Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-3-9
pubmed:abstractText
Activation of presynaptic inhibitory receptors or high-frequency synaptic stimulation normally inhibits excitatory synaptic transmission by reducing transmitter release. We have explored the interactions between these two pathways for reducing synaptic strength and found that for synapses stimulated at high rates, agonists of the GABA(B) receptor become excitatory and strengthen transmission. At an auditory glutamatergic synapse featuring strong synaptic depression, the GABA(B) agonist baclofen reduced by 90% postsynaptic currents elicited at low frequency. By contrast, synaptic currents elicited at high frequencies were 5-fold larger in baclofen and had a markedly increased likelihood of firing well-timed postsynaptic action potentials. Presynaptic GABA(B) receptors may thus regulate transmitter release to enable sustained transmission at higher stimulus frequencies, thereby extending the dynamic range of neural circuits.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0896-6273
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-41
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Enhancement of synaptic efficacy by presynaptic GABA(B) receptors.
pubmed:affiliation
Neuroscience Training Program, University of Wisconsin-Madison, 53706, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.