Trends in Neurosciences
ReviewNormal aging: regionally specific changes in hippocampal synaptic transmission
References (75)
Behav. Neural Biol.
(1993)- et al.
Neurobiol. Aging
(1988) Neurobiol. Aging
(1989)- et al.
Neurobiol. Aging
(1991) - et al.
Trends Neurosci.
(1992) - et al.
Neurobiol. Aging
(1991) Neurobiol. Aging
(1993)- et al.
Electroencephalog. Clin. Neurophysiol.
(1986) - et al.
Neurobiol. Aging
(1993) - et al.
Electroencephalog. Clin. Neurophysiol.
(1983)
Brain Res.
Brain Res.
Neuroscience
Neurobiol. Aging
Neurobiol. Aging
Neurobiol. Aging
Brain Res.
Brain Res.
Neurobiol. Aging
Neurobiol. Aging
Neurobiol. Aging
Neurobiol. Aging
Neurobiol. Aging
Neurobiol. Aging
Mech. Ageing Develop.
Neurobiol. Aging
Brain Res.
Brain Res.
Neurobiol. Aging
Brain Res.
Arch. Gerontol. Geriatr.
Brain Res.
Neurobiol. Aging
Brain Res.
Brain Res.
Brain Res.
Psychol. Rev.
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2021, Neurochemistry InternationalCitation Excerpt :Neuroaging also involve increase threshold for long term potentiation (LTP) induction and the lowering of threshold for long term depression (LTD) induction suggesting that a shift in LTP/LTD balance results in the declination of synaptic transmission and excessive synaptic depression (Barnes, 1994; Foster et al., 2001). Further this shifts in synaptic plasticity during aging is due to the reduced influx of Ca2+ through NMDARs and increased influx Ca2+ through voltage operated calcium channels (Barnes, 1994; Bodhinathan et al., 2010; Lehohla et al., 2008; Norris et al., 1996; Potier et al., 2000; Shankar et al., 1998; Thibault and Landfield, 1996) resulting in the disruption of neuronal Ca2+ homeostasis and cell death (Toescu and Verkhratsky, 2004; Toescu and Vreugdenhil, 2010). Excessive Ca2+ levels is also responsible for overloading of Ca2+ into mitochondria responsible for mitochondrial dysfunction (Petrosillo et al., 2004), and the release of cytochrome c (Vercesi et al., 1997; Iverson and Orrenius, 2004) further responsible for the initiation of apoptotic signaling pathway (Boehning et al., 2003) suggesting severe mitochondrial dysfunction an underlying event responsible for the neuronal degeneration (Gerlach et al., 1991; Kong and Xu, 1998; Panov et al., 2005).