Thalamic projections from trigeminal and certain other nuclei of the brainstem of the rat have been investigated using the technique of retrograde transport of horseradish peroxidase (HRP). The pattern of trigeminothalamic projections is very specifically related to the individual subnuclei of the complex. The Main Sensory Nucleus (MSN) provides profuse cross connections to the ventrobasal thalamus (VB); these arise exclusively from medium and small-sized neurons, but never from the large cells. In addition to these crossed connections, a small ipsilateral dorsal trigeminothalamic tract arises from the dorsal third of the most rostral part of the MSN; this is the only ipsilateral connection to VB found in the trigeminal complex. Subnucleus Oralis has no projections to the thalamus; it is suggested that it may be concerned primarily with reflex activation of the facial nucleus, with which it is co-extensive in the rostro-caudal axis. Subnucleus Interpolaris has a well-defined crossed projection of moderate size which arises from the large, medium and some of the small neurons. Subnucleus Caudalis has a sparse output to the thalamus and differs in its projections from rostral to caudal. At the most rostral level, all layers (marginal, transitional gelatinosa and magnocellularis) contain neurons which project to the thalamus; particularly conspicuous in this respect are the marginal neurons, most of which are strongly labelled. The presence of gelatinosa neurons projecting to the thalamus emphasizes a point made in earlier reports, that these neurons do not form an homogeneous population. At caudal levels, the marginal neurons are the major source of thalamic projections, while connections to the thalamus form deeper lying neurons are infrequent. With a single exception, the medullary reticular nuclei contained no neurons with thalamic connections; a small number of reticulo-thalamic neurons were found in the ventral pontine area. Marked labelling of the medial cuneate nucleus and moderate labelling of the gracilis and lateral cuneate nuclei occurred contralaterally to the injection site. A small numebr of medial cuneate and gracile neurons project to the ipsilateral thalamus. Projections from the solitary nucleus were always ipsialteral. The boundaries of individual subnuclei of the lateral sensory trigeminal complex in the rat have been redefined on the basis of cytological criteria; these are in good accord with the corresponding thalamic projection patterns.
Intraluminal membrane-bound bodies were occasionally identified but they did not appear to be producing significant obstruction. The tight endothelial junctions remained intact and there was no evidence of accelerated micropinocytosis. Severe neuronal injury frequently preceded the development of the microvascular obstruction and was more widespread than the zones of impaired perfusion.PROGRESSIVE microcirculatory obstruction in areas of focal cerebral ischemia has been demonstrated with the carbon perfusion technique by Crowell and Olsson 1 and by Little and associates.2 Light microscopic examination has shown that the obstruction lies primarily at the capillary level and appears to be related to compression of the capillary channels by the developing cerebral edema.2 Severe neuronal alterations were invariably identified before the development of the obstruction and were frequently present in areas of unimpaired perfusion. These findings suggested that the obstruction of the parenchymal vessels does not play a primary role in the production of a cerebral infarct.The object of this investigation was to study the fine structure of the microvasculature in areas of focal cerebral ischemia and to define the nature of the microcirculatory obstruction. The relationship between the parenchymal changes and the developing obstruction was also studied in order to elucidate further the significance of the obstruction. MethodsThe techniques used for the production of the ischemic lesions and carbon perfusion have been described in detail. The main steps in the procedure were as follows. (1) The right middle cerebral artery (MCA) in eight squirrel monkeys was occluded with a miniature aneurysm clip through a transorbital exposure. (2) Arterial blood samples (0.3 ml) were taken hourly for the determination of pH, Pao,, and Paco,. Rectal temperature and arterial blood pressure were constantly monitored. (3) Animals in groups of two were perfused after ischemic periods of 90 minutes, three hours, six hours, and 12 hours. They were initially perfused with 100 ml normal saline followed immediately by a mixture of colloidal carbon (250 ml) and phosphate-buffered 4% paraformaldehyde (250 ml). The clip was removed immediately prior to perfusion. (4) The brains were left undisturbed for two hours following perfusion. Then they were carefully removed from the skulls and placed in jars containing 50 ml phosphate-buffered 4% paraformaldehyde at 4°C for 24 hours. (5) The brains were cut coronally into 5 mm slices and the tissue was examined macroscopically. Thin (5 y. and 25 n) coronal sections were prepared from paraffin-embedded slices of both hemispheres and stained with hematoxylin and eosin and with thionine. (6) Multiple specimens were taken from the gray and white matter of both hemispheres of each brain. Tissue was taken from the poorly stained, intermediate, and surrounding well-stained areas of those brains which had macroscopic evidence of impaired perfusion. It was postfixed in phosphate-buffered 1% osmium tetroxide for two ...
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