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Electrodes were implanted into the rat hippocampus in both hemispheres for increasing periods of up to 60 days, and the effects of trauma and electrical stimulation of enzymes controlling cell metabolism in the region of implantation were examined and assessed in relation to studies on humans. In the unstimulated hippocampus as a control, enzyme changes were mainly confined to a narrow area of tissue damage surrounding the electrode. The enzyme changes in response to trauma varied widely; some enzymes controlling tissue respiration showed early and rapid changes, increasing in hyperactive, swollen glial cells and vascular endothelium and decreasing in nerve cells and neuropile. Acid phosphatase activity also increased rapidly in glial cells; other phosphate-releasing enzymes increased more gradually with time. A turning point in these chages was apparent between 25 and 40 days, followed by a reversion to more normal levels at 60 days. Electrical stimulation of the hippocampus in the contralateral hemisphere produced no detectable enzyme changes from those of the unstimulated hippocampus.
Electrodes were implanted into the rat hippocampus in both hemispheres for increasing periods of up to 60 days, and the effects of trauma and electrical stimulation of enzymes controlling cell metabolism in the region of implantation were examined and assessed in relation to studies on humans. In the unstimulated hippocampus as a control, enzyme changes were mainly confined to a narrow area of tissue damage surrounding the electrode. The enzyme changes in response to trauma varied widely; some enzymes controlling tissue respiration showed early and rapid changes, increasing in hyperactive, swollen glial cells and vascular endothelium and decreasing in nerve cells and neuropile. Acid phosphatase activity also increased rapidly in glial cells; other phosphate-releasing enzymes increased more gradually with time. A turning point in these chages was apparent between 25 and 40 days, followed by a reversion to more normal levels at 60 days. Electrical stimulation of the hippocampus in the contralateral hemisphere produced no detectable enzyme changes from those of the unstimulated hippocampus.
Thymidine-H3 radioautography was used to study the proliferative response to penetrating wounds of the mouse spinal cord. In one group of animals mononuclear leukocytes which i n a t r a t e nervous tissue wounds were labeled by injecting thymidine-H3 prior to injury. In two other experimental groups the cells which synthesized DNA in the nervous tissue following the injury were labeled by giving either a single injection of isotope shortly before sacrifice or by giving four injections during the 24 hours prior to sacrifice. The animals were sacrificed over a five day period following spinal cord injury. Although the labeled nuclei in a l l three groups were similar in appearance, their distribution about the lesion was very different. The labeled blood cells were greatly concentrated at the wound, while the cells that responded to injury by DNA synthesis were much more evenly spread throughout the tissue. When these distributions were converted to straight lines and compared statistically, there was a very low probability that the group of cells labeled before injury and the two groups labeled after injury were samples from the same population. Although mononuclear leukocytes do proliferate in and around nervous tissue wounds, other cells originally present in the nervous tissue must also proliferate.
Administration of x-rays (4000 I) to lumbar spinal cords of three-dayold rats caused a loss of neuroglia with an inhibition of myelinogenesis, neuronal damage and necrosis. In contrast, the loss of neuroglia following administration of 2000 r is temporary, with myelinogenesis occurring later than normal. Preliminary observations suggested that differences in vascular responses to these two amounts of x-rays might account for these differing fates of the spinal cords; therefore, this investigation was designed to study further the reactions of the intramedullary vessels.Rats, irradiated when three days of age, were killed 1 to 27 days later. Some were killed by perfusion with Monolite Fast Blue BNVSA Paste, a substance retained in the vessels and readily visualized on microscopic examination. The remaining rats were decapitated, and spinal cords were stained by Gomori's method for alkaline phosphatase. The earliest consistent alteration, a decreased number of vessels, was noted seven days following irradiation with either dose. Rats receiving 4000 r had marked losses of blood vessels, vasodilatation and necrosis by 15 days post-irradiation; whereas, a decreased number of vessels was the only change noted in rats irradiated with 2000 I. Alterations in rats receiving 4000 r remained the same or became more severe throughout the study; spinal cords in rats receiving 2000 r returned to normal. These vascular alterations correlate well with the changes in other spinal cord components described previously by this investigator.Ionizing radiation affects the immature spinal cord in a manner that is dose dependent (Gilmore, '63b, '65, '66; Rodgers, '65). When 2000 r or 4000 r of soft x-rays are administered to a 5 mm length of spinal cord in three-day-old rats, there is a loss of neuroglia within two days following irradiation and a consequent state of hypo-or a-myelination (Gilmore, '63b, '66; Rodgers, '65). These changes are found in all animals of both groups during the first eleven days following irradiation. After this time, however, the status of the irradiated areas is markedly different in the two groups. In the animals receiving 2000 r the neuroglia are restored, and delayed myelinogenesis takes place, so that by one month following irradiation, the spinal cords appear to be normal (Gilmore, '66). In contrast, when 4000 r of x-rays are administered the changes are quite different in that necrosis develops in many spinal cords by three weeks post-irradiation (Gilmore and Arrington, '67). Preliminary observations of vascular alterations in a few rats studied by Gilmore and Arrington ('67) showed that hemorrhages and vasodilatation begin to appear approximately two ANAT. REC., 163: 89-100.weeks following irradiation. These findings suggest that the vasculature can influence the manner in which the spinal cord reponds after exposure to ionizing radiation and these differing alterations in spinal cord parenchyma may reflect differences in the type and severity of vascular changes. It would seem reasonable to ...
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