ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Prolonged postinhibitory rebound firing in the cerebellar nuclei mediated by group I metabotropic glutamate receptor potentiation of L-type calcium currents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Characterizing optogenetically mediated rebound effects in anaesthetized mouse primary visual cortex.The Journal of physiology · 2025Article
- Activation of mGluR1 negatively modulates glutamate-induced phase shifts of the circadian pacemaker in the mouse suprachiasmatic nucleus.Neurobiology of sleep and circadian rhythms · 2023Article
- Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons.Journal of pain research · 2022Article
- Social Deficits and Cerebellar Degeneration in Purkinje CellFrontiers in molecular neuroscience · 2022Article
- Disruption of rat deep cerebellar perineuronal net alters eyeblink conditioning and neuronal electrophysiology.Neurobiology of learning and memory · 2021Article
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- The Dynamic Basis of Respiratory Rhythm Generation: One Breath at a Time.Annual review of neuroscience · 2018Review
- Perineuronal Nets in the Deep Cerebellar Nuclei Regulate GABAergic Transmission and Delay Eyeblink Conditioning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- L-type calcium channels refine the neural population code of sound level.Journal of neurophysiology · 2016Article
- L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone-induced depolarization in thalamic paraventricular nucleus neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Article
- Determinants of rebound burst responses in rat cerebellar nuclear neurons to physiological stimuli.The Journal of physiology · 2016Article
- Pathogenesis of severe ataxia and tremor without the typical signs of neurodegeneration.Neurobiology of disease · 2016Article
- Metabotropic Glutamate Receptors: MODULATORS OF CONTEXT-DEPENDENT FEEDING BEHAVIOUR IN C. ELEGANS.The Journal of biological chemistry · 2015Article
- Integration of Purkinje cell inhibition by cerebellar nucleo-olivary neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Maturation of membrane properties of neurons in the rat deep cerebellar nuclei.Developmental neurobiology · 2014Article
- Convergent rhythm generation from divergent cellular mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Modeling the generation of output by the cerebellar nuclei.Neural networks : the official journal of the International Neural Network Society · 2013Review
- NMDA receptor-dependent synaptic activation of TRPC channels in olfactory bulb granule cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Synchrony and neural coding in cerebellar circuits.Frontiers in neural circuits · 2012Article
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2 authors at 1 institution in 1 country.
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Abstract
Neurons in the cerebellar nuclei fire at accelerated rates for prolonged periods after trains of synaptic inhibition that interrupt spontaneous firing. Both in vitro and in vivo, however, this prolonged rebound firing is favored by strong stimulation of afferents, suggesting that neurotransmitters other than GABA may contribute to the increased firing rates. Here, we tested whether metabotropic glutamate receptors modulate excitability of nuclear cells in cerebellar slices from mouse. In current clamp, the prolonged rebound firing rate after high-frequency synaptic stimulation was reduced by a variety of group I mGluR antagonists, including CPCCOEt [7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester], JNJ16259685 (3,4-dihydro-2H-pyrano[2,3-b]quinolin-7-yl)-(cis-4-methoxycyclohexyl)-methanone) plus MPEP, or 3-MATIDA (α-amino-5-carboxy-3-methyl-2-thiopheneacetic acid) plus MPEP, as long as both mGluR1 and mGluR5 were blocked. This mGluR-dependent acceleration of firing was reduced but still evident when IPSPs were prevented by GABA(A) receptor antagonists. In voltage clamp, voltage ramps revealed a non-inactivating, low-voltage-activated, nimodipine-sensitive current that was enhanced by the selective group I mGluR agonist s-DHPG [(S)-3,5-dihydroxyphenylglycine]. This putative L-type current also increased when mGluRs were activated by trains of evoked synaptic currents instead of direct application of agonist. In current clamp, blocking L-type Ca channels with the specific blocker nifedipine greatly reduced prolonged poststimulus firing and occluded the effect of adding group I mGluR antagonists. Thus, potentiation of a low-voltage-activated L-type current by synaptically released glutamate accounted nearly fully for the mGluR-dependent acceleration of firing. Together, these data suggest that prolonged rebound firing in the cerebellar nuclei in vivo is most likely to occur when GABA(A) and mGluRs are simultaneously activated by concurrent excitation and inhibition.
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