Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Mockett, Bruce G.; Guévremont, Diane; Wutte, Magdalena; Hulme, Sarah R.; Williams, Joanna M.; Abraham, Wickliffe C.

doi:10.1523/jneurosci.6656-10.2011

Cited by 98 publications

(139 citation statements)

References 64 publications

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“…In contrast to the metaplasticity of LTP in the hippocampus (Bortolotto and Collingridge, 1998), we found CaMKII was not required for this form of metaplasticity in the ACC, though its inhibition did tend to reduce the level of priming. Moreover, a recent study showed in the hippocampus that CaMKII was important in mediating DHPG-induced mGluR-LTD but not PKC (Mockett et al, 2011). These results indicate that intracellular mechanisms mediated by priming group I mGluR in LTD may be doserelated and region-dependent.…”

Section: Loss Of Cortical Ltd After Amputationmentioning

confidence: 76%

Plasticity of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in the Anterior Cingulate Cortex after Amputation

et al. 2012

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Long-term depression (LTD) is a key form of synaptic plasticity important in learning and information storage in the brain. It has been studied in various cortical regions, including the anterior cingulate cortex (ACC). ACC is a crucial cortical region involved in such emotion-related physiological and pathological conditions as fear memory and chronic pain. In the present study, we used a multielectrode array system to map cingulate LTD in a spatiotemporal manner within the ACC. We found that low-frequency stimulation (1 Hz, 15 min) applied onto deep layer V induced LTD in layers II/III and layers V/VI. Cingulate LTD requires activation of metabotropic glutamate receptors (mGluRs), while L-type voltage-gated calcium channels and NMDA receptors also contribute to its induction. Peripheral amputation of the distal tail impaired ACC LTD, an effect that persisted for at least 2 weeks. The loss of LTD was rescued by priming ACC slices with activation of mGluR1 receptors by coapplying (RS)-3,5-dihydroxyphenylglycine and MPEP, a form of metaplasticity that involved the activation of protein kinase C. Our results provide in vitro evidence of the spatiotemporal properties of ACC LTD in adult mice. We demonstrate that tail amputation causes LTD impairment within the ACC circuit and that this can be rescued by activation of mGluR1.

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Section: Loss Of Cortical Ltd After Amputationmentioning

confidence: 76%

Plasticity of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in the Anterior Cingulate Cortex after Amputation

et al. 2012

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“…7e, f). In addition, it was reported that activation of mGluR I may alter CaMKII activity in various types of central neurons (Choe and Wang 2001;Mockett et al 2011). We tested the possible involvement of this signaling pathway.…”

Section: Involvement Of Ca 21 -Dependent Plc/pkc and Camkii Signalingmentioning

confidence: 99%

Activation of group I metabotropic glutamate receptors regulates the excitability of rat retinal ganglion cells by suppressing Kir and I h

Cui

Miao

et al. 2016

Brain Struct Funct

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Group I metabotropic glutamate receptor (mGluR I) activation exerts a slow postsynaptic excitatory effect in the CNS. Here, the issues of whether and how this receptor is involved in regulating retinal ganglion cell (RGC) excitability were investigated in retinal slices using patch-clamp techniques. Under physiological conditions, RGCs displayed spontaneous firing. Extracellular application of LY367385 (10 µM)/MPEP (10 µM), selective mGluR1 and mGluR5 antagonists, respectively, significantly reduced the firing frequency, suggesting that glutamate endogenously released from bipolar cells constantly modulates RGC firing. DHPG (10 µM), an mGluR I agonist, significantly increased the firing and caused depolarization of the cells, which were reversed by LY367385, but not by MPEP, suggesting the involvement of the mGluR1 subtype. Intracellular Ca-dependent PI-PLC/PKC and calcium/calmodulin-dependent protein kinase II (CaMKII) signaling pathways mediated the DHPG-induced effects. In the presence of cocktail synaptic blockers (CNQX, D-AP5, bicuculline, and strychnine), which terminated the spontaneous firing in both ON and OFF RGCs, DHPG still induced depolarization and triggered the cells to fire. The DHPG-induced depolarization could not be blocked by TTX. In contrast, Ba, an inwardly rectifying potassium channel (Kir) blocker, and Cs and ZD7288, hyperpolarization-activated cation channel (I ) blockers, mimicked the effect of DHPG. Furthermore, in the presence of Ba/ZD7288, DHPG did not show further effects. Moreover, Kir and I currents could be recorded in RGCs, and extracellular application of DHPG indeed suppressed these currents. Our results suggest that activation of mGluR I regulates the excitability of rat RGCs by inhibiting Kir and I.

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“…It seems that activation of mGluR I-induced increase in [Ca 2ϩ ] i in rat Müller cells could be due to Ca 2ϩ release from both IP 3 -and ryanodine-sensitive Ca 2ϩ stores. Changes in calcium/calmodulindependent protein kinase II (CaMKII) activity, which have been reported in various types of central neurons (Choe and Wang, 2001;Mockett et al, 2011), were unlikely involved in DHPG-induced suppression of Kir currents in Müller cells. Bath application of CaMKII inhibitors KN-62 (5 M)/KN-93 (10 M) did not change the Kir currents.…”

Section: Camentioning

confidence: 99%

Group I mGluR-Mediated Inhibition of Kir Channels Contributes to Retinal Müller Cell Gliosis in a Rat Chronic Ocular Hypertension Model

Miao

Dong

et al. 2012

J. Neurosci.

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Müller cell gliosis, which is characterized by upregulated expression of glial fibrillary acidic protein (GFAP), is a universal response in many retinal pathological conditions. Whether down-regulation of inward rectifying K ϩ (Kir) channels, which commonly accompanies the enhanced GFAP expression, could contribute to Müller cell gliosis is poorly understood. We investigated changes of Kir currents, GFAP and Kir4.1 protein expression in Müller cells in a rat chronic ocular hypertension (COH) model, and explored the mechanisms underlying Müller cell gliosis. We show that Kir currents and Kir4.1 protein expression in Müller cells were reduced significantly, while GFAP expression was increased in COH rats, and these changes were eliminated by MPEP, a group I metabotropic glutamate receptors (mGluR I) subtype mGluR5 antagonist. In normal isolated Müller cells, the mGluR I agonist (S)-3,5-dihydroxyphenylglycine (DHPG) suppressed the Kir currents and the suppression was blocked by MPEP. The DHPG effect was mediated by the intracellular Ca 2ϩ -dependent PLC/IP 3 -ryanodine/PKC signaling pathway, but the cAMP-PKA pathway was not involved. Moreover, intravitreal injection of DHPG in normal rats induced changes in Müller cells, similar to those observed in COH rats. The DHPG-induced increase of GFAP expression in Müller cells was obstructed by Ba 2ϩ , suggesting the involvement of Kir channels. We conclude that overactivation of mGluR5 by excessive extracellular glutamate in COH rats could contribute to Müller cell gliosis by suppressing Kir channels.

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Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Cited by 98 publications

References 64 publications

Plasticity of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in the Anterior Cingulate Cortex after Amputation

Plasticity of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in the Anterior Cingulate Cortex after Amputation

Activation of group I metabotropic glutamate receptors regulates the excitability of rat retinal ganglion cells by suppressing Kir and I h

Group I mGluR-Mediated Inhibition of Kir Channels Contributes to Retinal Müller Cell Gliosis in a Rat Chronic Ocular Hypertension Model

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