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Su, H., Sochivko, D., Becker, A., Chen, J., Jiang, Y., Yaari, Y. and Beck, H. (2002) Upregulation of T-Type Ca2+ Channels Causes a Long-Lasting Modification of Neuronal Firing Mode after Status Epilepticus. Journal of Neuroscience, 22, 3645-3655.

has been cited by the following article:

• TITLE: Progressive Obesity in Female Rats from Synergistic Interactions between Drugs and Whole Body Application of Weak, Physiologically Patterned Magnetic Fields

  AUTHORS: Linda S. St-Pierre, Michael A. Persinger

  KEYWORDS: Obesity, Drug-Induce Obesity, Weak Magnetic Fields, Drug-Magnetic Field Synergisms

  JOURNAL NAME: Journal of Behavioral and Brain Science, Vol.4 No.6, June 27, 2014

  ABSTRACT: Prepubescent female rats treated with the atypical neuroleptic acepromazine but not ketamine, prazosin, or doxepin, after lithium/pilocarpine-induced seizures gradually became obese over their lifetimes if spontaneous seizures developed. Mild increases in weight gain were induced when prepuberal females were given pilocarpine and acepromazine while being exposed briefly (1.5 hr) to a frequency-modulated magnetic field known to induce seizures. Weekly (1.5 hr) exposures to physiologically-patterned magnetic fields over 36 wks had no effect on weight gain while continuous periseizure exposure to 50 Hz fields above about 1 μT facilitated mild weight gains and protracted aggression. Perinatal exposure to a very weak, a 7 Hz magnetic field or a nitric oxide inhibitor retarded the weight gain induced by the obesity procedure. These results indicate that synergisms during a single episode between neuronal electrical lability and pharmacological states can initiate a process of weight gain that progresses to extreme obesity. We suggest that at least a component of the global “epidemic of obesity” could be related to a synergism between the insidious emergence of amplitude modulations within biologically compatible electromagnetic frequencies from the proliferation of communication systems and the pervasive utilization of pharmacology to treat transient disorders of ontogeny within the human population.