Neural damage in the rat thalamus after cortical infarcts.

Abstract

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in A xonal lesions cause not only anterograde degen-/ \ eration in distal segments of axons but also A. V . retrograde cell death in some neural centers. 1 -2 Central nervous system lesions thus can damage neural structures remote from the primary lesions. We have reported widespread degeneration of corticofugal axons and their terminals in rat brainstem and spinal cord after cortical infarction produced by middle cerebral artery (MCA) occlusion (MCAO). 3Several anatomic studies have shown retrograde neuronal degeneration in mammalian thalamus after decortication. 1 -2 "* Recent positron emission tomographic studies have revealed hypometabolic states in the ipsilateral thalamus of patients with focal cortical or capsular infarcts after MCAO. 56 We consequently examined the thalamus in rats after unilateral MCAO. Our model consistently produces infarcts in the lateral parietal cortical area, with variable involvement of the parasagittal frontoparietal cortex but little direct ischemic damage to subcortical structures. Received October 18, 1989; accepted January 9, 1990. somatosensory cortex and receive thalamocortical fibers from specific thalamic nuclei, that is, the ventroposteromedial and ventroposterolateral nuclei. 8The ventroposteromedial nucleus is the specific somatosensory relay nucleus for face sensation, while the ventroposterolateral nucleus serves the body, fore limbs, and hind limbs.8 Materials and MethodsWe studied 23 adult male Long-Evans hooded rats weighing 250-350 g. The rats were anesthetized with 40 mg/kg i.p. pentobarbital. The right MCA was exposed via a subtemporal craniotomy preserving the zygomatic arch so that the rats could feed after surgery. 37 The MCA was occluded and divided 1-2 mm below the rhinal fissure. The rats usually showed mild contralateral hemiparesis and a tendency to circle toward the lesioned site after MCA. Such symptoms, however, disappeared within 24 hours. The rats were housed in boxes containing sterile hardwood chips and fed ad libitum. They regained their preoperative weights within a week.The rats were randomly sacrificed 1 (n=4), 2 (n=3), or 3 (n=3) days or 1 (n=6), 3 (n=3), or 6 (n=4) weeks after MCAO by transcardiac perfusion with 4% paraformaldehyde or 10% forma...

Calcium Accumulation following Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats

“…In the thalamus, 45 Ca accumulation was limited to the ventral posterior nucleus, which has fiber con nections in anatomic proximity to the postcentral gyrus of the cerebral cortex. Damage in this area may be due to retrograde degeneration resulting from thalamocortical fiber damage caused by the ischemic insult to the postcentral gyrus (Matthews, 1973;Fujie et al, 1990;Nagasawa and Kogure, 1990;Iizuka et al, 1990). In this study, we fo und a direct-proportion relationship between damaged tween the two correlation coefficients shows 15 that the probability of the distribution of the plotted values for calcium accumulation in the thalamus and cortex is greater than that seen in ... E the striatum and cortex (Z = 1.9834; P < 0.05).…”

Evaluation of a Motor Deficit after Chronic Focal Cerebral Ischemia in Rats

“…This phenomenon is possibly related to changes in the intact hemisphere, which could improve functioning of the uninvolved limb, or which could cause chronic defi cits based on secondary damage. It has been noted that after infarction in the territory of the MCA, in the chronic phase progressive shrinkage occurs in the ipsilateral thalamus and SN (Fujie et al, 1990;Tamura et al, 1990;Iizuka et al, 1990). Thus, secondary damage or diaschi sis of the contralateral hemisphere may contribute to this phenomenon (Andrews et aI., 1991;Feeney and Baron, 1986).…”

A Master Key to Assess Stroke Consequences Across Species: The Adhesive Removal Test

“…Indeed, ischemia is known to cause secondary degeneration in non-ischemic remote brain areas such as the ipsilateral thalamus (mostly the ventroposteromedial and ventroposterolateral nuclei (Iizuka et al, 1990)) as well as in the substantia nigra . These regions that do not belong to the territory of the MCA, are connected to the primary lesion site.…”

“…These regions that do not belong to the territory of the MCA, are connected to the primary lesion site. As regards to secondary thalamus shrinkage, retrograde as well as anterograde degeneration due, respectively, to cortical lesion (Iizuka et al, 1990) (Wallerian) and to basal ganglia lesion and/or extensive vasogenic edema (Dihne et al, 2002) are thought to be responsible. Whether the extent of these degenerative changes is or not directly correlated to the size of primary lesion is still under controversy Iizuka et al, 1990).…”

“…As regards to secondary thalamus shrinkage, retrograde as well as anterograde degeneration due, respectively, to cortical lesion (Iizuka et al, 1990) (Wallerian) and to basal ganglia lesion and/or extensive vasogenic edema (Dihne et al, 2002) are thought to be responsible. Whether the extent of these degenerative changes is or not directly correlated to the size of primary lesion is still under controversy Iizuka et al, 1990). No matter how, in a rat stroke model, the final thalamic atrophy appears to be correlated with ischemia-induced deficits observed in the adhesive-removal test (especially its sensory component) .…”