Title : Epigenetic suppression of GAD65 expression mediates persistent pain.

Pub. Date : 2011 Oct 9

PMID : 21983856






6 Functional Relationships(s)
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1 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus
2 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus
3 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus
4 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus
5 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus
6 We show here that in the rat brainstem nucleus raphe magnus, which is important for central mechanisms of chronic pain, persistent inflammatory and neuropathic pain epigenetically suppresses Gad2 (encoding glutamic acid decarboxylase 65 (GAD65)) transcription through histone deacetylase (HDAC)-mediated histone hypoacetylation, resulting in impaired gamma-aminobutyric acid (GABA) synaptic inhibition. gamma-Aminobutyric Acid glutamate decarboxylase 2 Rattus norvegicus