Induction of NMDA Receptor-Dependent Long-Term Depression in Visual Cortex Does Not Require Metabotropic Glutamate Receptors

1999 ◽  
Vol 82 (6) ◽  
pp. 3594-3597 ◽  
Author(s):  
Nathaniel B. Sawtell ◽  
Kimberly M. Huber ◽  
John C. Roder ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Nmda Receptor ◽  
Metabotropic Glutamate Receptors ◽  
Low Frequency ◽  
Long Term Depression ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Frequency Stimulation ◽  
Visual Cortical

We tested the role of group I mGluRs in the induction of long-term depression (LTD) in the visual cortex, using the novel mGluR antagonist LY341495 and mice lacking mGluR5, the predominant phosphoinositide (PI)-linked mGluR in the visual cortex. We find that LY341495 is a potent blocker of glutamate-stimulated PI hydrolysis in visual cortical synaptoneurosomes, and that it effectively antagonizes the actions of the mGluR agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (ACPD) on synaptic transmission in visual cortical slices. However, LY341495 has no effect on the induction of LTD by low-frequency stimulation. Furthermore, mice lacking mGluR5 show normal NMDA receptor-dependent LTD. These results indicate that group I mGluR activation is not required for the induction of NMDA receptor-dependent LTD in the visual cortex.

scholarly journals NMDA receptor-dependent long-term depression in the lateral habenula: implications in physiology and depression

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Miseon Kang ◽  
Jihyun Noh ◽  
Jun-mo Chung
Keyword(s):  
Nmda Receptor ◽  
Neuronal Activity ◽  
Acute Stress ◽  
Low Frequency ◽  
Induction Phase ◽  
Long Term Depression ◽  
Lateral Habenula ◽  
Promising Therapeutic Target ◽  
Frequency Stimulation

Abstract Abnormally increased neuronal activity in the lateral habenula (LHb) is closely associated with depressive-like behavior. Despite the emphasis on the pathological importance of NMDA receptor (NMDAR)-dependent long-term depression (LTD) and the involvement of calcium permeable AMPA receptor (CP-AMPAR) as major Ca2+ source, the functions of NMDAR and CP-AMPAR on LTD modulation in the LHb still have not been fully investigated. Here, we found that NMDAR-dependent LTD by low frequency stimulation was induced in both synaptic and extrasynaptic regions in the LHb. In addition, CP-AMPAR was necessary for the activation of NMDAR in the induction phase of NMDAR-dependent LTD. The acute stress, which induced depressive behavior, had a blocked effect on synaptic NMDAR-dependent LTD but left extrasynaptic NMDAR-dependent LTD intact. These findings show that NMDAR-dependent LTD in LHb plays an important role in regulating neuronal activity, which is probable to be excessively increased by repeated stress, via maintaining homeostasis in both synaptic and extrasynaptic regions of the LHb. Moreover, NMDAR and CP-AMPAR may serve as a depression-related modulator and be regarded as a promising therapeutic target for treatment of psychopathology such as depression.

Brain-derived neurotrophic factor blocks long-term depression in rat visual cortex

1996 ◽  
Vol 76 (6) ◽  
pp. 4198-4201 ◽  
Author(s):  
Y. Akaneya ◽  
T. Tsumoto ◽  
H. Hatanaka
Keyword(s):  
Visual Cortex ◽  
Neurotrophic Factor ◽  
Tyrosine Kinases ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
Brain Derived Neurotrophic Factor ◽  
Long Term Depression ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

1. Brain-derived neurotrophic factor (BDNF) has been reported to play a role in long-term potentiation (LTP) in hippocampus, but whether it is involved also in long-term depression (LTD) is not yet known. In this study, we tested whether BDNF and its gene family, nerve growth factor (NGF), have any effect on synaptic transmission and LTD in visual cortical slices of young rats. 2. An application of BDNF at the concentration of 20 ng/ml did not significantly change layer II/III field responses evoked by layer IV stimulation at 0.1 Hz, although at 200 ng/ml it enhanced responses. BDNF at 20 ng/ml prevented LTD of field responses from being induced by low-frequency stimulation (1 Hz for 15 min) of layer IV. NGF did not have such effects in the same concentration range as that of BDNF. 3. The action of BDNF was antagonized by K252a, an inhibitor of receptor tyrosine kinases. When K252a alone was applied to slices, LTD of stronger magnitude than in control slices was induced by low-frequency stimulation. 4. These results suggest that endogeneous BDNF may prevent synapses from being depressed by low-frequency inputs in the developing visual cortex.

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