RGD Reference Report - Mechanism of GABA involvement in post-traumatic trigeminal neuropathic pain: Activation of neuronal circuitry composed of PKCgamma interneurons and pERK1/2 expressing neurons.

General

Mechanism of GABA involvement in post-traumatic trigeminal neuropathic pain: Activation of neuronal circuitry composed of PKCgamma interneurons and pERK1/2 expressing neurons.
Authors:	Dieb, W Hafidi, A
Citation:	Dieb W and Hafidi A, Eur J Pain. 2014 May 28. doi: 10.1002/ejp.525.
RGD ID:	9588557
Pubmed:	PMID:24890317 (View Abstract at PubMed)
DOI:	DOI:10.1002/ejp.525 (Journal Full-text)
BACKGROUND: GABA disinhibition within the spinal dorsal horn has been implicated in pain hypersensitivity on injury in different neuropathic models. However, GABA alteration has been explored in only one study on trigeminal neuropathic pain. METHODS: The present study investigated the implication of GABA in trigeminal dynamic mechanical allodynia (DMA) obtained after chronic constriction of the infraorbital nerve (CCI-IoN), and explored the cellular and molecular mechanisms by which GABA dysfunction induced DMA. RESULTS: Our data demonstrated a significant decrease in labelling in two GABA cell markers, glutamate acid decarboxylase (GAD67), and parvalbumin, in the medullary dorsal horn (MDH) of allodynic rats in comparison to sham rats. Increasing GABA by intracisternal injections of vigabatrin (VGB), a blocker of the catabolic enzyme GABA transaminase, alleviated pain behaviour and restored normal GABA cell marker expression in allodynic MDH. Interestingly, intracisternal VGB administration also significantly decreased PKCgamma staining, i.e., of its phosphorylated active form and the number of pERK1/2 positive cells within the MDH. These two markers were highly expressed in allodynic MDH. CONCLUSION: The circuitry composed of PKCgamma and pERK1/2 cells is silent under physiological conditions but is activated after CCI-IoN, therefore, switching touch stimuli to pain sensation. The decrease of GABA transmission constituted a key factor in the activation of this neuronal circuitry, which opens the gate for non-noxious stimuli to reach nociceptive projection neurons in lamina I.

RGD Manual Disease Annotations Click to see Annotation Detail View

Only show annotations with direct experimental evidence (0 objects hidden)

Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
Hyperalgesia	treatment	ISO	Abat (Rattus norvegicus)	9588557; 9588557		RGD
Hyperalgesia	treatment	IMP		9588557		RGD

Objects Annotated

Genes (Rattus norvegicus)

Abat (4-aminobutyrate aminotransferase)

Genes (Mus musculus)

Abat (4-aminobutyrate aminotransferase)

Genes (Homo sapiens)

ABAT (4-aminobutyrate aminotransferase)

Additional Information

Gene Annotator (Functional Annotation) unavailable	Gene Annotator (Annotation Distribution) unavailable	Variant Visualizer (Genomic Variants) unavailble Variant Visualizer (Genomic Variants) unavailable
Gene Annotator (Functional Annotation)	Gene Annotator (Annotation Distribution)	Variant Visualizer (Genomic Variants)

InterViewer (Protein-Protein Interactions) unavailable	Gviewer (Genome Viewer) unavailable	Variant Visualizer (Damaging Variants) unavailble Variant Visualizer (Damaging Variants) unavailable
InterViewer (Protein-Protein Interactions)	GViewer (Genome Viewer)	Variant Visualizer (Damaging Variants)

Gene Annotator (Annotation Comparison) unavailable	OLGA (Gene List Generator) unavailable
Gene Annotator (Annotation Comparison)	OLGA (Gene List Generator)	Excel (Download)

MOET (Multi-Ontology Enrichement) unavailable	GOLF (Gene-Ortholog Location Finder) unavailable
MOET (Multi-Ontology Enrichement)	GOLF (Gene-Ortholog Location Finder)

Create Name:

Description:

Send us a Message

Mechanism of GABA involvement in post-traumatic trigeminal neuropathic pain: Activation of neuronal circuitry composed of PKCgamma interneurons and pERK1/2 expressing neurons.