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The Journal of Neuroscience, December 5, 2007, 27(49):13520-13531; doi:10.1523/JNEUROSCI.3151-07.2007

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Cellular/Molecular
Lack of Synapsin I Reduces the Readily Releasable Pool of Synaptic Vesicles at Central Inhibitory Synapses

Pietro Baldelli,^1,2 Anna Fassio,^1,2 Flavia Valtorta,^3,4 and Fabio Benfenati^1,2

¹Department of Neuroscience and Brain Technologies, The Italian Institute of Technology, 16163 Genova, Italy, ²Department of Experimental Medicine, Section of Physiology, University of Genova, 16132 Genova, Italy, and ³S. Raffaele Scientific Institute, Vita-Salute University and ⁴IIT Unit of Molecular Neuroscience, 20132 Milano, Italy

Correspondence should be addressed to Dr. Pietro Baldelli, Department of Experimental Medicine, University of Genova, Viale Benedetto XV, 3, 16132 Genova, Italy. Email: pietro.baldelli{at}unige.it

Synapsins (Syns) are synaptic vesicle (SV) phosphoproteins that play a role in neurotransmitter release and synaptic plasticity by acting at multiple steps of exocytosis. Mutation of SYN genes results in an epileptic phenotype in mouse and man suggesting a role of Syns in the control of network excitability. We have studied the effects of the genetic ablation of the SYN1 gene on inhibitory synaptic transmission in primary hippocampal neurons. Inhibitory neurons lacking SynI showed reduced amplitude of IPSCs evoked by isolated action potentials. The impairment in inhibitory transmission was caused by a decrease in the size of the SV readily releasable pool, rather than by changes in release probability or quantal size. The reduction of the readily releasable pool was caused by a decrease in the number of SVs released by single synaptic boutons in response to the action potential, in the absence of variations in the number of synaptic contacts between couples of monosynaptically connected neurons. The deletion of SYN1 did not affect paired-pulse depression or post-tetanic potentation, but was associated with a moderate increase of synaptic depression evoked by trains of action potentials, which became apparent at high stimulation frequencies and was accompanied by a slow down of recovery from depression. The decreased size of the SV readily releasable pool, coupled with a decreased SV recycling rate and refilling by the SV reserve pool, may contribute to the epileptic phenotype of SynI knock-out mice.

Key words: synapsin; GABA release; synaptic transmission; knock-out mice; quantal analysis; synaptic plasticity; epilepsy

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Received July 11, 2007; revised Oct. 16, 2007; accepted Oct. 17, 2007.

Correspondence should be addressed to Dr. Pietro Baldelli, Department of Experimental Medicine, University of Genova, Viale Benedetto XV, 3, 16132 Genova, Italy. Email: pietro.baldelli{at}unige.it

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				A. Corradi, A. Zanardi, C. Giacomini, F. Onofri, F. Valtorta, M. Zoli, and F. Benfenati Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment J. Cell Sci., September 15, 2008; 121(18): 3042 - 3051. [Abstract] [Full Text] [PDF]

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