Low frequency stimulation modifies receptor binding in rat brain.

摘要

Experiments were designed to reproduce the antiepileptic effects of low frequency stimulation (LFS) during the amygdala kindling process and to examine LFS-induced changes in receptor binding levels of different neurotransmitters in normal brain. Male Wistar rats were stereotactically implanted in the right amygdala with a bipolar electrode. Rats ( [Formula: see text] ) received twice daily LFS (15min train of 1Hz, 0.1ms at an intensity of 100 to 400microA) immediately after amygdala kindling stimulation (1s train of 60Hz biphasic square waves, each 1ms at amplitude of 200-500microA) during 20 days. The LFS suppressed epileptogenesis (full attainment of stage V kindling) but not the presence of partial seizures (lower stages of kindling) in 85.7% of the rats. Thereafter, normal rats ( [Formula: see text] ) received amygdala LFS twice daily for 40 trials. Animals were sacrificed 24h after last stimulation and their brain used for labeling micro opioid, benzodiazepine (BZD), alpha(1)-adrenergic, and adenylyl cyclase binding. Autoradiography experiments revealed increased BZD receptor binding in basolateral amygdala (20.5%) and thalamus (29.3%) ipsilateral to the place of stimulation and in contralateral temporal cortex (18%) as well as decreased values in ipsilateral frontal cortex (24.2%). Concerning micro receptors, LFS decreased binding values in ipsilateral sensorimotor (7.2%) and temporal (5.6%) cortices, dentate gyrus (5.8% ipsi and 6.8% contralateral, respectively), and contralateral CA1 area of dorsal hippocampus (5.5%). LFS did not modify alpha(1) receptor and adenylyl cyclase binding values. These findings suggest that the antiepileptic effects of LFS may involve activation of GABA-BZD and endogenous opioid systems.