TY - JOUR ID - 148089992 TI - Physiological Correlates of Abnormal Behaviors in Magnesium-Deficient Rats. AU - Fukui, M. AU - Goto, Y. AU - Nakamura, M. AU - Abe, S. AU - Kato, M. PY - 1993 DB - UniCat KW - Abnormal behavior. KW - Activity. KW - Appearance. KW - Auditory stimulation. KW - Auditory. KW - Behavior. KW - Bradyarrhythmia. KW - Brain. KW - Central-nervous-system. KW - Control. KW - Diet. KW - Ecg. KW - Eeg. KW - Electrocardiogram. KW - Entorhinal cortex. KW - Epilepsy. KW - Epileptiform activity. KW - Events. KW - Experiment. KW - Expression. KW - Extracellular magnesium. KW - Floor. KW - Hippocampal slices. KW - Hippocampal spikes. KW - Hippocampus. KW - Limb. KW - Limbic system. KW - Magnesium deficiency. KW - Nervous system. KW - Nervous-system. KW - Noise. KW - Physiological. KW - Rat. KW - Rats. KW - Response. KW - Seizure. KW - Seizures. KW - Spike. KW - Stimulation. KW - System. KW - Telemetry. UR - https://www.unicat.be/uniCat?func=search&query=sysid:148089992 AB - In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions ER -