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Corticotropin‐releasing factor infusion into nucleus incertus suppresses medial prefrontal cortical activity and hippocampo‐medial prefrontal cortical long‐term potentiation
Author(s) -
Farooq Usman,
Rajkumar Ramamoorthy,
Sukumaran Shalini,
Wu You,
Tan Wei Hao,
Dawe Gavin Stewart
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12242
Subject(s) - prefrontal cortex , neuroscience , long term potentiation , infralimbic cortex , stimulation , nucleus , neuroplasticity , chemistry , electrophysiology , psychology , receptor , cognition , biochemistry
The medial prefrontal cortex ( mPFC ) in the rat has been implicated in a variety of cognitive processes, including working memory and expression of fear memory. We investigated the inputs from a brain stem nucleus, the nucleus incertus ( NI ), to the prelimbic area of the m PFC . This nucleus strongly expresses corticotropin‐releasing factor type 1 ( CRF 1 ) receptors and responds to stress. A retrograde tracer was used to verify connections from the NI to the mPFC . Retrogradely labelled cells in the NI expressed CRF receptors. Electrophysiological manipulation of the NI revealed that stimulation of the NI inhibited spontaneous neuronal firing in the mPFC . Similarly, CRF infusion into the NI , in order to mimic a stressful condition, inhibited neuronal firing and burst firing in the mPFC . The effect of concurrent high‐frequency stimulation of the NI on plasticity in the hippocampo‐prelimbic medial prefrontal cortical ( HP ‐ mPFC ) pathway was studied. It was found that electrical stimulation of the NI impaired long‐term potentiation in the HP ‐ mPFC pathway. Furthermore, CRF infusion into the NI produced similar results. These findings might account for some of the extra‐pituitary functions of CRF and indicate that the NI may play a role in stress‐driven modulation of working memory and possibly other cognitive processes subserved by the m PFC .

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