| From Fruit Flies to Barnacles, Histamine Is the Neurotransmitter of Arthropod Photoreceptors Neuron, Volume 22, Issue 3, 1 March 1999, Pages 431-433 Ann E Stuart Full Text | PDF (75 kb) |
| Transmitter timecourse in the synaptic cleft: its role in central synaptic function Trends in Neurosciences, Volume 19, Issue 5, 1 May 1996, Pages 163-171 J.D Clements Abstract . (1996) 19, 163–171 Abstract | Full Text | PDF (2501 kb) |
| Synapse-Specific Contribution of the Variation of Transmitter Concentration to the Decay of Inhibitory Postsynaptic Currents Biophysical Journal, Volume 80, Issue 3, 1 March 2001, Pages 1251-1261 Zoltan Nusser, David Naylor and Istvan Mody Abstract Synaptic transmission is characterized by a remarkable trial-to-trial variability in the postsynaptic response, influencing the way in which information is processed in neuronal networks. This variability may originate from the probabilistic nature of quantal transmitter release, from the stochastic behavior of the receptors, or from the fluctuation of the transmitter concentration in the cleft. We combined nonstationary noise analysis and modeling techniques to estimate the contribution of transmitter fluctuation to miniature inhibitory postsynaptic current (mIPSC) variability. A substantial variability (∼30%) in mIPSC decay was found in all cell types studied (neocortical layer2/3 pyramidal cells, granule cells of the olfactory bulb, and interneurons of the cerebellar molecular layer). This large variability was not solely the consequence of the expression of multiple types of GABA receptors, as a similar mIPSC decay variability was observed in cerebellar interneurons that express only a single type () of GABA receptor. At large synapses on these cells, all variance in mIPSC decay could be accounted for by the stochastic behavior of ∼36 pS channels, consistent with the conductance of GABA receptors at physiological temperatures. In contrast, at small synapses, a significant amount of variability in the synaptic cleft GABA transient had to be present to account for the additional variance in IPSC decay over that produced by stochastic channel openings. Thus, our results suggest a synapse-specific contribution of the variation of the spatiotemporal profile of GABA to the decay of IPSCs. Abstract | Full Text | PDF (253 kb) |
Copyright © 1996 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 71, Issue 5, 2413-2426, 1 November 1996
doi:10.1016/S0006-3495(96)79435-3
Research Article
J. Kleinle, K. Vogt, H.R. Lüscher, L. Müller, W. Senn, K. Wyler and J. Streit
Physiologisches Institut, Universität Bern, Switzerland. kleinle@iam.unibe.ch
A three-dimensional model for release and diffusion of glutamate in the synaptic cleft was developed and solved analytically. The model consists of a source function describing transmitter release from the vesicle and a diffusion function describing the spread of transmitter in the cleft. Concentration profiles of transmitter at the postsynaptic side were calculated for different transmitter concentrations in a vesicle, release scenarios, and diffusion coefficients. From the concentration profiles the receptor occupancy could be determined using alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor kinetics. It turned out that saturation of receptors and sufficiently fast currents could only be obtained if the diffusion coefficient was one order of magnitude lower than generally assumed, and if the postsynaptic receptors formed clusters with a diameter of roughly 100 nm directly opposite the release sites. Under these circumstances the gradient of the transmitter concentration at the postsynaptic membrane outside the receptor clusters was steep, with minimal cross-talk among neighboring receptor clusters. These findings suggest that for each release site a corresponding receptor aggregate exists, subdividing an individual synapse into independent functional subunits without the need for specific lateral diffusion barriers.