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The Journal of Neuroscience, August 15, 2002, 22(16):7177-7194
Impairment of L-type Ca2+ Channel-Dependent Forms of
Hippocampal Synaptic Plasticity in Mice Deficient in the Extracellular
Matrix Glycoprotein Tenascin-C
Matthias R.
Evers,
Benedikt
Salmen,
Olena
Bukalo,
Astrid
Rollenhagen,
Michael R.
Bösl,
Fabio
Morellini,
Udo
Bartsch,
Alexander
Dityatev, and
Melitta
Schachner
Zentrum für Molekulare Neurobiologie, Universität
Hamburg, D-20246 Hamburg, Germany
The extracellular matrix glycoprotein tenascin-C (TN-C) has been
suggested to play important functional roles during neural development,
axonal regeneration, and synaptic plasticity. We generated a
constitutively TN-C-deficient mouse mutant from embryonic stem cells
with a floxed tn-C allele, representing a standard for
future analysis of conditionally targeted mice. The gross morphology of
the CNS was not detectably affected, including no evidence for
perturbed nerve cell migration, abnormal oligodendrocyte distribution,
or defective myelination. Despite the apparent normal histology of the
hippocampus and normal performance in the water maze, theta-burst
stimulation (TBS) of Schaffer collaterals elicited reduced long-term
potentiation (LTP) in the CA1 region of TN-C-deficient mutants, as
compared with wild-type littermates. However, high-frequency stimulation evoked normal LTP not only in CA1, but also at mossy fiber-CA3 and medial and lateral perforant path-granule cell synapses in the dentate gyrus. Low-frequency stimulation failed to induce long-term depression in the CA1 region of TN-C-deficient animals. Recordings of TBS-induced LTP in the presence of nifedipine, an antagonist of L-type voltage-dependent Ca2+ channels
(VDCCs), did not affect LTP in TN-C-deficient mice, but reduced LTP in
wild-type mice to the levels seen in mutants. Furthermore, chemical
induction of a L-type VDCC-dependent LTP in the CA1 region by
application of the K+ channel blocker
tetraethylammonium resulted in impaired LTP in TN-C mutants. Thus,
reduction in L-type VDCC-mediated signaling appears to mediate the
deficits in certain forms of synaptic plasticity in constitutively
TN-C-deficient mice.
Key words:
tenascin-C; knock-out mutation; extracellular matrix
glycoprotein; gene targeting; hippocampus; long-term potentiation; long-term depression; CA1; CA3; dentate gyrus; water maze; TEA; L-type
voltage-dependent Ca2+ channels; VDCC; nifedipine
Copyright © 2002 Society for Neuroscience 0270-6474/02/22167177-18$05.00/0
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