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J Neurophysiol (December 1, 2002). 10.1152/jn.00928.2001
Submitted on 9 November 2001
Accepted on 21 August 2002
Department of Neurophysiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan
Kudoh, Masaharu,
Masashi Sakai, and
Katsuei Shibuki.
Differential Dependence of LTD on Glutamate Receptors in the
Auditory Cortical Synapses of Cortical and Thalamic Inputs. J. Neurophysiol. 88: 3167-3174, 2002. Pyramidal
neurons in the auditory cortex (AC) receive glutamatergic inputs from
the medial geniculate body (MGB inputs) and other pyramidal neurons
(pyramidal inputs). We found that the induction of long-term depression
(LTD) in supragranular layers was only partially suppressed by 50 µM
D-(
)-2-amino-5-phosphonovalerate (APV), an antagonist of
N-methyl-D-aspartate (NMDA) receptors (NMDARs),
and 500 µM (+)-
-methyl-4-carboxyphenylglycine (MCPG), an
antagonist of metabotropic glutamate receptors (mGluRs). However, LTD
was not observed in the mixture of APV and MCPG. We hypothesized that
the mixed dependence of LTD on glutamate receptors could be attributed
to the heterogeneity of MGB inputs and pyramidal inputs. To test this
hypothesis, the angle of slicing and other recording conditions were
adjusted so that postsynaptic potentials were recorded in normal
slices, but not in the slices prepared from the rats with MGB lesion.
In these experiments, LTD was suppressed by MCPG alone. The conditions
were adjusted to minimize the contribution of MGB inputs in field
potentials. In these experiments, the induction of LTD was suppressed
by APV alone. Interestingly, the induction of LTD was partially
suppressed by 20 µM nifedipine, a blocker of L-type
Ca2+ channels, in the slices prepared from the
rats with MGB lesions, but not in normal slices. These findings suggest
that the induction of LTD requires activation of mGluRs in the synapses
of MGB inputs and of NMDARs in the synapses of pyramidal inputs.
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