Changes of neuropeptides and their receptors in experimental stroke gerbil brains

Haba, K.; Ogawa, Norio; Asanuma, Masato; Hirata, Hiroshi; Sora, Yukiko H.; Mori, Akitane

doi:10.1016/0022-510x(92)90192-n

Cited by 8 publications

(1 citation statement)

References 26 publications

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“…Experimental studies have demonstrated that ischemic brain failure after carotid artery ligation is followed by an increase of /3-endorphin concentration in the ischemic hemisphere. 22 In conclusion, our study demonstrates an alteration of plasma /3-endorphin concentrations in stroke patients, which also persists in the convalescent period. A link between the /3-endorphin secretory pattern and functional outcome cannot be established with certainty by our study because of the relatively small number of cases.…”

Section: Discussionmentioning

confidence: 80%

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

Franceschini

Gandolfo

Cataldi

et al. 1994

Stroke

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Background and Purpose Abnormalities of hypothalamopituitary-adrenocortical axis function have been observed frequently in stroke patients. The aim of this study was to investigate plasma /S-endorphin and cortisol 24-hour secretory patterns in patients early after stroke and in the convalescent period to evaluate a possible influence of brain damage on hormonal circadian pattern.Methods Patients (n=15; age, 46 to 75 years) were evaluated in the first 24 hours and 10 days after hospital admission for ischemic cerebral stroke and compared with 15 age-and sex-matched normal subjects. Blood samples for /3-endorphin and cortisol determination were drawn every 4 hours from 8 AM to 8 PM and every 2 hours from midnight to 6 AM.Results Mean 24-hour /J-endorphin and cortisol levels, recorded in the acute phase, were significantly (P<.05) higher

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Section: Discussionmentioning

confidence: 80%

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

Franceschini

Gandolfo

Cataldi

et al. 1994

Stroke

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Vasopressin binding in the cerebral cortex of the mongolian gerbil is reduced by transient cerebral ischemia

Vallet

Bouras

Barberis

et al. 1995

J of Comparative Neurology

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In Mongolian gerbils, the content of vasopressin in the cerebral cortex, the striatum, and the hypothalamus is increased after induction of acute cerebral ischemia. We used an iodinated vasopressin analogue and light microscopic autoradiography to study the distribution of vasopressin V1 receptors in the brain of adult male gerbils and to evaluate the effects of a transient bilateral cerebral ischemia (6 minutes) on the density of this receptor population. The animals were killed immediately or 10, 30, or 100 hours after transient bilateral occlusion of the common carotid arteries. In control animals, specific [125I]-VPA binding sites were present in various structures of the brain (olfactory bulb, anterior olfactory nucleus, lateral septum, bed nucleus of the stria terminalis, median preoptic area, ventral pallidum, substantia innominata, amygdala, thalamus, hypothalamic mammillary nuclei, superior colliculus, subiculum, central gray, nucleus of the solitary tract, hypoglossal nucleus). The strongest labeling was detected in the cerebral cortex, layers 5-6. After 30-100 hours of survival time following ischemia there was a marked decrease in [125I]-VPA binding site density in these cerebral cortex layers. To a lesser degree, a decrease was also detected in the lateral septal nucleus. In contrast, labeling in other noncortical structures remained unchanged. All animals with 100 hours recovery showed a loss of cells in hippocampus (CA1 layer) and striatum. In addition, ischemia induced concomitant and proliferative changes in cortical and hippocampal astrocytes assessed by glial fibrillary acid protein immunoreactivity. These observations indicate a role for vasopressin in the cerebral cortex either on neurons or on glial cells and the modulation of vasopressin receptor expression by transient cerebral ischemia.

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Variable response of the Mongolian gerbil to unilateral carotid occlusion: Magnetic resonance imaging and neuropathological characterization

et al. 1995

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In the present investigation, we estimated both the evolution and the severity of ischemic damage following unilateral carotid occlusion (UCO) in Mongolian gerbils by using conventional magnetic resonance imaging (MRI, i.e. T2 weighted imaging) and histological techniques. Immediately after UCO, the animals showed different clinical effects. The mortality (46%) detected within the first 48h was considered an "stroke-sensitivity", the "stroke-resistant" animals showed wide variability in terms of both temporal evolution and the extent of ischemic damage. The signal hyperintensity and negative MRI observed during the first 30h after UCO did not always correlate with the cerebral damage presented after 14 days, although a close correlation was established between the T2 weighted images taken more than 30h after UCO and neuropathology: the gerbils negative to imaging showed no morphological changes, whereas an enhanced signal was always prognostic of ischemic injury. Moreover, late MRI documented ventricular dilatation. Histopathology showed that the ischemic damage differed among the stroke-resistant gerbils and was often bilateral. The present study confirms the differences in gerbil susceptibility to hemispheric infarction after permanent UCO and suggests that conventional MRI may be a useful non-invasive method for i) identifying the stroke-resistant animals prone to mature ischemic injury and ii) monitoring the evolution of therapeutic efficacy without sacrificing animals.

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Changes of neuropeptides and their receptors in experimental stroke gerbil brains

Cited by 8 publications

References 26 publications

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

Vasopressin binding in the cerebral cortex of the mongolian gerbil is reduced by transient cerebral ischemia

Variable response of the Mongolian gerbil to unilateral carotid occlusion: Magnetic resonance imaging and neuropathological characterization

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