACh) . When SP was applied simultaneously with ACh, the depolarization was increased in some neurons, but was cancelled to produce no resting potential change in others. It is thus suggested that SP as a co-transmitter modifies the action of main transmitter ACh, but tha modification differs from neuron to neuron. Actions of NO was not demonstrated clearly. Less
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