Sensory (nociceptive) stimulation evokes Fos expression in the subthalamus of hemiparkinsonian rats.
OBJECTIVE
In an effort to understand cell activity patterns and sensorimotor integration in Parkinson's disease, we have explored the expression of the Fos protein in the subthalamus after sensory (nociceptive) stimulation of hemiparkinsonian Sprague-Dawley rats [6-hydroxydopamine [6OHDA]-lesioned]. Fos is a marker for neuronal activity in most areas of the brain and the subthalamus is a major driving force of the basal ganglia and target for surgical intervention in parkinsonian patients.


METHODS
The medial forebrain bundle (major tract carrying dopaminergic nigrostriatal axons) was injected with either 6OHDA or saline (controls). A week later, some rats were subjected to mechanical stimulation (pinching; activating nociceptive pathways) of the hindpaw for 2 hours, while others received no stimulation. Thereafter, brains were processed using routine tyrosine hydroxylase (TH; marker for dopaminergic cells) or Fos immunocytochemistry.


RESULTS
In the cases that had saline injections combined with mechanical stimulation or with no stimulation, as well as those that had 6OHDA lesions combined with no stimulation, there were no Fos+ cells in the subthalamus. However, in the cases that had 6OHDA-lesions combined with mechanical stimulation, there were many Fos+ cells within the subthalamus of both sides, particularly on the ipsilateral side.


CONCLUSIONS
Our results indicate that after an increase in sensory (nociceptive) activity, via mechanical stimulation, there is an induction of Fos expression in the subthalamus of 6OHDA-lesioned cases. We suggest that activating nociceptive pathways exacerbates the abnormal cell activity in the basal ganglia generated by the hemiparkinsonian condition.
Heise
Claire E
CE
Department of Anatomy and Histology, University of Sydney, NSW, Australia.
Reyes
Stefanie
S
Mitrofanis
John
J
D000818:Animals; D002452:Cell Count; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000502:physiology*; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D016761:Oncogene Proteins v-fos / Q000378:metabolism*; D016627:Oxidopamine / Q000009:adverse effects; D010146:Pain / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000473:pathology*; D010812:Physical Stimulation / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020530:Subthalamus / Q000378:metabolism*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D016761:Oncogene Proteins v-fos; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase