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Participation of Catecholamines and Nitric Oxide in Regulation of Apoptosis in Nonapeptidergic Neurons of the Rat Hypothalamus

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Participation of Catecholamines and Nitric Oxide in Regulation of Apoptosis in Nonapeptidergic Neurons of the Rat Hypothalamus

Content Provider	Springer Nature Link
Author	Taranukhin, A. G. Glazova, M. V. Yevteyeva, S. E. Yamova, L. A. Chernigovskaya, E. V.
Copyright Year	2002
Abstract	The goal of this work was to study effects of blockade of catecholamine (CA) synthesis on activation of neuronal NO synthase (nNOS) and to elucidate the role of NO in activation of pro- and anti-apoptotic signal proteins in nonapeptidergic neurons of supraoptic (SON) and paraventricular (PVN) nuclei of hypothalamus. The experiment was carried out on adult male Wistar rats. Dehydration for 5 days was used as an apoptosis-activating factor in vasopressinergic neurosecretory cells of SON and PVN of hypothalamus in adult rats. To find out the role of CA, a part of the animals subjected to dehydration were administered intraperitoneally, for the last 3 consecutive experimental days, with an inhibitor of CA synthesis, α-methyl-p-tyrosine (α-MT) at a dose of 200 mg/kg body weight. A marker of the programmed cell death initiation, pro-apoptotic protein caspase-9, as well as anti-apoptotic protein bcl-2 and nNOS, were revealed using an immunohistochemical technique. Evaluation of immunopositive substance (nNOS, caspase-9, and bcl-2) in neurosecretory cells of SON and PVN were carried out quantitatively by determination of optical density of the stained material in perikarya, using a computerized digital television image analyzer and software PhotoM. On comparing the nNOS amount with the level of pro- and anti-apoptotic protein expression, we have come to the conclusion that a decrease of the brain CA level increases the nNOS and caspase-9 expression. This allows suggesting that an increased level of NO mediates activation of the pro-apoptotic protein caspase-9 and initiates apoptosis in neurons of SON and PVN of hypothalamus. The lack of neuronal loss in SON under conditions of decrease CA synthesis on the background of dehydration might be due to increased expression of the anti-apoptotic protein bcl-2, whose increased elevated level seems to prevent the further rise of the caspase-9 level and, thereby, protects cells from death. An increased level of bcl-2 in neurons of PVN correlated with high amounts of nNOS and caspase-9, but there also was observed no cell loss. It is suggested that suppression of apoptosis in PVN is due either to the bcl-2 effects at later stages of apoptosis, or to other mechanisms that inhibit active caspases.
Starting Page	781
Ending Page	786
Page Count	6
File Format	PDF
ISSN	00220930
Journal	Journal of Evolutionary Biochemistry and Physiology
Volume Number	38
Issue Number	6
e-ISSN	16083202
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2002-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Biochemistry Evolutionary Biology
Content Type	Text
Resource Type	Article
Subject	Physiology Biochemistry Ecology, Evolution, Behavior and Systematics

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Regulation of Apoptosis in Nonapeptidergic Neurons of Rat Hypothalamus by Catecholamines in Experiments in vitro

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Role of Different Types of Adrenoreceptors in Regulation of Functional Activity of Vasopressinergic Neurosecretory Cells of Rat Hypothalamus

Participation of Catecholamines and Nitric Oxide in Regulation of Apoptosis in Nonapeptidergic Neurons of the Rat Hypothalamus

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