PMID- 10884315
OWN - NLM
STAT- MEDLINE
DCOM- 20000803
LR  - 20191023
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 20
IP  - 14
DP  - 2000 Jul 15
TI  - Properties and plasticity of paired-pulse depression at a central synapse.
PG  - 5312-20
AB  - Synaptic depression was studied at the axo-axonic connection between the goldfish 
      Mauthner axon and identified cranial relay interneurons using simultaneous 
      presynaptic and postsynaptic recordings and a paired-pulse stimulus paradigm. We 
      used interstimulus intervals (ISIs) ranging from 10 msec to 1 sec and a cycle 
      time of approximately 5 sec. Depression (Delta EPSP/EPSP1) was maximal at the 
      shorter intervals (80%) and decreased exponentially with a tau approximately 400 
      msec (360 +/- 107 msec, mean +/- SD). We found the amplitudes of the first and 
      second EPSP were not correlated, indicating the magnitude of depression does not 
      depend on the amount of transmitter released by the conditioning stimulus. At 
      short ISIs, the latency of EPSP2 was 23% longer than that of EPSP1 and recovered 
      to control with tau approximately 400 msec, whereas rise time and decay time were 
      not altered significantly. The latency distribution, which is determined by the 
      timing of the first quantum released each trial, was used to derive alpha(t), the 
      rate of evoked exocytosis after an action potential. alpha(t) was biphasic, and 
      both components were consistently delayed during depression. Presynaptic 
      manipulations of putative intracellular regulatory pathways, such as Ca(2+) and 
      GTPgammaS injections, preferentially affected the amplitude of EPSP1 or EPSP2. 
      These results are not consistent with simple depletion of the available pool of 
      synaptic vesicles as the major mechanism underlying depression. They rather 
      suggest that it is attributable to a modification or refractoriness of the 
      release process and that there may be multiple pathways subserving evoked 
      exocytosis.
FAU - Waldeck, R F
AU  - Waldeck RF
AD  - Department of Neurobiology and Anatomy, MCP-Hahnemann University of the Health 
      Sciences, Philadelphia, Pennsylvania 19129, USA.
FAU - Pereda, A
AU  - Pereda A
FAU - Faber, D S
AU  - Faber DS
LA  - eng
GR  - NS21838/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (postsynaptic density proteins)
RN  - 37589-80-3 (Guanosine 5'-O-(3-Thiotriphosphate))
RN  - EC 3.6.5.1 (Heterotrimeric GTP-Binding Proteins)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Action Potentials/physiology
MH  - Animals
MH  - Brain Stem/cytology/metabolism/*physiology
MH  - Calcium/metabolism/pharmacology
MH  - Electric Stimulation
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Goldfish
MH  - Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
MH  - Heterotrimeric GTP-Binding Proteins/metabolism
MH  - Nerve Tissue Proteins/metabolism
MH  - Neural Inhibition/*physiology
MH  - Neuronal Plasticity/*physiology
MH  - Reaction Time
MH  - Synapses/*physiology
PMC - PMC6772341
EDAT- 2000/07/07 11:00
MHDA- 2000/08/06 11:00
PMCR- 2001/01/15
CRDT- 2000/07/07 11:00
PHST- 2000/07/07 11:00 [pubmed]
PHST- 2000/08/06 11:00 [medline]
PHST- 2000/07/07 11:00 [entrez]
PHST- 2001/01/15 00:00 [pmc-release]
AID - 20/14/5312 [pii]
AID - 4338 [pii]
AID - 10.1523/JNEUROSCI.20-14-05312.2000 [doi]
PST - ppublish
SO  - J Neurosci. 2000 Jul 15;20(14):5312-20. doi: 10.1523/JNEUROSCI.20-14-05312.2000.