EVIDENCE FOR A THALAMOCORTICAL DYSRHYTHMIA IN MICE TREATED WITH ACUTE COCAINE BINGE.

V. BISAGNO; V. PESKIN; S.I. WIKINSKI; F. J. URBANO

Tandil, Buenos Aires

Congreso; XL REUNION ANUAL DE LA SOCIEDAD ARGENTINA DE FARMACOLOGÍA EXPERIMENTAL; 2008

SOCIEDAD ARGENTINA DE FARMACOLOGÍA EXPERIMENTAL

Cocaine intake might induce brain anomalies with broad behavioral consequences. Altered thalamocortical dynamics are in the basis for several types of both neurological and neuropsychiatic diseases, currently grouped under the name thalamocortical dysrhythmia syndrome (TCDs; Llinas et al., 1999). Abnormal activity of thalamic relay neurons is suggested to be related to an increase of low frequency oscillatory activity due to protracted activation of the T-type calcium channels related to a hyperpolarization due to excess GABAergic inhibition. In our experiments using an acute cocaine binge protocol (3 X 15mg/kg, i.p. inj.., 1 hour apart)., in vivo, EEG recordings showed a significant increment of delta-, theta- and alpha-band activity in the experimental group that was partially reversed after a 24 hour washout period. We measured the enzyme involved in GABA synthesis, GAD, by immunocytochemistry in thalamic nuclei and parietal cortex. No significant differences were found between groups. Preliminary results showed comparable spine density in cortical and thalamic nuclei (using Golgi staining techniques) between saline and cocaine treated mice. Our results suggest that acute cocaine binge induced a transitory TCD. Future experiments will further explore the role of GABA on this phenomenon.