Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-7-29
pubmed:abstractText
The effect of glutamate and aspartate iontophoresis on extracellular pH was investigated in the turtle cerebellum in vitro. Both amino acids produced a rapid alkaline transient, typically followed by a prolonged acidification. These responses could be evoked in all layers of the cerebellum. Transition from bicarbonate to N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered media amplified the pH shifts. Similar alkaline-acid transients could be evoked in the molecular layer by electrical stimulation of the parallel fibers or the ipsilateral peduncle, or by superfusion of glutamate or aspartate. However, no alkaline shifts were evoked in the granular layer by either parallel fiber or peduncle stimulation. In contrast, the iontophoretically induced alkaline shifts were largest in the granular layer. Compared with the stimulus-evoked alkalinizations, the iontophoretic alkaline shifts were relatively insensitive to Mn2+ or Cd2+. These data suggest that the activity-dependent alkalinization of brain extracellular space is generated by a bicarbonate-independent mechanism related to excitatory synaptic transmission. The results are consistent with a flux of hydrogen ions through cationic channels, but do not support a direct role for voltage-dependent Ca2+ channels. In view of the sensitivity of ion channels to changes in external pH, and the magnitude of the amino acid-induced pH shifts, these results indicate that extracellular pH could play an important modulatory role in excitatory synaptic transmission.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
257-67
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1711651-Animals, pubmed-meshheading:1711651-Aspartic Acid, pubmed-meshheading:1711651-Bicarbonates, pubmed-meshheading:1711651-Cadmium, pubmed-meshheading:1711651-Calcium Channel Blockers, pubmed-meshheading:1711651-Cerebellum, pubmed-meshheading:1711651-Electric Stimulation, pubmed-meshheading:1711651-Extracellular Space, pubmed-meshheading:1711651-Female, pubmed-meshheading:1711651-Glutamates, pubmed-meshheading:1711651-Glutamic Acid, pubmed-meshheading:1711651-HEPES, pubmed-meshheading:1711651-Hydrogen-Ion Concentration, pubmed-meshheading:1711651-Ion Channel Gating, pubmed-meshheading:1711651-Ion Channels, pubmed-meshheading:1711651-Iontophoresis, pubmed-meshheading:1711651-Male, pubmed-meshheading:1711651-Manganese, pubmed-meshheading:1711651-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:1711651-Synaptic Transmission, pubmed-meshheading:1711651-Turtles
pubmed:year
1991
pubmed:articleTitle
Extracellular alkaline-acid pH shifts evoked by iontophoresis of glutamate and aspartate in turtle cerebellum.
pubmed:affiliation
Department of Neurosurgery, New York University Medical Center, NY 10016.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.