2-Deoxyglucose uptake and histologic changes in rat thalamus after neocortical ablations

Cooper, R. M.; Thurlow, G.A.; Rooney, B.J.

doi:10.1016/0014-4886(84)90052-9

Cited by 31 publications

(12 citation statements)

References 15 publications

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“…Iizuka et al 11 also reported a similar result using the same model and concluded that their findings were consistent with retrograde neuronal degeneration. A similar degeneration of thalamic neurons has been well-documented after cortical ablation, 12 -13 a classical technique for showing neuronal links in the central nervous system. Since 1870, when Gudden provided evidence of an intimate link between the thalamus and cerebral cortex by showing that ablation of the cortex led to the death and disappearance of cell bodies in the thalamus, several studies have shown neuronal death and later atrophy in the ipsilateral thalamus following cortical ablation.…”

Section: Discussionmentioning

confidence: 53%

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

Tamura

Tahira

Nagashima

et al. 1991

Stroke

120

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We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted £2 days after the stroke and who were followed by computed tomography for >1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken <2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (/xO.Ol) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction. (Stroke 1991^22:615-618) I t has been widely believed that neuronal alterations following cerebral ischemia progress rapidly. 1 Therefore, the main issue of neuropathologic studies after cerebral ischemia has been acute neuronal changes in the ischemic area. In 1982, Kirino 2 found a strikingly slow process of neuronal change in the hippocampal CA1 subfield following brief cerebral ischemia, which he called "delayed neuronal death." Since then, delayed neuropathologic changes following cerebral ischemia have attracted widespread attention. These changes are also found in the area exposed to ischemia.The aim of this study was to analyze neuropathologic changes in a distant, nonischemic area after focal cerebral ischemia. We particularly focused on delayed neuropathologic changes of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery (MCA). Subjects and MethodsA total of 109 patients with cerebral infarction were admitted to our clinic from 1985 through 1989.From the Department of Neurosurgery, Teikyo University School of Medicine, Tokyo, Japan.Supported in part by a grant-in-aid for scientific research from the Ministry of Education, Science and Culture of Japan and by a research grant for cardiovascular diseases from the Ministry of Health and Welfare.Address for correspondence: Akira Tamura, MD, Department of Neurosurgery, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173, Japan.Received November 7, 1990; accepted January 31, 1991. From among these patients, we selected 33 who 1) were admitted <,2 days after the first attack of stroke, 2) had a single low-density area on an initial or follow-up computed tomogram (CT film) in the MCA territory, 3) were followed by symmetrical CT at the level of the thalamus for > 1 year, and 4) developed no symptomatic or asymptomatic recurrence of stroke on CT. In these patients, the area of the thalamus on each side was randomly measured with a computerized digitizer on the CT films at the level of the thalamus according to a CT atlas 3 1, 3, and 6 months and 1 and 2 years after the stroke. The CT films were taken in parallel planes at an angle of 15° to the infraorbitomeatal lin...

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Section: Discussionmentioning

confidence: 53%

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

Tamura

Tahira

Nagashima

et al. 1991

Stroke

120

View full text Add to dashboard Cite

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“…These altered CA levels following cortical injury may result from damage to CA axons, producing a shift from transmitter production to protein synthesis for repair (Ross, Joh, & Reis, 1975). Evidence for RFD after injury to the brain is also provided by several histochemical studies (Cooper, Thurlow, & Rooney, 1984;Dail, Feeney, Murray, Linn, & Boyeson, 1981;Frey & Agranoff, 1983;Pappius & Wolfe, 1983;Reinstein, Isaacson, & Dunn, 1979;Schwartz, Sharp, Gunn, & Evarts, 1976) and by studies employing electrophysiological techniques (Glassman, 1970;Glassman & Malamut, 1976;Kempinsky, 1954Kempinsky, , 1956Kempinsky, , 1958Pittman, Feeney, & Spiker, 1976).…”

Section: Discussionmentioning

confidence: 97%

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

et al. 1985

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Cerebral metabolic effects of locus coeruleus (LC) lesion or drugs affecting LC were investigated after unilateral injury of sensorimotor cortex in rats. Sensoriomotor cortex ablation produced a widespread depression of cerebral 14C-2-deoxyglucose utilization which was reversed by amphetamine (AMP, 2 mg/kg) and worsened by haloperidol (HAL, 0.4 mg/kg). Lesion of LC alone did not affect cerebral oxidative metabolism, measured by a stain for the enzyme alphaglycerophosphate dehydrogenase (a-GPDH). Lesion of LC prior to undercut laceration of motor cortex shortened time to onset of a-GPDH cortical paling. Treatment with AMP (2 mg/kg) blocked cortical paling ofthe enzyme stain at 4 days postinjury, an effect prevented by concomitant HAL (0.3 or 0.6 mg/kg). Apomorphine (1 mg/kg) did not block cortical paling. These data parallel effects of these drugs on recovery of function. The results suggest that a metabolic "remote functional depression" (RFD) is alleviated by catecholamine activation after cortical injury, whereas onset of RFD is accelerated by LC lesions and exacerbated by catecholamine blockade.The locus coeruleus (LC) may have an important role in neuronal development and plasticity (Felton, Hallman,

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“…An explanation for the increase in hippocampal CMR g lc 7 days after ischemia is that activation of astro cytes, as demonstrated in this study, is responsible for that. Cooper et al (1984) have already pointed out that it is important to consider glial contribution to DOG uptake in rats subjected to brain damage. However, other possible reasons for increases in CMR g lc in postischemic brain tissue are also known.…”

Section: Discussionmentioning

confidence: 99%

Postischemic Neuronal Damage Causes Astroglial Activation and Increase in Local Cerebral Glucose Utilization of Rat Hippocampus

Rischke

Krieglstein

1991

J Cereb Blood Flow Metab

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Summary:The purpose of the present study was to de termine the consequences of postischemic neuronal dam age on CMRglc. Forebrain ischemia of \0 min duration was induced in male Wi star rats. The extent of neuronal damage and the numbers of immunocytochemically de tected astrocytes in the hippocampal CAl subfield as well as CMRglc were determined 2, 5, 7, and 14 days after ischemia. CBF was additionally measured 7 days post ischemia. CMRglc was decreased in cortical and thalamic structures up to 5 days postischemia, and was normalized again on day 7 after ischemia. In the hippocampal areas, CMRglc was decreased only on day 2 after ischemia, was normalized after 5 days, and increased in the stratum

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2-Deoxyglucose uptake and histologic changes in rat thalamus after neocortical ablations

Cited by 31 publications

References 15 publications

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

Postischemic Neuronal Damage Causes Astroglial Activation and Increase in Local Cerebral Glucose Utilization of Rat Hippocampus

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