Psychiatry related information on Kcnj9

• 3. Cocaine-stimulated increases in horizontal locomotor activity in wild-type, Kir3.2 knockout, Kir3.3 knockout, and Kir3.2/3.3 double knockout mice, with only minor differences observed between the mouse lines [1].

High impact information on Kcnj9

• On the other hand, coexpression of GIRK3 with GIRK2 suppressed the GIRK2 alone response [2].
• In adult hippocampus, high levels of Kir3.3 channel protein exist in axons that run with the mossy fiber tract [3].
• Axonal sorting of Kir3.3 defines a GABA-containing neuron in the CA3 region of rodent hippocampus [3].
• Axonal sorting of Kir3.3 appears to be typical of a group of large inhibitory neurons, including Purkinje cells and a novel type of interneuron in CA3 [3].
• Kir3.3 and the vesicular GABA transporter could be identified in subpopulations of large synaptic terminals that probably derive from Kir3.3 neurons [3].

Biological context of Kcnj9

• Multiple mRNA variants of Girk1, Girk3, and Girk4 were identified, existing by virtue of alternative splicing and/or usage of distinct transcription initiation sites [4].
• 3. Resting membrane potentials of LC neurons in brain slices from Kir3.2 knock-out, Kir3.3 knock-out, and Kir3.2/3.3 double knock-out mice were depolarized by 15-20 mV relative to LC neurons from wild-type mice [5].

Anatomical context of Kcnj9

• G-protein-gated potassium channels containing Kir3.2 and Kir3.3 subunits mediate the acute inhibitory effects of opioids on locus ceruleus neurons [5].
• Coexpression of GIRK2wv with GIRK1, GIRK2, or GIRK3 in Xenopus oocytes along with expression of subunit combinations linked as dimers and tetramers was used to investigate the effects of the pore mutation on channel selectivity and gating as a function of relative subunit position and number within a heterotetrameric complex [6].

Associations of Kcnj9 with chemical compounds

• In contrast, Kir3.2 and Kir3.3 knockout mice exhibited dramatically reduced intravenous self-administration of cocaine relative to wild-type mice over a range of cocaine doses [1].
• A single locus is partially responsible for the genetic mediation of pain inhibition, and genetic variation associated with the potassium channel gene, Kcnj9, is a prime candidate for explaining the variable response to these analgesic drugs [7].

Other interactions of Kcnj9

• In general, GIRK1 showed the least fluctuation in its levels of expression during development, while dynamic changes were found with the levels of GIRK2 and GIRK3 transcripts [8].
• Hot-plate paw-lick latencies for wild-type, Kir3.2 knockout, Kir3.3 knockout, and Kir3.4 knockout mice were measured at 52 degrees C and 55 degrees C, following the s.c. injection of either saline or 10 mg/kg morphine [9].
• We conclude that G protein-gated potassium channels containing Kir3.2 and/or Kir3.3 play a significant role in responses to moderate thermal stimuli [9].
• On the other hand, mbGIRK2 and mbGIRK3 are more similar to GIRK1 (60%) than to ROMK1 and IRK1 (50%) [10].

References