PMID- 16371459
OWN - NLM
STAT- MEDLINE
DCOM- 20060925
LR  - 20131121
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 95
IP  - 4
DP  - 2006 Apr
TI  - Neuronal firing before and after burst discharges in the monkey basal ganglia is 
      predictably patterned in the normal state and altered in parkinsonism.
PG  - 2120-33
AB  - It is known that burst discharges in basal ganglia neurons are more common in 
      parkinsonism than under normal conditions, but changes in the structure of burst 
      or peri-burst epochs have not been reported. In this study, the temporal 
      structure of bursts and the timing of neuronal discharges that precede or follow 
      them were examined in neuronal spike trains recorded in the subthalamic nucleus 
      (STN) and the external and internal pallidal segment (GPe, GPi) in two awake 
      Rhesus monkeys before and after they were rendered hemiparkinsonian by unilateral 
      intracarotid infusion of the dopaminergic neurotoxin 
      1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Bursts were detected by the 
      "surprise" method. In the normal state, interspike intervals (ISIs) preceding or 
      following bursts were frequently significantly longer than the average baseline 
      ISI, and their duration was correlated with the burst length (i.e., the number of 
      spikes/burst). Significant correlations were also found in all three structures 
      between the burst length and the duration of interburst intervals. The incidence 
      of burst discharges and the proportion of time spent in bursts increased in GPe, 
      STN, and GPi after MPTP treatment. Burst lengths became more tightly related to 
      preburst ISIs in the STN after MPTP treatment and to postburst ISI duration in 
      all three structures. These results show that bursts in spontaneous GPe, STN, and 
      GPi discharge are often preceded or followed by long ISIs, and that burst length, 
      the length of pre- and postburst ISIs, and the length of interburst intervals are 
      related to one another. Complex changes in these interactions may contribute to 
      abnormal information processing in parkinsonism.
FAU - Wichmann, Thomas
AU  - Wichmann T
AD  - Department of Neurology, Emory University, Atlanta, GA 30322, USA. 
      twichma@emory.edu
FAU - Soares, Jesus
AU  - Soares J
LA  - eng
GR  - P01 NS-38399/NS/NINDS NIH HHS/United States
GR  - R01 NS-42250/NS/NINDS NIH HHS/United States
GR  - RR-000165/RR/NCRR NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20051221
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Neurotoxins)
RN  - 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
SB  - IM
MH  - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology
MH  - Action Potentials/drug effects
MH  - Algorithms
MH  - Animals
MH  - Basal Ganglia/physiology/*physiopathology
MH  - Cerebral Cortex/physiology/physiopathology
MH  - Electrophysiology
MH  - Macaca mulatta
MH  - Neurons/drug effects/*physiology
MH  - Neurotoxins/pharmacology
MH  - Parkinsonian Disorders/*physiopathology
MH  - Subthalamic Nucleus/physiology/physiopathology
MH  - Synaptic Transmission/drug effects
MH  - Thalamus/physiology/physiopathology
MH  - Time Factors
EDAT- 2005/12/24 09:00
MHDA- 2006/09/26 09:00
CRDT- 2005/12/24 09:00
PHST- 2005/12/24 09:00 [pubmed]
PHST- 2006/09/26 09:00 [medline]
PHST- 2005/12/24 09:00 [entrez]
AID - 01013.2005 [pii]
AID - 10.1152/jn.01013.2005 [doi]
PST - ppublish
SO  - J Neurophysiol. 2006 Apr;95(4):2120-33. doi: 10.1152/jn.01013.2005. Epub 2005 Dec 
      21.