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 from senescent mammals is almost completely unknown. To address this issue, we investigated whether IGF-1 effects 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 among other functions that have been found impaired in the brain from 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, & [alpha]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 (2-4 weeks), young-adult (7 months), and senescent (28-29) rats. These results supports 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.