Localization and regulation of vasopressin mRNA in human neurons

Rivkees, Scott A.; Chaar, M.; Hanley, Daniel F.; Maxwell, Marius; Reppert, Steven M.; Uhl, George R.

doi:10.1002/syn.890030311

Cited by 25 publications

(5 citation statements)

References 39 publications

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“…Different agonal states may also cause physiological changes in mRNAs antemortem, and these altered rnRNA levels could persist postmortem. Except for a few studies (Guillemette et al ., 1986;Rivkees et al, 1989 ;Harrison and Pearson, 1990;Burke et al, 1991 ;Harrison et al ., 1991Harrison et al ., , 1993, changes in mRNA levels resulting from altered physiology immediately antemortem have not been considered as a variable when evaluating mRNA changes in postmortem brain . Most communications only match brains for postmortem study by age, sex, presence of disease, postmortem interval, and, sometimes, cause of death.…”

Section: Discussionmentioning

confidence: 99%

Heat‐Shock 70 Messenger RNA Levels in Human Brain: Correlation with Agonal Fever

Morrison‐Bogorad

Zimmerman²,

Pardue³

1995

Journal of Neurochemistry

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Systematic review of antemortem clinical information on randomly selected Alzheimer disease (AD) patients revealed that -40% of the patients had a recorded fever of X39 .2°C at or near death . Using isolation and quantitation techniques appropriate for analysis of human brain mRNAs, we found that low levels of inducible heatshock protein 70 (hsp70) mRNAs were present in cerebellum of afebrile AD patients and that mRNA levels were usually lower in two brain regions affected in AD, i .e ., hippocampus and temporal cortex . Levels of hsp70 mRNAs were increased three-to 33-fold in cerebellum of febrile patients compared with levels in patients whose recorded temperatures were -37 .5°C . Levels of hsp70 mRNAs were also increased in hippocampus and cortex of these febrile patients, but to a lesser extent than cerebellum . Heat-shock cognate 70 (hsc70) mRNAs were present at highest levels in afebrile cerebellum and were also present in the other brain regions . In cerebellum of patients with the highest temperatures, hsc70 mRNAs were induced severalfold over basal levels . Although there was a low and variable induction of hsc70 mRNAs in temporal cortex of these patients, there was no evidence for any induction in hippocampus . Increased heatshock 70 mRNA levels did not correlate with hypoxia, coma, hypertension, hypoglycemia, seizures, or medication . These results indicate that a specific agonal stress, namely fever, can increase the levels of heat shock 70 mRNAs in AD brain ; however, there is no evidence to suggest that affected regions of AD brain have higher overall levels of these mRNAs . Failure to obtain adequate agonal state information could result in inaccurately identifying short-term stress-related changes in postmortem brain as neuropathology characteristic of a chronic disease state . Key Words : Alzheimer disease-Agonal stress-Heat-shock response-hsp70 mRNA induction .

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Section: Discussionmentioning

confidence: 99%

Heat‐Shock 70 Messenger RNA Levels in Human Brain: Correlation with Agonal Fever

Morrison‐Bogorad

Zimmerman²,

Pardue³

1995

Journal of Neurochemistry

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“…The difference between the studies appears to be an improved sensitivity of their nonradioactive hybridization, which in most circumstances has been less than that afforded by radiolabelled probes. In support of this interpretation, Rivkees et al (1989), using a 35S-labelled probe, found a smaller percentage reduction in vasopressin mRNA associated with increasing PMI, and their data suggested a postmortem half-life for rat vasopressin mRNA of 24 h. Clearly, the threshold for detection of a mRNA will affect the apparent degree, though not necessarily the statistical significance, of any difference in amount of mRNA that exists between the groups being compared. Moreover, because ISHH and northern blotting in practice allow only relative, not absolute, quantification, caution should be exercised when interpreting a percentage change in RNA abundance with these methods, whether in relation to PMI or to other variables (see Wiesner and Zak, 1991).…”

Section: Pmi and Detection Of Specific Mrnasmentioning

confidence: 91%

“…Many mRNAs are affected by acute or chronic drug administration, including neuroleptics (Romano et al, 1987;De la Concha et al, 1991), opiates (Lightman and Young, 1987), and alcohol (Mochly-Rosen et al, 1988). Other influences that may be pertinent for some mRNAs include the time of day at which death occurred (Lausson et al, 1989), dehydration (Rivkees et al, 1989), hypoglycaemia (Suda et al, 1988), stresses of various kinds (Daval et al, 1989;Nichols et al, 1990), and neuronal activity (Nishimori et al, 1989;Steward et al, 1991).…”

Section: The Effect Of As On Brain Rnamentioning

confidence: 99%

Pre‐and Postmortem Influences on Brain RNA

Barton

Pearson

Najlerahim

et al. 1993

Journal of Neurochemistry

243

142

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Many potentially valuable techniques for the understanding of human neurobiological and neuropathological processes require the use of RNA obtained from postmortem tissue. As with earlier neurochemical studies, there are two particular problems posed by such tissue in comparison with tissue from experimental animals. These are the postmortem interval and the condition of the patient prior to death, referred to as the agonal state. We review the nature and extent of the effects of postmortem interval and agonal state on RNA in brain tissue, with particular reference to the study of neuropsychiatric disorders. Perhaps surprisingly, postmortem interval has at most a modest effect on RNA. Abundant intact and biologically active RNA is present in tissue frozen 36 h or more after death. Postmortem interval does not account for the marked variability observed among human brains in all RNA parameters. Despite the overall stability of RNA after death, some evidence suggests that individual RNAs may undergo postmortem decay. Less attention has been paid to the effects of agonal state. The existing data indicate that events in the premortem period such as hypoxia and coma can affect the amount of some messenger RNAs. The nature of agonal state influences depends on the messenger RNA in question, though the basis for this selective vulnerability is unknown. No agonal state effect on overall RNA level or activity has been found. The data show that postmortem brain tissue can be used for RNA research. However, considerable attention must be paid to controlling for the influences of pre-and postmortem factors, especially when quantitative analyses are performed.

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“…Based on the above observations, we suggest that somatic illnesses leading to prolonged osmotic or nonosmotic stimulation of VP release induce an activity-related increase in TH expression within the human neurosecretory neurons. Although animal data suggest that genetic factors could also be responsible for a variable number of TH-IR neurons in the hypothalamus [66], we consider this increased expression of TH in the human PVN and SON as activity-related since it is evident specifically in patients with clinical conditions of increased and prolonged demand for VP secretion and it appears to parallel the increased expression of VP mRNA observed in hypovolemic or dehydrated patients [67, 68]. …”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Tyrosine Hydroxylase Immunoreactivity in Paraventricular and Supraoptic Neurons in Illnesses with Prolonged Osmotic or Nonosmotic Stimulation of Vasopressin Release

Panayotacopoulou¹,

Malidelis²,

Fliers³

et al. 2002

Neuroendocrinology

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Our previous studies indicated that in the human paraventricular (PVN) and supraoptic (SON) nuclei, tyrosine hydroxylase (TH) – the first and rate-limiting enzyme in catecholamine synthesis – is localized mainly in magnocellular neurons and that antemortem factors regulate its expression. The purpose of the present study was to investigate the distribution of TH-immunoreactive (TH-IR) perikarya of the hypothalami of a large sample of well-documented adult subjects without neurological, psychiatric or endocrinological disease in order to identify factors that could regulate the expression of TH in the human neurosecretory neurons. Our material consisted of the hypothalami of 38 subjects studied immunohistochemically for TH using the peroxidase-antiperoxidase method. Striking individual differences were observed among the subjects studied concerning the number and distribution of TH-IR perikarya within the PVN and SON. These differences were evident throughout the entire rostrocaudal length of the hypothalamus and appeared to be related neither to the age or sex of the subjects nor to the postmortem interval or staining procedures. In the sample studied, a large number of TH-IR perikarya were observed specifically in all subjects that had suffered from right-sided heart failure due to pulmonary hypertension, liver cirrhosis or dehydration. In all the above illnesses, increased production and secretion of vasopressin (VP) are reported to occur due to a decrease in ‘effective’ blood volume or to osmotic stimulation. We conclude that somatic illnesses leading to prolonged osmotic or nonosmotic stimulation of VP release may induce increased expression of TH immunoreactivity in the human neurosecretory neurons related to neuronal activation.

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Localization and regulation of vasopressin mRNA in human neurons

Cited by 25 publications

References 39 publications

Heat‐Shock 70 Messenger RNA Levels in Human Brain: Correlation with Agonal Fever

Heat‐Shock 70 Messenger RNA Levels in Human Brain: Correlation with Agonal Fever

Pre‐and Postmortem Influences on Brain RNA

Increased Expression of Tyrosine Hydroxylase Immunoreactivity in Paraventricular and Supraoptic Neurons in Illnesses with Prolonged Osmotic or Nonosmotic Stimulation of Vasopressin Release

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