Lee C, Rajkumar R, Suri S, Chin WM, Dawe GS (2011) The nucleus incertus contributes to the anxiety-like behaviour in rats. Neuroscience 2011 Abstracts 901.09. Society for Neuroscience, Washington, DC.
Summary: The nucleus incertus (NI), the principal source of relaxin-3 (Rln3) in the brain, is found in the periventricular gray, ventral and medial to the posterodorsal tegmental nucleus (PDTg). Several neuroanatomical studies have indicated that the NI projects to putative correlates of anxiety, especially the amygdala. Relaxin family peptide receptor type-3 (Rxfp3), the native receptor for Rln3, is expressed in the amygdala. These studies have hence predicted that the NI is strategically located to control neural circuits that underlie anxiety-like behaviour in rodents. Presence of Rln3-immunoreactive nerve fibres in the amygdala suggested the involvement of the Rln3/Rxfp3 system. Corticotrophin-releasing factor receptors type-1 (Crfr-1), one of the important anxiolytic drug targets, are prominently expressed in the NI neurons. Based on the aforesaid anatomical and receptor distribution reports, the present investigation was designed to clarify the function of the NI in anxiety-like behaviour of rats. We hypothesized that lesioning of the NI and the resulting decrease in Rln3 would affect the regulation of stress and anxiety response in rats. Firstly, the effect of NI neuron ablation, by CRF-Saporin toxin, on fear conditioning and elevated plus maze (EPM) exploration paradigms was evaluated. Secondly, the firing rates of NI neurons as the rat explored the EPM were assessed. Lastly, the effects of high frequency simulation of the NI on the expression of immediate early genes (IEG) in the amygdala were studied. The results revealed that, in a cued fear conditioning paradigm, NI-lesioned rats exhibited greater fear, indicated by longer freezing periods in the test phase, than sham-lesioned rats. Likewise, in the EPM, NI-lesioned rats made fewer entries into and spent less time in the open arms demonstrating an anxious phenotype. In addition, the NI also showed distinct firing patterns in the open and closed arms of the EPM. Stimulation of the NI activated the medial amygdaloid (MeA) nucleus as indicated by the increased expression of markers of neuronal activation. To sum up, the present study shows a significant contribution of the NI and NI-MeA pathway in the anxiety-like behaviour of rats. It also suggests that the NI and/or Rln3 have a role in the regulation of anxiety-like behaviour, implicating them as targets for anxiety-related disorders.
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