Jianguo Chen
Dr. med.
Role of Metabotropic Glutamate Receptors for Induction of Homosynaptic Long-term
Depression in Rat Spinal Dorsal Horn
Geboren am 28, 04, 1963 in Hubei, VR China.
Reifeprüfung am 07, 07, 1980
Studiengang der Fachrichtung Medizin vom 01, 09, 1980 bis 30, 06, 1985, vom 01, 09, 1987
bis 30, 06, 1990, und vom 01, 10, 1996 bis 30, 06, 1998
Physikum am 15, 07, 1982 an der Xiannin Medical College, Hubei, Chnia.
Klinisches Studium in Xiannin Medical College, Hubei, China
Praktisches Jahr in Xiannin Medical College, Hubei, China
Staatsexamen am 30, 06, 1985 an der Xiannin Medical College, Hubei, China
Promotionsfach: Physiologie
Doktorvater: Prof. Dr. med. Jürgen Sandkühler
We have previously reported that low-frequency stimulation of primary afferent Aδ-fibers
may induce long-term depression (LTD) at synapses between Aδ-fibers and neurons in lamina
II of spinal dorsal horn of young rat. Here we show for the first time that this form of LTD is
homosynaptic in nature and activation of metabotropic glutamate receptors (mGluRs) is
required for its induction. Synaptic transmission between dorsal root afferents and neurons in
lamina II of spinal dorsal horn was examined by intracellular recording in a transverse slice-
dorsal root preparation of rat spinal cord. When the dorsal root was spliced into two halfs,
conditioning stimulation given at 1 Hz, 0.7 mA, 0.1 ms, 900 pulses induced an LTD of EPSP
amplitudes to 60 ± 12 % of control only in the conditioned pathway, whereas the synaptic
transmission in the other non-conditioned pathway was not changed. Coactivation of group I
and group II, but not group III mGluRs is required for the generation of this form of LFS-
induced LTD, since non-selective mGluRs antagonist (S)-MCPG, specific group I mGluRs
antagonist (S)-4C-PG and group II mGluRs antagonist MSOPPE, but not group III mGluRs
selective antagonist MSOP blocked the LTD induction. Moreover, the induction of LTD was
severely impaired by intracellular injection of Ca2+ fast chelator BAPTA, indicating a rise in
postsynaptic free Ca2+ concentration is involved in the induction of LTD. On the other hand,
activation of mGluRs by (1S, 3R)-ACPD induces an LTD only under conditions of
disinhibition. The (1S, 3R)-ACPD-induced LTD is NMDA receptor independent and may be
mediated by pertussis toxin (PTX)-insensitive G-proteins, since this (1S, 3R)-ACPD-induced
LTD could still be induced in the presence of NMDA receptor antagonist D-AP5 and after the
slices were preincubated with PTX. Both of LFS-induced LTD and (1S, 3R)-ACPD-induced
LTD in spinal dorsal horn may be relevant to antinociception.
