NDLI: Vasopressinergic, Oxytocinergic, and Somatostatinergic Neuronal Activity after Adrenalectomy and Immobilization Stress

Content Provider	Springer Nature Link
Author	Franco Bourland, Rebecca E.
Copyright Year	1998
Abstract	Twenty days after bilateral adrenalectomy (ADX) or immediately after the last of three 6-h long immobilization periods, the levels of hypothalamic and neurohypophyseal L-[$^{35}$S]Cys-labeled arginine vasopressin (AVP), oxytocin (OT), and somatostatin-14 (SRIF) (only stressed animals) were measured simultaneously in male Wistar rats, after third ventricular administration of the labeled precursor, via guide-cannulae. The acetic acid-extracted labeled peptide fractions were purified by two sequential HPLC steps. After a 4 h period of labeling, only L-[$^{35}$S]Cys-AVP was selectively increased in the hypothalami of ADX-ized rats, compared to the sham-operated animals, possibly reflecting a significant activation of the paraventricular parvocellular (PVC) AVP/corticotropin-releasing factor (CRF) neurons. The increased accumulation of neurohypophyseal L-[$^{35}$S]Cys-labeled AVP and OT in these animals, without changes in the endogenous levels of these peptides, as measured by UV absorbance, also suggests a moderate activation of the magnocellular (MGC) AVP and OT neurons, as a consequence of adrenal insufficiency. In response to immobilization stress, levels of L-[$^{35}$S]Cys-OT were selectively increased in the hypothalami and corresponding neurohypophyses, 2 h and 4 h after receiving the label, concomitantly with a statistically significant reduction in the stores of OT in the neural lobes. AVP and SRJF biosynthesis remained unaffected by immobilization; the neurohypophyseal AVP stores likewise remained unchanged. These observations suggest the selective activation of MGC-OT neurons in response to chronic immobilization stress. Selective increases in hypothalamic L-[$^{35}$S]Cys-AVP in ADX-ized rats, and in hypothalamic L-[$^{35}$S]Cys-OT in chronically stress-immobilized rats, are presented as a measure of PVC-AVP/CRF and MGC-OT neuronal activation, respectively.
Starting Page	695
Ending Page	701
Page Count	7
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	23
Issue Number	5
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1998-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Neuronal Apoptosis Induced by Endoplasmic Reticulum Stress

Neurotrophic Factor Effects on Oxidative Stress–Induced Neuronal Death

Oxidative Stress Alters Physiological and Morphological Neuronal Properties

Gonadal Steroids and Neuronal Function

5-HT$_{1A}$ Receptor Agonist Reverses Adrenalectomy-Induced Loss of Granule Neuronal Morphology in the Rat Dentate Gyrus

GFAPβ mRNA Expression in the Normal Rat Brain and after Neuronal Injury

Antianxiety-Like Activity of Gallic Acid in Unstressed and Stressed Mice: Possible Involvement of Nitriergic System

Mitochondrial Function in Apoptotic Neuronal Cell Death

Proteomic Analysis of Neuronal Hypoxia In vitro

Vasopressinergic, Oxytocinergic, and Somatostatinergic Neuronal Activity after Adrenalectomy and Immobilization Stress

Similar Documents

Neuronal Apoptosis Induced by Endoplasmic Reticulum Stress

Neurotrophic Factor Effects on Oxidative Stress–Induced Neuronal Death

Oxidative Stress Alters Physiological and Morphological Neuronal Properties

Gonadal Steroids and Neuronal Function

5-HT$_{1A}$ Receptor Agonist Reverses Adrenalectomy-Induced Loss of Granule Neuronal Morphology in the Rat Dentate Gyrus

GFAPβ mRNA Expression in the Normal Rat Brain and after Neuronal Injury

Antianxiety-Like Activity of Gallic Acid in Unstressed and Stressed Mice: Possible Involvement of Nitriergic System

Mitochondrial Function in Apoptotic Neuronal Cell Death

Proteomic Analysis of Neuronal Hypoxia In vitro

Vasopressinergic, Oxytocinergic, and Somatostatinergic Neuronal Activity after Adrenalectomy and Immobilization Stress