Abstract
It has been demonstrated that stress impairs performance of skilled reaching and walking tasks in rats due to the action of glucocorticoids involved in the stress response. Skilled reaching and walking are controlled by the primary motor cortex (M1); however, it is not known whether stress-related impairments in skilled motor tasks are related to functional and/or structural alterations within the M1. We studied the effects of single and repeated injections of corticosterone (twice daily for 7 days) on spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) recorded from layer II/III pyramidal neurons in ex vivo slices of the M1, prepared 2 days after the last administration of the hormone. We also measured the density of dendritic spines on pyramidal cells and the protein levels of selected subunits of AMPA, NMDA, and GABAA receptors after repeated corticosterone administration. Repeatedly administered corticosterone induced an increase in the frequency but not in the amplitude of sEPSCs, while a single administration had no effect on the recorded excitatory currents. The frequency and amplitude of sIPSCs as well as the excitability of pyramidal cells were changed neither after single nor after repeated corticosterone administration. Treatment with corticosterone for 7 days did not modify the density of dendritic spines on pyramidal neurons. Corticosterone influenced neither the protein levels of GluA1, GluA2, GluN1, GluN2A, and GluN2B subunits of glutamate receptors nor those of α1, β2, and γ2 subunits of the GABAA receptor. The increase in sEPSCs frequency induced by repeated corticosterone administration faded out within 7 days. These data indicate that prolonged administration of exogenous corticosterone selectively and reversibly enhances glutamatergic, but not GABAergic transmission in the rat motor cortex. Our results suggest that corticosterone treatment results in an enhancement of spontaneous glutamate release from presynaptic terminals in the M1 and thereby uncovers a potential mechanism underlying stress-induced motor functions impairment.
Highlights
In the rat brain, the primary motor cortex (M1) contains motor maps, which are representations of how movements are organized [8, 32]
We have previously investigated the effects of repeated corticosterone administration lasting 7 and 21 days, on field potentials evoked in layer II/III of the rat motor cortex [4]
We have previously reported that glutamatergic field potentials evoked in layer II/III of the frontal cortical area M1 by stimulation of underlying sites were increased after repeated corticosterone administration lasting 7 and 21 days
Summary
The primary motor cortex (M1) contains motor maps, which are representations of how movements are organized [8, 32]. Examples of M1-controlled motor functions in the rat include skilled limb use in reaching for food [49] and in rung ladder walking [1]. Motor skill learning is associated with a reorganization of movement representations within the rat M1 [19, 36]. The mechanism of motor skill learningrelated plasticity of the M1 involves activity-dependent, longterm strengthening of excitatory synaptic connections within the cortical layer II/III [37,38,39]. Motor skill learning has been reported to induce an increase in synapse number in the M1 [20]. Stress-related impairments in skilled motor tasks may be related to functional and/or structural plasticity of excitatory synapses within rat M1; this possibility has not yet been investigated
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