Premium
The effect of acute swim stress and learning in the water maze on hippocampal synaptic activity as well as plasticity in the dentate gyrus of freely moving rats
Author(s) -
Iqbal Mohamed Ariff,
Sulagna Das,
Anirban Basu
Publication year - 2012
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2012.03.226
Subject(s) - dentate gyrus , hippocampal formation , neuroscience , synaptic plasticity , psychology , hippocampus , cognitive psychology , medicine , receptor
E-mail address: anirban@nbrc.ac.in (A. Basu). Introduction: Japanese encephalitis virus (JEV), a neurotropic virus targets CNS and infects different brain regions including SVZ. Apart from infecting neurons and leading to substantial neuronal injury, JEV also infects neural stem/progenitors (NSPCs) which are essential for neuronal repair. In JEV, the survivors have long-term neurological deficits, correlate with depletion of NSPCs. The objective of the study is to see whether the fate or differentiation pattern of NSPCs change after virus infection. To determine the temporal profiling of fate specific genes and transcription factors. Methods: SVZ of BALB/c pups (postnatal day7) was dissected out and NSPCs were isolated and selected through passaging in growth factor supplemented selective media. Cells were subsequently infected with JEV at 5 MOI and allowed them to differentiate. ICC staining done for cell specific markers and RT and qRT-PCR were done to quantify the fate specific genes and transcription factors. Results: The experiments demonstrate that JEV infection inhibits migration and differentiation of neurospheres. In JEV infected neurosphere, the proportion of migrating and differentiating cells were decreased considerably. JEV infected NSPCs show an impaired ability to differentiate into both neurons and astrocytes. Differentiation of JEV infected NSPCs resulted in significantly reduced beta III tubulin+ve, MAP-2+ve and GFAP+ve cells. Further study is about the temporal profile of cell specific genes (beta III tubulin, DCX and GFAP) and transcription factors (Ngn1, Mash1 and NeuroD). It shows there is a significant reduction in neuron specific genes in JEV infected NSPCs and astrocytic differentiation is recovered in 3 days differentiation. Discussion: Thus it seems possible that JEV-infected NSPCs show hampered neurogenesis and migration in SVZ which is important for neuronal repair and CNS regeneration after insult/injury. Neuronal differentiation is more affected than astrocytic differentiation.