Facilitation of the Inhibitory Transmission by Gastrin-Releasing Peptide in the Anterior Cingulate Cortex

Cao, Xiao Yan; Mercaldo, Valentina; Li, Pingyang; Zhuo, Min

doi:10.1186/1744-8069-6-52

Cited by 16 publications

(26 citation statements)

References 48 publications

(62 reference statements)

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“…; Cao et al . ). To test the involvement of GRP‐GRPR in mediating the effects of NeuroD2 overexpression in regulating inhibitory synaptic tone, we used the GRPR antagonist RC‐3095 (2 μ m ) (Shumyatsky et al .…”

Section: Resultsmentioning

confidence: 97%

“…; Cao et al . ). GRP expresses across many brain areas including cortex, hippocampus and amygdala (Wada et al .…”

Section: Discussionmentioning

confidence: 97%

“…We also observed a decrease in GRP mRNA in cortical tissue taken from P14 KO animals compared to WT littermates (WT = 1 ± 0.05 vs. KO = 0.66 ± 0.1; mean ± SD, P = 0.02). GRP has a positive effect on inhibitory neurotransmission through activation of its receptor GRPR (Shumyatsky et al 2002;Cao et al 2010). To test the involvement of GRP-GRPR in mediating the effects of NeuroD2 overexpression in regulating inhibitory synaptic tone, we used the GRPR antagonist RC-3095 (2 μM) (Shumyatsky et al 2002).…”

Section: Neurod2 Promotes Inhibitory Synapses Through Regulation Of Gmentioning

confidence: 99%

“…GRP acts on the gastrin‐releasing peptide receptor (GRPR) to promote inhibitory neurotransmission (Cao et al . ). We found GRP mRNA was strongly decreased in NeuroD2 null neurons and the GRPR antagonist RC‐3059 partially blocked the increase in inhibitory synaptic inputs onto NeuroD2 overexpressing cells.…”

Section: Introductionmentioning

confidence: 97%

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The transcription factor NeuroD2 coordinates synaptic innervation and cell intrinsic properties to control excitability of cortical pyramidal neurons

Chen

Moran

Zhang

et al. 2016

The Journal of Physiology

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Key pointsr Synaptic excitation and inhibition must be properly balanced in individual neurons and neuronal networks to allow proper brain function.r Disrupting this balance may lead to autism spectral disorders and epilepsy. r We show the basic helix-loop-helix transcription factor NeuroD2 promotes inhibitory synaptic drive but also decreases cell-intrinsic neuronal excitability of cortical pyramidal neurons both in vitro and in vivo.r We identify two genes potentially downstream of NeuroD2-mediated transcription that regulate these parameters: gastrin-releasing peptide and the small conductance, calcium-activated potassium channel, SK2.r Our results reveal an important function for NeuroD2 in balancing synaptic neurotransmission and intrinsic excitability.r Our results offer insight into how synaptic innervation and intrinsic excitability are coordinated during cortical development.Abstract Synaptic excitation and inhibition must be properly balanced in individual neurons and neuronal networks for proper brain function. Disruption of this balance during development may lead to autism spectral disorders and epilepsy. Synaptic excitation is counterbalanced by synaptic inhibition but also by attenuation of cell-intrinsic neuronal excitability. To maintain proper excitation levels during development, neurons must sense activity over time and regulate the expression of genes that control these parameters. While this is a critical process, little is known about the transcription factors involved in coordinating gene expression to control excitatory/inhibitory synaptic balance. We show here that the basic helix-loop-helix transcription factor NeuroD2 promotes inhibitory synaptic drive but also decreases cell-intrinsic neuronal excitability of cortical pyramidal neurons both in vitro and in vivo as shown by ex vivo analysis of a NeuroD2 knockout mouse. Using microarray analysis and comparing wild-type and NeuroD2 knockout cortical networks, we identified two potential gene targets of NeuroD2 that contribute to these processes: gastrin-releasing peptide (GRP) and the small conductance, calcium-activated potassium channel, SK2. We found that the GRP receptor antagonist RC-3059 and the SK2 specific blocker apamin partially reversed the effects of increased NeuroD2 expression on inhibitory synaptic drive and action potential repolarization, respectively. Our results reveal an important

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Section: Resultsmentioning

confidence: 97%

“…; Cao et al . ). GRP expresses across many brain areas including cortex, hippocampus and amygdala (Wada et al .…”

Section: Discussionmentioning

confidence: 97%

Section: Neurod2 Promotes Inhibitory Synapses Through Regulation Of Gmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

See 2 more Smart Citations

The transcription factor NeuroD2 coordinates synaptic innervation and cell intrinsic properties to control excitability of cortical pyramidal neurons

Chen

Moran

Zhang

et al. 2016

The Journal of Physiology

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“…NMBR is important for thermoregulation, but not necessary for smooth muscle contraction, or for suppression of feeding behavior (56). In the CNS, the physiological effect of GRPR has been studied in the anterior cingulated cortex, hippocampus and amygdala (8, 42, 69). In all these structures GRPR is expressed by inhibitory interneurons and GRPR mutant mice showed enhanced long-term potentiation and more persistent long-term fear memory.…”

Section: Nonhistaminergic Itch Signalingmentioning

confidence: 99%

Itch Signaling in the Nervous System

2011

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Itch is a major somatic sensation, along with pain, temperature and touch, detected and relayed by the somatosensory system. Itch can be an acute sensation, associated with mosquito bite, or a chronic condition, like atopic dermatitis (29, 59). The origins of the stimulus can be localized in the periphery or systemic, and associated with organ failure or cancer. Itch is also a perception originating in the brain. Itch is broadly characterized as either histamine-dependent (histaminergic) or histamine-independent (nonhistaminergic), both of which are relayed by subsets of C-fibers, and by the second-order neurons expressing gastrin-releasing peptide receptor (GRPR) and spinothalamic track (STT) neurons in the spinal cord of rodents. Historically, itch research has been primarily limited to clinical and psychophysical studies, and to histamine-mediated mechanisms. In contrast, little is known about signaling mechanisms underlying nonhistaminergic itch, despite the fact that the majority of chronic itch are mediated by nonhistaminergic mechanisms. During the past few years, important progress has been made in understanding of molecular signaling of itch, largely due to the introduction of mouse genetics. In this review, we examine some of molecular mechanisms underlying itch sensation with an emphasis on recent studies in rodents.

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Spinal Mechanisms of Itch Transmission

2017

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Peripheral itch stimuli are transmitted by sensory neurons to the spinal cord dorsal horn, which then transmits the information to the brain. The molecular and cellular mechanisms within the dorsal horn for itch transmission have only been investigated and identified during the past ten years. This review covers the progress that has been made in identifying the peptide families in sensory neurons and the receptor families in dorsal horn neurons as putative itch transmitters, with a focus on gastrin-releasing peptide (GRP)-GRP receptor signaling. Also discussed are the signaling mechanisms, including opioids, by which various types of itch are transmitted and modulated, as well as the many conflicting results arising from recent studies.

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Facilitation of the Inhibitory Transmission by Gastrin-Releasing Peptide in the Anterior Cingulate Cortex

Cited by 16 publications

References 48 publications

The transcription factor NeuroD2 coordinates synaptic innervation and cell intrinsic properties to control excitability of cortical pyramidal neurons

The transcription factor NeuroD2 coordinates synaptic innervation and cell intrinsic properties to control excitability of cortical pyramidal neurons

Itch Signaling in the Nervous System

Spinal Mechanisms of Itch Transmission

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