Increases in the numerical density of GAT-1 positive puncta in the barrel cortex of adult mice after fear conditioning.

Manabu Sakakibara,Ewa Siucinska,Adam Hamed,Malgorzata Jasinska

doi:10.1371/journal.pone.0110493

Manabu Sakakibara, Ewa Siucinska + Show 2 more

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https://doi.org/10.1371/journal.pone.0110493

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Abstract

Three days of fear conditioning that combines tactile stimulation of a row of facial vibrissae (conditioned stimulus, CS) with a tail shock (unconditioned stimulus, UCS) expands the representation of “trained” vibrissae, which can be demonstrated by labeling with 2-deoxyglucose in layer IV of the barrel cortex. We have also shown that functional reorganization of the primary somatosensory cortex (S1) increases GABAergic markers in the hollows of “trained” barrels of the adult mouse. This study investigated how whisker-shock conditioning (CS+UCS) affected the expression of puncta of a high-affinity GABA plasma membrane transporter GAT-1 in the barrel cortex of mice 24 h after associative learning paradigm. We found that whisker-shock conditioning (CS+UCS) led to increase expression of neuronal and astroglial GAT-1 puncta in the “trained” row compared to controls: Pseudoconditioned, CS-only, UCS-only and Naïve animals. These findings suggest that fear conditioning specifically induces activation of systems regulating cellular levels of the inhibitory neurotransmitter GABA.

Highlights

Previous work on the primary somatosensory cortex (S1, barrel cortex) has demonstrated that there is expansion of the ‘‘trained’’ barrels after animals acquire whisker shock conditioning [1] or whisker-trace-eyeblink conditioning [2]
In tail shock alone (UCS-only group n = 6), the whisker stimulation described above was omitted, but a single tail shock was applied for the same duration and the same number of times as in whisker-shock conditioning (CS+UCS) group
This shows that a tail shock applied alone produced a definite observable response, i.e. reduction of head turnings

Summary

Introduction

Previous work on the primary somatosensory cortex (S1, barrel cortex) has demonstrated that there is expansion of the ‘‘trained’’ barrels after animals acquire whisker shock conditioning [1] or whisker-trace-eyeblink conditioning [2]. Learning in adult animals generates structural [4,5,6] functional [3] or small scale changes [7] in primary sensory cortex. Large scale changes are associated with structural and functional deficiency of the cortical circuits [8,9]. The pioneering studies of Hendry and Jones [12,13] demonstrated activity dependent regulation of layer IV immunostained GABAergic neurons in the monkey visual cortex. The inhibitory system in the primary somatosensory cortex of rodents can be affected by increasing peripheral stimulation [14]. Several reports have suggested that both excitatory and inhibitory circuits in the neocortex are strongly regulated by experience [15,16,17,18]

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