The basolateral amygdala (BL) is a putative site for regulating anxiety, where inhibition and excitation respectively lead to decreases and increases in anxiety-like behaviors. The BL contains local networks of GABAergic interneurons that are subdivided into classes based on neurochemical content, and are hypothesized to regulate unique functional responses of local glutamatergic projection neurons. Recently it was demonstrated that lesioning a portion of the BL interneuronal population, those interneurons that express neurokinin1 receptors (NK1r), resulted in anxiety-like behavior. In the current study, these NK1r expressing cells of the BL are further phenotypically characterized, demonstrating approximately 80% co-expression with GABA thus confirming them as GABAergic interneurons. These NK1r interneurons also colocalize with two distinct populations of BL interneurons as defined by the neuropeptide content. Of the NK1r positive cells, 41.8% are also positive for neuropeptide Y (NPY) and 39.7% of the NK1r positive cells are also positive for cholecystokinin (CCK). In addition to enhancing the phenotypic characterization, the extent to which the NK1r cells of amygdala nuclei contribute to anxiety-like responses was also investigated. Lesioning the NK1r expressing interneurons, with a stable form of substance P (SSP; the natural ligand for NK1r) coupled to the targeted toxin saporin (SAP), in the anterior and posterior divisions of the BL was correlated to increased anxiety-like behaviors compared to baseline and control treated rats. Furthermore the phenotypic and regional selectivity of the lesions was also confirmed.
|Original language||English (US)|
|Number of pages||11|
|State||Published - May 5 2009|
- substance P
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