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Developmental changes in release properties of the CA3-CA1 glutamate synapse in rat hippocampus.

Wasling, Pontus, 1970 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
Hanse, Eric, 1962 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
Gustafsson, Bengt, 1946 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
 (creator_code:org_t)
American Physiological Society, 2004
2004
Engelska.
Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 92:5, s. 2714-24
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Developmental changes in release probability (Pr) and paired-pulse plasticity at CA3-CA1 glutamate synapses in hippocampal slices of neonatal rats were examined using field excitatory postsynaptic potential (EPSP) recordings. Paired-pulse facilitation (PPF) at these synapses was, on average, absent in the first postnatal week but emerged and became successively larger during the second postnatal week. This developmental increase in PPF was associated with a reduction in Pr, as indicated by the slower progressive block of the N-methyl-D-aspartate (NMDA) EPSP by the noncompetitive NMDA receptor antagonist MK-801. This developmental reduction in Pr was not homogenous among the synapses. As shown by the MK-801 analysis, the Pr heterogeneity observed among adult CA3-CA1 synapses is present already during the first postnatal week, and the developmental Pr reduction was found to be largely selective for synapses with higher Pr values, leaving Pr of the vast majority of the synapses essentially unaffected. A reduction in Pves, the release probability of the individual vesicle, possibly caused by reduction in Ca2+ influx, seems to explain the reduction in Pr. In vivo injection of tetanus toxin at the end of the first postnatal week did not prevent the increase in PPF, indicating that this developmental change in release is not critically dependent on normal neural activity during the second postnatal week.

Nyckelord

Aging
physiology
Animals
Calcium Channel Blockers
pharmacology
Dizocilpine Maleate
pharmacology
Excitatory Postsynaptic Potentials
drug effects
physiology
Glutamic Acid
physiology
Hippocampus
growth & development
physiology
Male
Pyramidal Cells
drug effects
physiology
Rats
Rats
Wistar
Receptors
N-Methyl-D-Aspartate
drug effects
physiology
Synapses
physiology
omega-Conotoxin GVIA
pharmacology

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