Short-term synaptic plasticity is altered in mice lacking synapsin I.
Synapsin I, the major phosphoprotein of synaptic vesicles, is thought to play a central role in neurotransmitter release. Here we introduce a null mutation into the murine synapsin I gene by homologous recombination. Mice with no detectable synapsin I manifest no apparent changes in well-being or gross nervous system function. Thus, synapsin I is not essential for neurotransmitter release. Electrophysiology reveals that mice lacking synapsin I exhibit a selective increase in paired pulse facilitation, with no major alterations in other synaptic parameters such as long-term potentiation. In addition to potential redundant functions shared with other proteins, synapsin I in normal mice may function to limit increases in neurotransmitter release elicited by residual Ca2+ after an initial stimulus.
Rosahl
T W
TW
Department of Molecular Genetics, Howard Hughes Medical Institute, University of Texas Southwestern Medical School, Dallas 75235.
Geppert
M
M
Spillane
D
D
Herz
J
J
Hammer
R E
RE
Malenka
R C
RC
Südhof
T C
TC
D000818:Animals; D001483:Base Sequence; D002395:Catecholamines / Q000502:physiology; D005796:Genes; D006624:Hippocampus / Q000502:physiology; D066298:In Vitro Techniques; D051379:Mice; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D009473:Neuronal Plasticity; D018377:Neurotransmitter Agents / Q000378:metabolism; D009838:Oligodeoxyribonucleotides / Q000737:chemistry; D015183:Restriction Mapping; D016704:Synapsins / Q000502:physiology*; D009435:Synaptic Transmission; D013997:Time Factors
D002395:Catecholamines; D018377:Neurotransmitter Agents; D009838:Oligodeoxyribonucleotides; D016704:Synapsins