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Defects in the expression of <jats:italic>Notch<\/jats:italic> genes result in severe, often lethal developmental abnormalities. Notch3 is generally thought to have a similar proliferative, anti\u2010differentiation and gliogenic role to Notch1. However, in some cases, Notch3 has an opposite, pro\u2010differentiation effect. Here, we show that Notch3 segregates from Notch1 and is transiently expressed in adult rat and mouse spinal cord neuron precursors and immature neurons. This suggests that during the differentiation of adult neural progenitor cells, Notch signalling may follow a modified version of the classical lateral inhibition model, involving the segregation of individual Notch receptors. Notch3 knockout mice, otherwise neurologically normal, are characterized by a reduced number of mature inhibitory interneurons and an increased number of highly excitable immature neurons in spinal cord laminae I\u2013II. As a result, these mice have permanently lower nociceptive thresholds, similar to chronic pain. These results suggest that defective neuronal differentiation, for example as a result of reduced Notch3 expression or activation, may underlie human cases of intractable chronic pain, such as fibromyalgia and neuropathic pain.<\/jats:p>","DOI":"10.1111\/jcmm.12362","type":"journal-article","created":{"date-parts":[[2014,8,28]],"date-time":"2014-08-28T04:45:54Z","timestamp":1409201154000},"page":"2103-2116","source":"Crossref","is-referenced-by-count":37,"title":["Notch3 is necessary for neuronal differentiation and maturation in the adult spinal cord"],"prefix":"10.1111","volume":"18","author":[{"given":"Gabriel","family":"Rusanescu","sequence":"first","affiliation":[{"name":"MGH Center for Translational Pain Research Department of Anesthesia Critical Care and Pain Medicine Massachusetts General Hospital Charlestown MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianren","family":"Mao","sequence":"additional","affiliation":[{"name":"MGH Center for 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