Loss of Somatal Neuropeptide Y Immunoreactivity in the Rat Hippocampus Following Transient Cerebral Ischemia

Ff, Johansen; Mm, O'Hare

doi:10.1097/00008506-198912000-00007

Cited by 22 publications

(9 citation statements)

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“…This loss of immunocytochemical reactivity coincides with an actual loss of neurons in the dentate hilus (Johansen, Lin & Schousboe, 1989;Johansen & O'Hare, 1989;Ternder et al, 1990). Since we, however, in other studies have found that the levels of immunocytochemical staining for glutamic acid decarboxylase (GAD), neuropeptide Y, and parvalbumin, respectively, can increase, disappear permanently, or decrease transiently in hippocampal neurons that otherwise survive an ischaemic insult (Johansen et al, 1989Johansen & O'Hare, 1989), we wanted to determine whether the hilar SS-i neurons actually died or merely lost their S S immunoreactivity after ischaemia. For this purpose we decided to examine the hilar SS-i neurons 40 h after ischaemia in the electron microscope (EM), and correlate the observed changes with the ischaemic cell changes described by others (Brown & Brierley, 1972).…”

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confidence: 71%

Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections

Sørensen¹,

Tønder²,

Zimmer³

et al. 1992

Neuropathology Appl Neurobio

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In a light microscopical study, we previously showed that more than 80% of somatostatin (SS) immunoreactive (-i) neurons in the hilus of the dorsal part of the rat dentate gyrus are lost 4 days after ischemia. In order to verify that the loss of SS immunostaining is due to an actual loss of the SS-i neurons and not merely a loss in expression of SS immunoreactivity, we have now performed an ultrastructural study of these neurons before and 40 h after 20 min of global cerebral ischaemia in adult rats. The normal SS-i neurons were multipolar and fusiform in shape. The SS-i product was associated with the endoplasmic reticulum and occasionally the Golgi apparatus. The cell nuclei had indentations of the nucleolemma and contained intranuclear rods. After ischaemia, many SS-i neurons in the dentate hilus showed increased electron density of both the cell nucleus and the cytoplasm. In addition the cytoplasm was heavily vacuolated with the SS-i associated with some of these vacuoles. Other SS-i neurons had, in addition to the vacuoles a more homogeneous, and abnormal electron lucent nucleus and cytoplasm. These ultrastructural changes correspond to previously reported irreversible, ischaemic cell changes of neurons. Based on this we conclude that the SS immunoreactivity in the dentate hilus of the dorsal hippocampus is lost after ischaemia because of neuronal necrosis. As a minor part of this study, we examined whether the ischaemia-susceptible SS-i neurons in dentate hilus had commissural axonal projections. This was done utilizing double fluorescence microscopy of retrograde axonal transport of the fluorescent dye, Fluoro-Gold, and the observation that vulnerable SS-i neurons display homogeneously dispersed immunostaining 40 h after ischaemia. Fluoro-Gold was injected unilaterally into the dorsal dentate gyrus 5 days prior to ischaemia. Then, 40 h after ischaemia, sections were stained for SS immunofluorescence, and examined, in the dentate hilus contralateral to the injection, for neuronal co-localization of both events. Cell counts revealed double-labelling of 13% of all neurons which displayed one of the events. This observation suggests that at least some of the ischaemia-susceptible SS-i neurons in dentate hilus do project commissurally. The pathophysiological significance of ischaemic loss of commissurally projecting SS-i neurons in dentate hilus remains to be determined.

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mentioning

confidence: 71%

Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections

Sørensen¹,

Tønder²,

Zimmer³

et al. 1992

Neuropathology Appl Neurobio

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“…As the BCCAO model used here presents chronic and moderate ischemia, the altered amounts of these specific GABAergic cells could be different in comparison to the results in acute ischemia. The numbers of PV-and NPY-positive cells slowly reduced in the hippocampus in acute cerebral ischemia, and SOM-positive cells decreased in transient global ischemia as well, but they tend to be resistant to ischemia when co-localized with PV [36][37][38][39]. Meanwhile, Luo et al [23] recently reported the unchanged amounts of GABAergic cells in the prefrontal cortex during CCH, and suggested that deficits of cognitive ability induced by CCH may also result from the GABAergic interneuron dysfunction (such as alteration of electrophysiological properties).…”

Section: Research Weiping Liu and Qianfa Longmentioning

confidence: 99%

Parvalbumin and Neuropeptide Y Neuronal Loss in the Hippocampal CA1 Subarea is Associated with Cognitive Deficits in a Rat Model of Chronic Cerebral Hypoperfusion

Hei¹,

Wei²,

Yi³

et al. 2018

Neuropsychiatry

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BackgroundPermanent bilateral common carotid artery occlusion (BCCAO) produces a chronic cerebral hypoperfusion (CCH) state, which may cause cognitive impairments in aging, Alzheimer's disease and vascular dementia. Recent studies have noticed the crucial role of gamma amino butyric acid (GABA)ergic system in regulation of cognitive ability in a rat model of CCH, but the pathological processes of hippocampal GABAergic interneurons in CCH has not been systematically investigated so far. Here we investigated the altered amounts of GABAergic interneurons, namely parvalbumin (PV)-, neuropeptide Y (NPY)-and somatostatin (SOM)-positive cells and their possible relationship with cognitive deficits. Methods 55 male Sprague Dawley (SD) rats were randomly divided into BCCAO group (n=33, treated with permanent BCCAO) and sham group (n=22, same operation without ligation). Four weeks later, Morris Water Maze was used to analyze the cognitive deficits, and immunohistochemistry or western blotting was employed to investigate the GABAergic expression in the hippocampus of the rat model.

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“…u piramidalnim ćelijama [20]. Johansen izveštava da se SS-IR u hipokampu pri ishemiji ne menja [22]. Johansen izveštava da se SS-IR u hipokampu pri ishemiji ne menja [22].…”

Section: Somatostatin I Ishemijaunclassified

Expression of somatostatine in ischemia of rat brain

Babovic¹,

Srdić-Galić²,

Soldatovic-Stajic

et al. 2013

Med pregl

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Loss of Somatal Neuropeptide Y Immunoreactivity in the Rat Hippocampus Following Transient Cerebral Ischemia

Cited by 22 publications

References 0 publications

Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections

Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections

Parvalbumin and Neuropeptide Y Neuronal Loss in the Hippocampal CA1 Subarea is Associated with Cognitive Deficits in a Rat Model of Chronic Cerebral Hypoperfusion

Expression of somatostatine in ischemia of rat brain

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