Subconvulsive dose of pentylenetetrazole increases the firing rate of substantia nigra pars reticulata neurons in dystonic but not in nondystonic hamsters

Citation
M. Gernert et al., Subconvulsive dose of pentylenetetrazole increases the firing rate of substantia nigra pars reticulata neurons in dystonic but not in nondystonic hamsters, SYNAPSE, 33(4), 1999, pp. 259-267
Citations number
44
Categorie Soggetti
Neurosciences & Behavoir
Journal title
SYNAPSE
ISSN journal
08874476 → ACNP
Volume
33
Issue
4
Year of publication
1999
Pages
259 - 267
Database
ISI
SICI code
0887-4476(19990915)33:4<259:SDOPIT>2.0.ZU;2-U
Abstract
Dystonic attacks, including twisting movements, can be initiated by mild st ress in mutant (gene symbol dt(sz)) Syrian golden hamsters, an animal model of idiopathic paroxysmal dystonia. Previous studies suggested that dysfunc tions in basal ganglia, which are not restricted to periods of attacks, are involved in the dystonic syndrome in mutant hamsters. Therefore, in the pr esent study in anesthetized animals, we examined whether the spontaneous fi ring rate of extracellularly recorded neurons of the substantia nigra pars reticulata (SNr) differs between dt(sz) and age-matched nondystonic control hamsters. Furthermore, we investigated the responsiveness of these nondopa minergic, presumably GABAergic neurons to a subconvulsive dose (25mg/kgi.p. ) of systemically applied pentylenetetrazole (PTZ), which exerts prodystoni c effects in mutant hamsters. The mean basal (spontaneous) firing rate of S Nr neurons was not altered in mutant hamsters. However, within 5 min after i.p. injection of PTZ, the mean firing rate of SNr neurons significantly in creased to about 160% of predrug control values in dt(sz) but not in contro l hamsters. Although the present study failed to reveal changes in the basa l firing rate of SNr neurons in mutant hamsters, the abnormal response to P TZ is in line with previous pharmacological and biochemical data indicating disturbed function of the GABAergic system. Synapse 33:259-267, 1999. (C) 1999 Wiley-Liss, Inc.