Slow oscillatory activity of rat globus pallidus neurons in vitro.
The neurons in the external segment of the pallidum in the primate develop a characteristic firing pattern consisting of alternately occurring long, 2-20 s, strongly active phases and long completely silent phases when the subthalamo-pallidal excitatory inputs are blocked. The induction of the activity might be a factor in the development of dyskinesias after the loss of subthalamic output. In this study, we used globus pallidus (GPe) slice preparations obtained from juvenile rats to examined the conditions that support the alternatively occurring long depolarized and hyperpolarized phases which we refer to as the slow oscillation (SO). SO was not induced by the blockade of glutamatergic inputs but was induced by treatments that depolarized dendrites and, at the same time, hyperpolarized the somata with current injections. The treatments included elevation of extracellular K(+), application of K-current blockers and the lowering of extracellular Ca(2+). Application of TTX or intracellular BAPTA injection blocked the SO, while the SO could be maintained in hyperpolarization-activated inward current blockers, organic Ca-current blockers and up to 200 microm CdCl(2). These results suggest that Na currents play a major role in the generation of SO in vitro. It can be speculated that Na currents are involved in the development of active phases observed in the GPe after blockade of the glutamatergic inputs in vivo and that the unique property of GPe neurons in maintaining strong activity after the elimination of the glutamatergic driving force contributes to the development of motor disorders such as dyskinesia.
Hashimoto
Kenji
K
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, 855 Monroe Avenue, Memphis, TN 38163, USA.
Kita
Hitoshi
H
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D019256:Cadmium Chloride / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005917:Globus Pallidus / Q000166:cytology*; D066298:In Vitro Techniques; D009474:Neurons / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D010879:Piperazines / Q000494:pharmacology; D011724:Pyridazines / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D000779:Anesthetics, Local; D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D010879:Piperazines; D011724:Pyridazines; D011743:Pyrimidines; D011810:Quinoxalines; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; C082246:ICI D2788; D013779:Tetrodotoxin; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; C049853:gabazine; D019256:Cadmium Chloride; D002118:Calcium