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1 low-calcium environment that also inhibited basal release.
2 n of basal neurotransmission causing "leaky" basal release, (2) changes in either the size or mobiliz
3 stributions and signaling are dependent upon basal release and uptake, and on cytoneme-mediated movem
5 ude that MH-only mutations modestly increase basal release-channel activity in a manner insufficient
11 between the number of estrogen receptors and basal release of EDNO in the aorta of mice, and suggest
12 showed a primed phenotype with an increased basal release of IL-8 and MMP-9 and expressed a corticos
17 in group 3 exhibited better preservation of basal release of nitric oxide, as measured by contractio
24 microM elicited a 27 +/- 8% decrease in the basal release of SPLI and prevented the increase in the
25 In conclusion, dynorphin(1-8) reduces the basal release of SPLI and prevents the increase in the r
26 orsal horn through the perfusate reduced the basal release of SPLI by 29 +/- 9% and prevented the inc
30 roM) and dipyridamole (200 microM) depressed basal releases of glutamate and taurine and the ischemia
31 We have found that injury does not alter basal release or acetylcholine, but it results in a mark
32 h N-cadherin in postsynaptic neurons reduced basal release probability (p(r)) at inputs to the neuron
34 In THC-tolerant mice, an increase of the basal release probability was found at PF-PC synapses, i
35 ndritic activity is the major determinant of basal release probability, and we suggest that this feed
36 neurotransmission unaltered with respect to basal release probability, Ca2+ dependence of release, s
38 95% O(2) and 5% CO(2.) After determining the basal release, the hypothalami were challenged with 0, 0
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