title: Dopamine lesion-induced changes in subthalamic nucleus activity are not associated with alterations in firing rate or pattern in layer V neurons of the anterior cingulate cortex in anesthetized rats.
abstract: Dysfunctional activity in the subthalamic nucleus (STN) is thought to underlie movement deficits of patients with Parkinson's disease. Alterations in STN firing patterns are also evident in the anesthetized rat model of Parkinson's disease, where studies show that loss of striatal dopamine and concomitant changes in the indirect pathway are associated with bursty and oscillatory firing patterns in STN output. However, the extent to which alterations in cortical activity contribute to changes in STN activity is unclear. As pyramidal neurons in the cingulate cortex project directly to the STN, cingulate output was assessed after dopamine lesion by simultaneously recording single-unit and local field potential (LFP) activities in STN and anterior cingulate cortex in control, dopamine-lesioned and non-lesioned hemispheres of urethane-anesthetized rats. Correlated oscillations were observed in cross-correlograms of spike trains from STN and cingulate layer V neurons with broad waveforms indicative of pyramidal neurons. One-2 weeks after dopamine cell lesion, firing rate, incidence of bursty and 0.3-2.5 Hz oscillatory activity of neurons and LFP power in the STN all increased significantly. In contrast, firing rate, incidence of bursty and 0.3-2.5 Hz oscillatory activity of cingulate layer V putative pyramidal neurons and power in cingulate LFPs did not differ significantly between dopamine-lesioned, non-lesioned or control hemispheres, despite significant loss of dopamine in the lesioned cingulate cortex. Data show that alterations in STN activity in the dopamine-lesioned hemisphere are not associated with alterations in neuronal activity in layer V of the anterior cingulate cortex in anesthetized rats.
authors: Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Building 35 Room 1C 905, Bethesda, MD 20892-3702, USA. parrbl@ninds.nih.gov
authors: Louise C
authors: LC
authors: Parr-Brownlie
authors: Stacey L
authors: SL
authors: Poloskey
authors: Kalynda K
authors: KK
authors: Flanagan
authors: Graeme
authors: G
authors: Eisenhofer
authors: Debra A
authors: DA
authors: Bergstrom
authors: Judith R
authors: JR
authors: Walters
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000758:Anesthesia; D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D005071:Evoked Potentials / Q000502:physiology; D005583:Fourier Analysis; D007839:Functional Laterality; D006179:Gyrus Cinguli / Q000166:cytology*; D008297:Male; D008474:Medial Forebrain Bundle / Q000293:injuries / Q000502:physiology; D016627:Oxidopamine / Q000633:toxicity; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020531:Subthalamic Nucleus / Q000187:drug effects* / Q000293:injuries*; D013565:Sympatholytics / Q000633:toxicity
chemical_list: D013565:Sympatholytics; D016627:Oxidopamine; D004298:Dopamine