PMID- 17581955
OWN - NLM
STAT- MEDLINE
DCOM- 20070719
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 27
IP  - 25
DP  - 2007 Jun 20
TI  - Integration of asynchronously released quanta prolongs the postsynaptic spike 
      window.
PG  - 6684-91
AB  - Classically, the release of glutamate in response to a presynaptic action 
      potential causes a brief increase in postsynaptic excitability. Previous reports 
      indicate that at some central synapses, a single action potential can elicit 
      multiple, asynchronous release events. This raises the possibility that the 
      temporal dynamics of neurotransmitter release may determine the duration of 
      altered postsynaptic excitability. In response to physiological challenges, the 
      magnocellular neurosecretory cells (MNCs) in the paraventricular nucleus of the 
      hypothalamus (PVN) exhibit robust and prolonged increases in neuronal activity. 
      Although the postsynaptic conductances that may facilitate this form of activity 
      have been investigated thoroughly, the role of presynaptic release has been 
      largely overlooked. Because the specific patterns of activity generated by MNCs 
      require the activation of excitatory synaptic inputs, we sought to characterize 
      the release dynamics at these synapses and determine whether they contribute to 
      prolonged excitability in these cells. We obtained whole-cell recordings from 
      MNCs in brain slices of postnatal day 21-44 rats. Stimulation of glutamatergic 
      inputs elicited large and prolonged postsynaptic events that resulted from the 
      summation of multiple, asynchronously released quanta. Asynchronous release was 
      selectively inhibited by the slow calcium buffer EGTA-AM and potentiated by brief 
      high-frequency stimulus trains. These trains caused a prolonged increase in 
      postsynaptic spike activity that could also be eliminated by EGTA-AM. Our results 
      demonstrate that glutamatergic terminals in PVN exhibit asynchronous release, 
      which is important in generating large postsynaptic depolarizations and prolonged 
      spiking in response to brief, high-frequency bursts of presynaptic activity.
FAU - Iremonger, Karl J
AU  - Iremonger KJ
AD  - Hotchkiss Brain Institute and Department of Physiology and Biophysics, University 
      of Calgary, Calgary, Alberta, Canada T2N 4N1.
FAU - Bains, Jaideep S
AU  - Bains JS
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
SB  - IM
MH  - Action Potentials/*physiology
MH  - Animals
MH  - Animals, Genetically Modified
MH  - Excitatory Postsynaptic Potentials/*physiology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rats, Wistar
MH  - Synapses/*physiology
MH  - Synaptic Vesicles/*metabolism
MH  - Time Factors
PMC - PMC6672686
EDAT- 2007/06/22 09:00
MHDA- 2007/07/20 09:00
PMCR- 2007/12/20
CRDT- 2007/06/22 09:00
PHST- 2007/06/22 09:00 [pubmed]
PHST- 2007/07/20 09:00 [medline]
PHST- 2007/06/22 09:00 [entrez]
PHST- 2007/12/20 00:00 [pmc-release]
AID - 27/25/6684 [pii]
AID - 3235239 [pii]
AID - 10.1523/JNEUROSCI.0934-07.2007 [doi]
PST - ppublish
SO  - J Neurosci. 2007 Jun 20;27(25):6684-91. doi: 10.1523/JNEUROSCI.0934-07.2007.