Transient increase in the expression of growth-associated protein-43 in the thalamus of spontaneously hypertensive rats with cortical infarction

To see whether or not regenerative reactions occurred in the thalamus after cortical infarction in stroke-prone spontaneously hypertensive (SH-SP) rat s, the expression of growth-associated protein (GAP)-43 was studied. The le ft middle cerebral artery (MCA) distal to the striate branches was permanen tly occluded. Three to 7 days after ischemia, linear- or spiral-shaped GAP- 43 immunoreactive structures increased in number and intensity in the left ventroposterior (VP) thalamic nucleus. Under electron microscopy, GAP-43 wa s localized to axons. Immunoblot analysis also showed a transient increase in GAP-43 after ischemia. Besides the thalamus, a population of neurons in the right spinal trigeminal nucleus and many axons in the left medial lemni scus and lateral spinothalamic tract contained GAP-43 immunoreaction produc ts. The transient elevation of GAP-43 immunoreactivity in the thalamus was apparently suppressed by ciliary neurotrophic factor (CNTF) infusion starti ng just after ischemia, possibly due to a preventive effect of CNTF on the secondary thalamic degeneration. These findings suggest that spinal trigemi nal nucleus neurons projecting into the thalamus via the medial lemniscus a nd lateral spinothalamic tract upregulate GAP-43 expression in response to cortical infarction and subsequent thalamic degeneration.