Activity-Dependent Neurotrophin Signaling Underlies Developmental Switch of Ca<sup>2+</sup>Channel Subtypes Mediating Neurotransmitter Release

Miki, Takafumi; Hirai, Hirokazu; Takahashi, Tomoyuki

doi:10.1523/jneurosci.3161-13.2013

Cited by 23 publications

(24 citation statements)

References 52 publications

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“…Purkinje neurons show activity-dependent BDNF/TrkB signaling, with reduced activity tending to result in reduced signaling [90]. As described previously, a mouse model of SCA1 shows reduced firing frequency that could be corrected through aminopyridine treatment.…”

Section: Transcriptional Dysregulation Of Ion Channel Genes In Polyq mentioning

confidence: 64%

“…There is some evidence to suggest that alterations in activitydependent secretion of neurotrophins, specifically the neurotrophin brain-derived neurotrophic factor (BDNF), are present in mouse models of disease. Because BDNF secretion in neurons is known to be regulated by neuronal activity [88][89][90], altered activity might be sufficient to produce pathologic changes in BDNF secretion. Indeed, there is emerging evidence for both HD and SCA1 that this may be the case.…”

Section: Transcriptional Dysregulation Of Ion Channel Genes In Polyq mentioning

confidence: 99%

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The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

Chopra

Shakkottai

2014

Neurotherapeutics

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Polyglutamine diseases are a class of neurodegenerative diseases that share an expansion of a glutamineencoding CAG tract in the respective disease genes as a central hallmark. In all of these diseases there is progressive degeneration in a select subset of neurons, and the mechanisms behind this degeneration remain unclear. Emerging evidence from animal models of disease has identified abnormalities in synaptic signaling and intrinsic excitability in affected neurons, which coincide with the onset of symptoms and precede apparent neuropathology. The appearance of these early changes suggests that altered neuronal activity might be an important component of network dysfunction and that these alterations in network physiology could contribute to symptoms of disease. Here we review abnormalities in neuronal function that have been identified in both animal models and patients, and highlight ways in which these changes in neuronal activity may contribute to disease symptoms. We then review the literature supporting an emerging role for abnormalities in neuronal activity as a driver of neurodegeneration. Finally, we identify common themes that emerge from studies of neuronal dysfunction in polyglutamine disease.

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Section: Transcriptional Dysregulation Of Ion Channel Genes In Polyq mentioning

confidence: 64%

Section: Transcriptional Dysregulation Of Ion Channel Genes In Polyq mentioning

confidence: 99%

The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

Chopra

Shakkottai

2014

Neurotherapeutics

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“…; Miki et al . ). Thus, short‐term plasticity by Ca 2+ channel modulation might also developmentally change.…”

Section: Discussionmentioning

confidence: 97%

Ca²⁺ current facilitation determines short‐term facilitation at inhibitory synapses between cerebellar Purkinje cells

Díaz-Rojas

Sakaba

Kawaguchi

2015

The Journal of Physiology

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Key pointsr Short-term facilitation takes place at GABAergic synapses between cerebellar Purkinje cells (PCs).r By directly patch clamp recording from a PC axon terminal, we studied the mechanism of short-term facilitation.r We show that the Ca 2+ currents elicited by high-frequency action potentials were augmented in a [Ca 2+ ] i -dependent manner.r The facilitation of synaptic transmission showed 4-5th power dependence on the Ca 2+ current facilitation, and was abolished when the Ca 2+ current amplitude was adjusted to be identical.r Short-term facilitation of Ca 2+ currents predominantly mediates short-term facilitation at synapses between PCs.Abstract Short-term synaptic facilitation is critical for information processing of neuronal circuits. Several Ca 2+ -dependent positive regulations of transmitter release have been suggested as candidate mechanisms underlying facilitation. However, the small sizes of presynaptic terminals have hindered the biophysical study of short-term facilitation. In the present study, by directly recording from the axon terminal of a rat cerebellar Purkinje cell (PC) in culture, we demonstrate a crucial role of [Ca 2+ ] i -dependent facilitation of Ca 2+ currents in short-term facilitation at inhibitory PC-PC synapses. Voltage clamp recording was performed from a PC axon terminal visualized by enhanced green fluorescent protein, and the Ca 2+ currents elicited by the voltage command consisting of action potential waveforms were recorded. The amplitude of presynaptic Ca 2+ current was augmented upon high-frequency paired-pulse stimulation in a [Ca 2+ ] i -dependent manner, leading to paired-pulse facilitation of Ca 2+ currents. Paired recordings from a presynaptic PC axon terminal and a postsynaptic PC soma demonstrated that the paired-pulse facilitation of inhibitory synaptic transmission between PCs showed 4-5th power dependence on that of Ca 2+ currents, and was completely abolished when the Ca 2+ current amplitude was adjusted to be identical. Thus, short-term facilitation of Ca 2+ currents predominantly mediates short-term synaptic facilitation at synapses between PCs.

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“…The mechanisms for gamma frequency activity in the PPT involve N-type calcium channels during REM sleep, and in the SubCD involve sodium-dependent sub-threshold oscillations [60]. Interestingly, BDNF modulates both N-type calcium and voltage-gated sodium channels [61–63]. These findings suggest a possible mechanism by which BDNF may regulate the manifestation of REM sleep by the PPT and SubCD.…”

Section: Discussionmentioning

confidence: 99%

The homeostatic regulation of REM sleep: A role for localized expression of brain-derived neurotrophic factor in the brainstem

Datta

Knapp

Koul-Tiwari

et al. 2015

Behavioural Brain Research

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Homeostatic regulation of REM sleep plays a key role in neural plasticity and deficits in this process are implicated in the development of many neuropsychiatric disorders. Little is known, however, about the molecular mechanisms that underlie this homeostatic regulation process. This study examined the hypothesis that, during selective REM sleep deprivation (RSD), increased brain-derived neurotrophic factor (BDNF) expression in REM sleep regulating areas is critical for the development of homeostatic drive for REM sleep, as measured by an increase in the number of REM sleep transitions. Rats were assigned to RSD, non-sleep deprived (BSL), or total sleep deprivation (TSD) groups. Physiological recordings were obtained from cortical, hippocampal, and pontine EEG electrodes over a 6-hour period, in which sleep deprivation occurred during the first 3 hours. In the RSD, but not the other conditions, homeostatic drive for REM sleep increased progressively. BDNF protein expression was significantly greater in the pedunculopontine tegmentum (PPT) and subcoeruleus nucleus (SubCD) in the RSD as compared to the TSD and BSL groups, areas that regulate REM sleep, but not in the medial preoptic area, which regulates non-REM sleep. There was a significant positive correlation between RSD-induced increases in number of REM sleep episodes and increased BDNF expression in the PPT and SubCD. These increases positively correlated with levels of homeostatic drive for REM sleep. These results, for the first time, suggest that selective RSD-induced increased expression of BDNF in the PPT and SubCD are determinant factors in the development of the homeostatic drive for REM sleep.

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Activity-Dependent Neurotrophin Signaling Underlies Developmental Switch of Ca²⁺Channel Subtypes Mediating Neurotransmitter Release

Cited by 23 publications

References 52 publications

The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

Ca²⁺ current facilitation determines short‐term facilitation at inhibitory synapses between cerebellar Purkinje cells

The homeostatic regulation of REM sleep: A role for localized expression of brain-derived neurotrophic factor in the brainstem

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Activity-Dependent Neurotrophin Signaling Underlies Developmental Switch of Ca2+Channel Subtypes Mediating Neurotransmitter Release

Cited by 23 publications

References 52 publications

The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

The Role for Alterations in Neuronal Activity in the Pathogenesis of Polyglutamine Repeat Disorders

Ca2+ current facilitation determines short‐term facilitation at inhibitory synapses between cerebellar Purkinje cells

The homeostatic regulation of REM sleep: A role for localized expression of brain-derived neurotrophic factor in the brainstem

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Activity-Dependent Neurotrophin Signaling Underlies Developmental Switch of Ca²⁺Channel Subtypes Mediating Neurotransmitter Release

Ca²⁺ current facilitation determines short‐term facilitation at inhibitory synapses between cerebellar Purkinje cells