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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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NK-3 receptors are expressed on mouse striatal gamma-aminobutyric acid-ergic interneurones and evoke [(3)H] gamma-aminobutyric acid release.

In the present study the ability of tachykinin agonists and antagonists to modulate gamma-aminobutyric acid (GABA) release has been correlated with tachykinin receptor expression in the mouse striatum. Significant GABA release was observed when striatal slices were challenged with the NK-3 receptor agonist senktide, the selectivity of which was confirmed using the NK-3 receptor antagonist SR142801. In situ hybridisation revealed co-expression of NK-3 receptors with nitric oxide synthase (NOS)/preprosomatostatin containing GABAergic interneurones. These findings suggest that tachykinins modulate GABA release within the striatum via interaction with NK-3 receptors on somatostatin/NOS interneurones.[1]

References

  1. NK-3 receptors are expressed on mouse striatal gamma-aminobutyric acid-ergic interneurones and evoke [(3)H] gamma-aminobutyric acid release. Preston, Z., Richardson, P.J., Pinnock, R.D., Lee, K. Neurosci. Lett. (2000) [Pubmed]
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