GABAB receptors inhibit low-voltage activated and high-voltage activated Ca2+ channels in sensory neurons via distinct mechanisms

Biochemical and Biophysical Research Communications

Volumn 465, Issue 2, 2015, Pages 188-193

  Huang, Dongyang ^a   Huang, Sha ^a   Peers, Chris ^b   Du, Xiaona ^a   Zhang, Hailin ^a   Gamper, Nikita ^a,b  

^a HEBEI MEDICAL UNIVERSITY   (China)

^b UNIVERSITY OF LEEDS   (United Kingdom)

Author keywords

Baclofen; GABAB receptors; Nociceptor; Opioid receptor; Redox mechanisms; T type Ca2+ channels

Indexed keywords

4 AMINOBUTYRIC ACID B RECEPTOR; BACLOFEN; CALCIUM CHANNEL; CALCIUM CHANNEL T TYPE; DITHIOTHREITOL; ENKEPHALIN[2 DEXTRO ALANINE 4 METHYLPHENYLALANINE 5 GLYCINE]; HIGH VOLTAGE ACTIVATED CALCIUM CHANNEL; PERTUSSIS TOXIN; REACTIVE OXYGEN METABOLITE; UNCLASSIFIED DRUG; 4 AMINOBUTYRIC ACID; 4 AMINOBUTYRIC ACID A RECEPTOR; 4 AMINOBUTYRIC ACID B RECEPTOR STIMULATING AGENT; CALCIUM CHANNEL L TYPE; CALCIUM CHANNEL N TYPE; GUANOSINE 5'-O-(2-THIODIPHOSPHATE); GUANOSINE DIPHOSPHATE; NUCLEOTIDE;

ADULT; ANALGESIA; ANIMAL CELL; ARTICLE; CALCIUM CURRENT; CONTROLLED STUDY; HEK293 CELL LINE; HUMAN; HUMAN CELL; IC50; NONHUMAN; OXIDATION REDUCTION REACTION; PAIN RECEPTOR; PRIORITY JOURNAL; RAT; SENSORY NERVE CELL; SPINAL CORD NERVE CELL; SPINAL GANGLION; WHOLE CELL PATCH CLAMP; ANALOGS AND DERIVATIVES; ANIMAL; CYTOLOGY; DRUG EFFECTS; METABOLISM; NOCICEPTION; PAIN; PATCH CLAMP TECHNIQUE; PATHOPHYSIOLOGY; PHYSIOLOGY; PRIMARY CELL CULTURE; SIGNAL TRANSDUCTION; SPRAGUE DAWLEY RAT;

MAMMALIA;

ANIMALS; BACLOFEN; CALCIUM CHANNELS, L-TYPE; CALCIUM CHANNELS, N-TYPE; CALCIUM CHANNELS, T-TYPE; DITHIOTHREITOL; ENKEPHALIN, ALA(2)-MEPHE(4)-GLY(5)-; GABA-B RECEPTOR AGONISTS; GAMMA-AMINOBUTYRIC ACID; GANGLIA, SPINAL; GUANOSINE DIPHOSPHATE; HEK293 CELLS; HUMANS; NOCICEPTION; PAIN; PATCH-CLAMP TECHNIQUES; PERTUSSIS TOXIN; PRIMARY CELL CULTURE; RATS; RATS, SPRAGUE-DAWLEY; RECEPTORS, GABA-A; RECEPTORS, GABA-B; SENSORY RECEPTOR CELLS; SIGNAL TRANSDUCTION; THIONUCLEOTIDES;

EID: 84940460774     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2015.07.137     Document Type: Article

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