alexa Low frequency stimulation modifies receptor binding in rat brain.
Pharmaceutical Sciences

Pharmaceutical Sciences

Biochemistry & Pharmacology: Open Access

Author(s): LpezMeraz ML, NeriBazn L, Rocha L

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Abstract 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 (n = 14) received twice daily LFS (15 min train of 1Hz, 0.1 ms at an intensity of 100 to 400 microA) immediately after amygdala kindling stimulation (1s train of 60 Hz biphasic square waves, each 1 ms at amplitude of 200-500 microA) 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 (n = 7) received amygdala LFS twice daily for 40 trials. Animals were sacrificed 24 h after last stimulation and their brain used for labeling mu 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 mu 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. This article was published in Epilepsy Res and referenced in Biochemistry & Pharmacology: Open Access

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