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The Journal of Neuroscience, May 24, 2006, 26(21):5786-5793; doi:10.1523/JNEUROSCI.4631-05.2006

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Cellular/Molecular
Synapsin Utilization Differs among Functional Classes of Synapses on Thalamocortical Cells

Anders Kielland,¹ Alev Erisir,² S. Ivar Walaas,¹ and Paul Heggelund¹

¹University of Oslo, Institute of Basic Medical Sciences, N-0317 Oslo, Norway, and ²University of Virginia, Department of Psychology, Charlottesville, Virginia 22904-4400

Correspondence should be addressed to Paul Heggelund, Department of Physiology, University of Oslo, Institute of Basic Medical Sciences, P.O. Box 1103 Blindern, Sognsvannsveien 9, N-0317 Oslo, Norway. Email: paul.heggelund{at}medisin.uio.no

Several proteins in nerve terminals participate in synaptic transmission between neurons. The synapsins, which are synaptic vesicle-associated proteins, have widespread distribution in the brain and are assumed essential for sustained recruitment of vesicles during high rates of synaptic transmission. We compared the role of synapsins in two types of glutamatergic synapses on thalamocortical cells in the dorsal lateral geniculate nucleus of mice: retinogeniculate synapses, which transmit primary afferent input at high frequencies and show synaptic depression, and corticogeniculate synapses, which provide modulatory feedback at lower frequencies and show synaptic facilitation. We used electrophysiological methods to determine effects of gene knock-out of synapsin I and II on short-term synaptic plasticity in paired-pulse, pulse-train, and posttetanic potentiation paradigms. The gene inactivation changed the plasticity properties in corticogeniculate, but not in retinogeniculate, synapses. Immunostaining with antibodies against synapsins in wild-type mice demonstrated that neither synapsin I nor II occurred in retinogeniculate terminals, whereas both occurred in corticogeniculate terminals. In GABAergic terminals, only synapsin I occurred. In corticogeniculate terminals of knock-out mice, the density of synaptic vesicles was reduced because of increased terminal size rather than reduced number of vesicles and the intervesicle distance was increased compared with wild-type mice. In the retinogeniculate terminals, no significant morphometric differences occurred between knock-out and wild-type mice. Together, this indicates that synapsin I and II are not present in the retinogeniculate terminals and therefore are not essential for sustained, high-rate synaptic transmission.

Key words: synaptic transmission; synapsin; facilitation; depression; PTP; synaptic terminals; synaptic vesicle clusters; thalamus; LGN

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Received Oct. 28, 2005; revised March 2, 2006; accepted April 19, 2006.

Correspondence should be addressed to Paul Heggelund, Department of Physiology, University of Oslo, Institute of Basic Medical Sciences, P.O. Box 1103 Blindern, Sognsvannsveien 9, N-0317 Oslo, Norway. Email: paul.heggelund{at}medisin.uio.no

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