Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of Mice Was Reduced in Aging.

Nuria García-Magro,Jonathan A Zegarra-Valdivia,Ignacio Torres-Aleman,Sara Troyas-Martinez,Angel Nuñez

doi:10.3390/cells11040717

Abstract

Aging is accompanied by a decline in cognition that can be due to a lower IGF-I level. We studied response facilitation induced in primary somatosensory (S1) cortical neurons by repetitive stimulation of whiskers in young and old mice. Layer 2/3 and 5/6 neurons were extracellularly recorded in young (≤ 6 months of age) and old (≥ 20 month of age) anesthetized mice. IGF-I injection in S1 cortex (10 nM; 0.2 μL) increased whisker responses in young and old animals. A stimulation train at 8 Hz induced a long-lasting response facilitation in only layer 2/3 neurons of young animals. However, all cortical neurons from young and old animals showed long-lasting response facilitation when IGF-I was applied in the S1 cortex. The reduction in response facilitation in old animals can be due to a reduction in the IGF-I receptors as was indicated by the immunohistochemistry study. Furthermore, a reduction in the performance of a whisker discrimination task was observed in old animals. In conclusion, our findings indicate that there is a reduction in the synaptic plasticity of S1 neurons during aging that can be recovered by IGF-I. Therefore, it opens the possibility of use IGF-I as a therapeutic tool to ameliorate the effects of heathy aging.

Highlights

It has been demonstrated that the insulin-like growth factor I (IGF-I) can be a potent stimulator of neuronal activity, participating in numerous brain processes
The functional implications of these changes must be explored because modulation of the excitability of neurons by IGF-I may be involved in synaptic plasticity such as long-term potentiation (LTP), which are critical for learning and memory processes
Whisker Responses Increased in the Presence of IGF-I in Young and Old Animals

Summary

Introduction

It has been demonstrated that the insulin-like growth factor I (IGF-I) can be a potent stimulator of neuronal activity, participating in numerous brain processes (see for review [1,2,3,4,5]). IGF-I increases the spontaneous firing rate as well as the response to afferent stimulation in target neurons [6,7,8,9,10,11]. The functional implications of these changes must be explored because modulation of the excitability of neurons by IGF-I may be involved in synaptic plasticity such as long-term potentiation (LTP), which are critical for learning and memory processes. When IGF-I is reduced, LTP is impaired [14,15]. Deprivation of IGF-I reversibly impairs learning [15,16]

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Results

Conclusion