Treatment of aged rat sensory neurons in short-term, serum-free culture with nerve growth factor reverses the effect of aging on neurite outgrowth, calcium currents, and neuronal survival

Ciliary Neurotrophic Factor-treated Astrocyte Conditioned Medium Regulates the L-type Calcium Channel Activity in Rat Cortical Neurons

“…Accumulated data have confirmed that FGF-2 [13][14][15][16][17] as well as NGF [18][19][20][21] not only promotes the expression of functional LCC, but also augments the amplitude of Ica-L in neurons. To investigate which component in CNTF-ACM is responsible for the upregulation of LCC activity in neurons, we assessed the concentration of FGF-2 and NGF in conditioned media by ELISA assay.…”

Novel mechanism of increased Ca2+ release following oxidative stress in neuronal cells involves type 2 inositol-1,4,5-trisphosphate receptors

“…Numerous studies have indicated the critical role for regulation of the intracellular Ca 2+ concentration in the pathogenesis of age-related neuronal dysfunction with a variety of techniques and human disease model systems (Landfield, 1987; Mattson and Chan, 2001; Mattson et al, 1989; Missiaen et al, 2000; Squier and Bigelow, 2000; Thibault et al, 1998). Perturbations in the intracellular Ca 2+ homoeostasis are often a result of oxidative stress and are typically correlated with deficits in nerve cell function, increased cell damage and cell death of neurons and require control of the intracellular Ca 2+ concentration to achieve improvement of the conditions (Baskys and Adamchik, 2001; Butterfield et al, 2001; Chen, 1998; Chen and Fernandez, 1999; Hall et al, 2001; Kontush, 2001; Leissring et al, 2000; Massheimer et al, 2000; Mattson and Chan, 2001; Mattson et al, 1989; Mattson et al, 2000; Missiaen et al, 2000; O'Neill et al, 2001; Squier and Bigelow, 2000; Thibault et al, 2001; Thibault et al, 1998; Tuppo and Forman, 2001; Veinbergs et al, 2002). IP 3 Rs are pivotal to the regulation of intracellular Ca 2+ and neuronal function (Berridge, 2009) and have been found involved in a variety of pathophysiological mechanisms, including those leading to AD (for review see, Stutzmann, 2005), by either direct or indirect modulation (Cheung et al, 2010; Crews et al, 1994; Ferrari-DiLeo and Flynn, 1993; Ferreiro et al, 2006; Garlind et al, 1995; Kasri et al, 2006; Kurumatani et al, 1998; Stokes and Hawthorne, 1987; Stutzmann et al, 2004; Young et al, 1988).…”

Behavioral and Cellular Level Changes in the Aging Somatosensory System

“…These findings suggest that age‐related deficits in thermal and mechanical responses are not simply a result of anatomical changes but might also reflect changes at the cellular and molecular level that alter sensory neuron response properties. Such change could include altered expression of genes encoding trophic factors and their receptors, neuropeptides, cell adhesion molecules, ion channels or genes related to mitochondrial function and calcium handling 8,9 …”

“…Such change could include altered expression of genes encoding trophic factors and their receptors, neuropeptides, cell adhesion molecules, ion channels or genes related to mitochondrial function and calcium handling. 8,9 Much of our understanding of changes that occur in aging sensory neurons is based on studies of anatomy and behavioral responses carried out in rodents. Sensory nerves of aging rodents exhibit slower nerve conduction velocity and action potential amplitude, and this decrease begins in early adulthood.…”