In vivo extracellular electrophysiology of pallidal neurons in dystonic and nondystonic hamsters

In the dt(sz) hamster, a model of idiopathic paroxysmal dystonia, recent fi ndings indicated a decreased neuronal activity within the globus pallidus ( GP) and an impaired gamma aminobutyric acid (GABA)ergic function when compa red to nondystonic controls. Therefore, in the present study, extracellular single-unit recordings combined with systemical application of a subconvul sant prodystonic dose of pentylenetetrazole (PTZ) were used to compare the electrophysiological properties of GP neurons in anesthetized dt(sz) hamste rs and nondystonic controls. The spontaneous discharge rate of GP neurons w as not decreased but a trend towards a wide-ranged distribution was found i n mutants compared to controls. Since the single-unit activity of striatal neurons was recently shown to be significantly increased in dt(sz) hamsters , the lack of significant changes in GP discharge rates was unpredicted, We suggest that this is due to antagonistic convergent striatal and subthalam ic inputs and to lateral monosynaptic inhibition known for striatum and GP, While no significant changes of the discharge rate of GP neurons could be detected, the spike morphology was significantly altered in dt(sz) hamsters , suggesting subtle impaired information processing in the GP. The lack of marked changes in basal firing pattern may be related to the anesthesia, Ad ministration of PTZ (25 mg/kg i.p.) at a subconvulsant dose, which aggravat es dystonia in awake dt(sz) hamsters, seemed to induce more marked changes in spike morphology and firing pattern in mutants than in controls, althoug h the discharge rate did not differ significantly between both animal group s in response to PTZ, In view of recent findings, we assume that GABAergic dysfunctions in dystonic hamsters are of regionally different extent. (C) 1 999 Wiley-Liss, Inc.