| Title |
The Mechanism of Presynaptic Long-Term Depression Mediated by Group I Metabotropic Glutamate Receptors |
| Authors |
Yuansheng Tan,Nobuaki Hori,and David O. Carpenter |
| Publication Info |
Society of Toxicology 23/2/187-203 |
| Date Published |
Dec 12, 2008 |
| Abstract |
1. Metabotropic glutamate receptors (mGluRs) are known to play a role in synaptic
plasticity. In a study of rat hippocampal brain slices, we find that a brief perfusion of a
group I mGluR agonist, (S)-3,5-dihydroxyphenylglycine (DHPG), induced a robust longterm
depression (DHPG-LTD) in area CA1.
2. The action was accompanied by an enhancement of the paired-pulse facilitation
(PPF) ratio.
3. At the same time DHPG enhanced ionophoretic responses to alpha-amino-3-
hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), kainic acid (KA), and N-methyl-Daspartate
(NMDA) in CA1 pyramidal neurons. This was only partially reversed by washing.
4. These observations indicate that DHPG exerts two opposing actions, suppression
of the synaptic transmission and facilitation of postsynaptic responses. However, the presynaptic
action dominates, since the net effect of monosynaptic activation is a reduction of
response.
5. Perfusion of DHPG reduced three calcium-dependent responses in CA3 pyramidal
neurons, which are presynaptic to CA1 neurons. These are calcium spike width and
amplitude, after-hyperpolarization (AHP), and spike frequency adaptation (SFA).
6. These results suggest that the DHPG-LTD results from modulation of the presynaptic
calcium currents by group l mGluRs. |
| Article |
/pdfs/tan-paper-6.pdf |
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