Subthalamic nucleus activity in the awake hemiparkinsonian rat: relationships with motor and cognitive networks.
Oscillatory activity in both beta and gamma ranges has been recorded in the subthalamic nucleus (STN) of Parkinson's disease (PD) patients and linked to motor function, with beta activity considered antikinetic, and gamma activity, prokinetic. However, the extent to which nonmotor networks contribute to this activity is unclear. This study uses hemiparkinsonian rats performing a treadmill walking task to compare synchronized STN local field potential (LFP) activity with activity in motor cortex (MCx) and medial prefrontal cortex (mPFC), areas involved in motor and cognitive processes, respectively. Data show increases in STN and MCx 29-36 Hz LFP spectral power and coherence after dopamine depletion, which are reduced by apomorphine and levodopa treatments. In contrast, recordings from mPFC 3 weeks after dopamine depletion failed to show peaks in 29-36 Hz LFP power. However, mPFC and STN both showed peaks in the 45-55 Hz frequency range in LFP power and coherence during walking before and 21 days after dopamine depletion. Interestingly, power in this low gamma range was transiently reduced in both mPFC and STN after dopamine depletion but recovered by day 21. In contrast to the 45-55 Hz activity, the amplitude of the exaggerated 29-36 Hz rhythm in the STN was modulated by paw movement. Furthermore, as in PD patients, after dopamine treatment a third band (high gamma) emerged in the lesioned hemisphere. The results suggest that STN integrates activity from both motor and cognitive networks in a manner that varies with frequency, behavioral state, and the integrity of the dopamine system.
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3702.
Claire
C
Delaville
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3702.
Alex J
AJ
McCoy
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3702.
Colin M
CM
Gerber
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3702.
Ana V
AV
Cruz
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3702 waltersj@ninds.nih.gov.
Judith R
JR
Walters
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D018663:Adrenergic Agents / Q000633:toxicity; D000818:Animals; D000978:Antiparkinson Agents / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D003072:Cognition Disorders / Q000209:etiology*; D004195:Disease Models, Animal; D018492:Dopamine Antagonists / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D007839:Functional Laterality / Q000502:physiology*; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D016627:Oxidopamine / Q000633:toxicity; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy / Q000473:pathology*; D051381:Rats; D020318:Rats, Long-Evans; D020531:Subthalamic Nucleus / Q000503:physiopathology*; D013997:Time Factors; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014851:Wakefulness
D018663:Adrenergic Agents; D000978:Antiparkinson Agents; D001552:Benzazepines; D018492:Dopamine Antagonists; C534628:SCH 23390; D007980:Levodopa; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase
Parkinson's disease; beta oscillation; dopamine; gamma oscillations; medial prefrontal cortex; subthalamic nucleus