Cortisol-induced effects on human cortical excitability
Received 12 June 2009; received in revised form 21 July 2009; accepted 26 July 2009. published online 21 August 2009.
Background
Cortisol may fulfill all criteria for a neuromodulator. However, it is not known whether it may rapidly influence motor system activity in humans.
Objective
Circulating cortisol levels were manipulated by administration of a single intravenous dose of hydrocortisone or saline solution, on separate days, to study changes in corticospinal and motor cortical excitability.
Methods
Motor-evoked potentials (MEPs) to single- and paired-pulse transcranial magnetic stimulation from the resting first dorsal interosseous muscle, and cortisol plasma levels were assessed before and after either a bolus of 20 mg of hydrocortisone or saline solution in seven healthy subjects.
Results
Mean cortisol plasma level rapidly rose, peaked between 5 and 10 minutes after hydrocortisone injection, to slowly decay afterward. Mean MEP amplitude significantly increased from preinjection levels, and mean standard deviation of MEPs significantly increased between 8-12 minutes postinjection. Short-intracortical inhibition, tested during the same period, was significantly decreased. No significant changes in the above measures were observed after saline solution administration.
Conclusions
Our results suggest that high circulating levels of cortisol rapidly increase corticospinal excitability and reduce gamma aminobutyric acid activity, as measured by short-intracortical inhibition, in humans. These effects, lasting about 10 minutes, were observed within 15 minutes from the pharmacological intervention. They are therefore compatible with a nongenomic mechanism. These findings are important in view of the notion that a decrease in intracortical gamma aminobutyric acid activity appears to be a prerequisite for motor learning and plastic processes in the human motor cortex.
aSezione di Neurofisiologia Clinica, Dipartimento di Scienze Neurologiche e del Comportamento, Universita' di Siena, Siena, Italy
bDipartimento di Fisiologia, Universita' di Siena, Siena, Italy
Correspondence: Dr. R. Mazzocchio, Sezione di Neurofisiologia Clinica, Dipartimento di Scienze Neurologiche, Neurochirurgiche e del Comportamento, Universita' di Siena, Policlinico “Le Scotte”, Viale Bracci, I-53100 Siena, Italy.
This study was supported by a grant from the University of Siena (Piano di Ateneo per la Ricerca, PAR 2007). There are no biomedical financial interests or potential conflicts of interest.
ABSTRACT