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Jain, Neeraj
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Preferred name
Jain, Neeraj
Alternative Name
Jain, N.
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ORCID
Scopus Author ID
7202533741
Now showing 1 - 2 of 2
- PublicationCortical reorganization following dorsal spinal injuries in newborn monkeys reveals a critical period in the development of the somatosensory cortex(2025-01)
; ;Hui-Xin Qi ;Arun Raman ;David LyonJon H. KaasLesions of the dorsal columns of the spinal cord in adult macaque monkeys lead to the loss of hand inputs and large-scale expansion of the face inputs in the hand region of the somatosensory cortex. Inputs from alternate spinal pathways do not reactivate the deafferented regions of area 3b. Here, we determined how transections of the dorsal columns done within a few days after birth affect the developing somatosensory cortex. Dorsal columns were transected between the 3rd and 12th postnatal day (PND), and the somatosensory cortex was mapped when the macaques were over 3 y old. There were two distinct outcomes depending on the age at the time of the lesion. In monkeys lesioned between the 3rd and 5th PND, neurons in the entire hand region of area 3b and the adjacent somatosensory cortex responded to touch on the hand. An alternate spinal pathway must have replaced the lost pathway. In monkeys lesioned between the 9th and 12th PND, neurons in the deafferented hand region did not respond to touch on the hand. There was medialward expansion of the face representation into the deafferented cortex and a lateral expansion of the arm representation as in lesioned adults. Thus, different mechanisms underlie the reorganization of area 3b and the adjacent somatosensory cortex following identical spinal cord injuries sustained as early or late newborns. The results suggest that alternate spinal cord pathways can develop within a critical period before the 9th PND, but not later. Copyright © 2025 the Author(s). - PublicationPrenatal protein deficiency causes age-specific alteration in number and distribution of inhibitory neurons in the somatosensory cortex during early postnatal development(2025-03)
;Arti Kumari ;V RemaPrenatal protein deficiency causes behavioral and cognitive dysfunctions in children. The deficits could be caused by altered acquisition and processing of sensory information in the brain. Although GABAergic neurons are the key regulators of neuronal activity, the effect of prenatal protein deficiency on GABA neurons in the brain is largely unknown. We fed pregnant mice diets with one-third (7%) or half (10%) the normal protein requirement (20% protein). After birth, the pups were fostered with normally fed lactating females. We used transgenic mice to show that protein deficiency in pregnant dams fed a 7% protein diet affected the number and distribution of GABA neurons in the somatosensory barrel cortex and individual cortical layers during early postnatal development of pups. If the mothers were fed a 10% protein diet, the effects on GABA neurons were much less. Development of barrels was also affected in pups born to mothers fed the 7% protein diet, but not the 10% group. In addition, high protein deficiency, i.e., the 7% protein diet, affected conception, hampered gestational weight gain, induced resorption of embryos, reduced litter sizes, and increased cannibalism, which was not observed in females on 10% protein diet. © Indian Academy of Sciences 2025.