Kazumi Yamamoto

Noradrenaline innervation of the spinal cord studied by the horseradish peroxidase method combined with monoamine oxidase staining

SummaryThe origin of the spinal cord noradrenaline (NA) has been investigated by means of the horseradish peroxidase (HRP) method, combined with monoamine oxidase staining (Glenner) to identify the NA neurons. Following the injection of HRP to the various levels of rat spinal cord, cervical to sacral cord, A1–3, 5–7 NA neuron groups were labeled with HRP. They showed almost the same distribution pattern regardless of difference in the injected segment. Labeled NA neurons in A6 were concentrated in the ventral division of the locus coeruleus, which continued to the labeled NA neurons in the subcoeruleus area. The HRP positive neurons in the pons outnumbered those of the medulla oblongata. As the NA neurons described above were considered to be the source of NA in the forebrain, such as the hypothalamus and preoptic area, the possibility that the same NA neurons might innervate both the forebrain and spinal cord has been presented.

Ultrastructural investigation of the CA1 region of the hippocampus after transient cerebral ischemia in gerbils

SummaryUltrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.

Descending projection of the nucleus tegmentalis latero-dorsalis to the spinal cord; studied by the horseradish peroxidase method following 6-hydroxy-DOPA administration.

Descending projection of the nucleus tegmentalis laterodorsalis (TLD) to the spinal cord was investigated using the horseradish peroxidase (HRP) method following the systemic administration of 6-hydroxy-DOPA (6-OH-DOPA). 6-OH-DOPA pretreatment resulted in an intense labeling of the cell group at the laterocaudal portion of TLD after the injection of HRP to the lower segments of the spinal cord. Whereas in untreated rats, cells at the laterocaudal portion of TLD were faintly labeled. Such indirect effect correlated with a reduction in the number of fluorescent catecholamine nerve terminals in the spinal cord after 6-OH-DOPA injection, suggesting that the descending projection from laterocaudal portion of TLD to the spinal cord might be influenced by the catecholamine neurons in the central nervous system.

Early Detection of Cerebral Ischemic Damage and Repair Process in the Gerbil by Use of an Immunohistochemical Technique

After occlusion of the right common carotid artery in the gerbil, we monitored the progression of ischemic damage and postischemic damage and the repair process in the brain immunohistochemically by using tubulin, creatine kinase BB-isoenzyme (CK-BB), and neuron-specific enolase as the neuronal markers and astroprotein, glial fibrillary acidic protein, and CK-BB as the astrocytic markers. The earliest ischemic lesion was detected in the hippocampus and the cerebral cortex after ischemia for 5 minutes as loss of the reaction in the neuropil, nerve cell bodies, and dendrites. The reaction disappeared more promptly in the dendrites than in the nerve cell bodies. The reaction for tubulin was the most sensitive for detection of the neuronal ischemic damage. After an ischemic period of 30 minutes and subsequent reestablishment of cerebral circulation, the immunohistochemical lesions affecting the neuronal structure expanded during the first 3 hours and then slowly afterward for up to 12 hours. Reactive astrocytes were already identified 24 hours after reperfusion. The current investigation demonstrated that early ischemic damage can be clearly visualized by use of the immunohistochemical technique soon after the onset of cerebral ischemia but that considerable heterogeneity exists not only in different anatomic regions but also within the neuronal structure. This technique has potential for further investigation of cerebral ischemia or other pathophysiologic conditions when used in combination with other morphologic, physiologic, or biochemical techniques.

Benign chondroblastoma of the occipital bone

We report the case of a 14-year-old boy with benign chondroblastoma in the occipital bone associated with a cerebellar hemorrhage. The clinical features, radiologic and histologic appearances, and histogenesis in this case are described. Other reports of benign chondroblastomas of the cranial bones are also discussed.