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Preservation of motor neuron Ca²⁺ channel sensitivity to insulin-like growth factor-1 in brain motor cortex from senescent rat

Hongqu Shan*, María Laura Messi*, Zhenlin Zheng*, Zhong-Min Wang* and Osvaldo Delbono*†‡

Despite the multiple effects on mammals during development, the effectiveness of the insulin-like growth factor-1 (IGF-1) to sustain cell function and structure in the brain of senescent mammals is almost completely unknown. To address this issue, we investigated whether the effects of IGF-1 on specific targets are preserved at later stages of life. Voltage-gated Ca²⁺ channels (VGCC) are well-characterized targets of IGF-1. VGCC regulate membrane excitability and gene transcription along with other functions that have been found to be impaired in the brain of senescent rodents. As the voluntary control of movement has been reported to be altered in the elderly, we investigated the expression, function and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca²⁺ channels to IGF-1, using the whole-cell configuration of the patch-clamp and RT-PCR in the specific region of the rat motor cortex that controls hindlimb muscle movement. We detected the expression of _1A, _1B and _1E genes encoding the HVA Ca²⁺ channels P/Q, N and R, respectively, but not _1C, _1D, _1S encoding the L-type Ca²⁺ channel in this region of the brain cortex. IGF-1 enhanced Ca²⁺ channel currents through P/Q- and N-type channels but not significantly through the R-type or LVA channels. IGF-1 enhanced the amplitude but did not modify the voltage dependence of Ca²⁺ channel currents in young (2- to 4-week-old), young adult (7-month-old) and senescent (28- to 29-month-old) rats. These results support the concept that despite the reported decrease in circulating (liver) and local (central nervous system) production of IGF-1 with ageing, key neuronal targets such as the VGCC remain responsive to the growth factor throughout life.

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