Linked Life Data

2905191

Source:http://linkedlifedata.com/resource/pubmed/id/2905191

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-2-21
pubmed:abstractText
Excitatory amino acid (EAA) receptors are present in the nucleus tractus solitarii (NTS), and there is growing evidence that L-glutamate (L-Glu) may activate neurons in this region to precipitate changes in autonomic discharge. To evaluate the potential role of EAA agonists in synaptic transmission in NTS, we studied the responses of single units in an in vitro brain slice preparation of NTS to electrical stimulation of one or both solitary tracts (TS) before, during and after superfusion with selected EAA antagonists. Dose-response studies demonstrated that the synaptic input to NTS units was substantially blocked by 2-amino-5-phosphonovaleric acid (APV) at perfusion concentrations of 1 mM, by kynurenic acid (KYN) at 10 mM, and glutamate diethylester (GDEE) at 10 mM. Using these concentrations, we examined the responses of single NTS neurons to afferent input from ipsilateral and contralateral TS stimulation before, during and after perfusion with each antagonist. KYN inhibited afferent input from one TS but not the other in 7 of 13 cells tested, inhibited both inputs in 4, and caused differential augmentation of input in two. APV caused differential inhibition of the two inputs in 4 of 9 cells tested, differential excitation in 1 and inhibition of both inputs in one. GDEE caused differential inhibition in 4 of 9 cells tested, differential excitation in 3 and inhibition of both inputs in one. When inputs from a single TS were examined, those blocked by APV were always blocked by KYN (5 of 16 inputs tested); there was overlap between the blocking effects of KYN and GDEE (4 of 12 inputs tested) and occasionally of APV and GDEE (one of 12 inputs tested). We also observed differential blocking effects of these agents on single inputs to the same neuron. Evoked responses were reduced or enhanced by only one of the two agents for 5 of 16 inputs tested with KYN and APV, 4 of 12 tested with KYN and GDEE, and 7 of 12 tested with APV and GDEE. The average reduction in synaptically evoked responses caused by blocking doses of antagonist was 85 +/- 6% for KYN, 63 +/- 28% for APV and 68 +/- 10% for GDEE. These data indicate that all 3 major EAA antagonists can selectively inhibit electrically evoked afferent input to NTS neurons and suggest a role for specific EAA receptors in mediating input to these neurons over different afferent pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
456
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
333-43
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2905191-2-Amino-5-phosphonovalerate, pubmed-meshheading:2905191-Action Potentials, pubmed-meshheading:2905191-Animals, pubmed-meshheading:2905191-Electric Stimulation, pubmed-meshheading:2905191-Functional Laterality, pubmed-meshheading:2905191-Glutamates, pubmed-meshheading:2905191-Kynurenic Acid, pubmed-meshheading:2905191-Male, pubmed-meshheading:2905191-Medulla Oblongata, pubmed-meshheading:2905191-Neurotransmitter Agents, pubmed-meshheading:2905191-Rats, pubmed-meshheading:2905191-Rats, Inbred Strains, pubmed-meshheading:2905191-Receptors, Amino Acid, pubmed-meshheading:2905191-Receptors, Cell Surface, pubmed-meshheading:2905191-Reference Values, pubmed-meshheading:2905191-Synapses, pubmed-meshheading:2905191-Synaptic Transmission, pubmed-meshheading:2905191-Valine
pubmed:year
1988
pubmed:articleTitle
Excitatory amino acid receptors intrinsic to synaptic transmission in nucleus tractus solitarii.
pubmed:affiliation
Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City 52242.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't