Recent laboratory and clinical studies demonstrate therapeutic efficacy of intracerebral
transplantation of carotid body (CB) in
Parkinson's disease, possibly through secretion of
neurotrophic factors. Here, we examined the role of CB in experimental
stroke. In the first experiment, we hypothesized that removal of CB would exacerbate
cerebral infarction and
stroke-related behavioral deficits. Eight-week-old, male Sprague-Dawley rats were randomly divided into two groups:
stroke with intact CB and
stroke with surgically removed CB. We used the
stroke model of temporary
middle cerebral artery occlusion. The ipsilateral CB was removed in animals assigned to treatment group exposed to
stroke with surgically removed CB. Behavioral tests, using the elevated body swing test, were conducted at days 1-3 after surgery.
Cerebral infarction was visualized by TTC staining on day 3 post-surgery. The data revealed no significant differences in behavioral deficits and
infarct volumes between the two groups. In the second experiment, CB cell
suspension grafts or control adult tissue grafts were intracerebally transplanted into the ischemic penumbra immediately (within 1 h) after
stroke surgery. The results revealed significant reduction of behavioral deficits and
infarct volumes, accompanied by increased levels of
neurotrophic factors, as detected by ELISA, in transplanted ischemic striatum collected from CB-grafted
stroke animals. These observations suggest that surgical resection of CB in the periphery did not alter
stroke pathology; however, CB when made available in the CNS, via intracerebral
transplantation, could protect against
stroke possibly through the synergistic release of
neurotrophic factors. The present study extends the use of CB as efficacious graft source for
transplantation.