Dendritic regression dissociated from neuronal death but associated with partial deafferentation in aging rat supraoptic nucleus

Dorothy G. Flood, Paul Coleman

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

As neurons are lost in normal aging, the dendrites of surviving neighbor neurons may proliferate, regress, or remain unchanged. In the case of age-related dendritic regression, it has been difficult to distinguish whether the regression precedes neuronal death or whether it is a consequence of loss of afferent supply. The rat supraoptic nucleus (SON) represents a model system in which there is no age-related loss of neurons, but in which there is an age-related loss of afferents. The magnocellular neurosecretory neurons of the SON, that produce vasopressin and oxytocin for release in the posterior pituitary, were studied in male Fischer 344 rats at 3, 12, 20, 27, 30, and 32 months of age. Counts in Nissl-stained sections showed no neuronal loss with age, and confirmed similar findings in other strains of rat and in mouse and human. Nucleolar size increased between 3 and 12 months of age, due, in part, to nucleolar fusion, and was unchanged between 12 and 32 months of age, indicating maintenance of general cellular function in old age. Dendritic extent quantified in Golgi-stained tissue increased between 3 and 12 months of age, was stable between 12 and 20 months, and decreased between 20 and 27 months. We interpret the increase between 3 and 12 months as a late maturational change. Dendritic regression between 20 and 27 months was probably the result of deafferentation due to the preceding age-related loss of the noradrenergic input to the SON from the ventral medulla.

Original languageEnglish (US)
Pages (from-to)575-587
Number of pages13
JournalNeurobiology of Aging
Volume14
Issue number6
DOIs
StatePublished - Jan 1 1993
Externally publishedYes

Fingerprint

Supraoptic Nucleus
Neurons
Inbred F344 Rats
Oxytocin
Dendrites
Vasopressins
Maintenance

Keywords

  • Aging
  • Dendrites
  • Fischer 344
  • Golgi
  • Hypothalamus
  • Neuronal number
  • Nucleoli
  • Rat
  • Supraoptic nucleus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Developmental Biology
  • Geriatrics and Gerontology
  • Clinical Neurology

Cite this

Dendritic regression dissociated from neuronal death but associated with partial deafferentation in aging rat supraoptic nucleus. / Flood, Dorothy G.; Coleman, Paul.

In: Neurobiology of Aging, Vol. 14, No. 6, 01.01.1993, p. 575-587.

Research output: Contribution to journalArticle

@article{1308c6bdaaf84437956ec4ad8099f4fb,
title = "Dendritic regression dissociated from neuronal death but associated with partial deafferentation in aging rat supraoptic nucleus",
abstract = "As neurons are lost in normal aging, the dendrites of surviving neighbor neurons may proliferate, regress, or remain unchanged. In the case of age-related dendritic regression, it has been difficult to distinguish whether the regression precedes neuronal death or whether it is a consequence of loss of afferent supply. The rat supraoptic nucleus (SON) represents a model system in which there is no age-related loss of neurons, but in which there is an age-related loss of afferents. The magnocellular neurosecretory neurons of the SON, that produce vasopressin and oxytocin for release in the posterior pituitary, were studied in male Fischer 344 rats at 3, 12, 20, 27, 30, and 32 months of age. Counts in Nissl-stained sections showed no neuronal loss with age, and confirmed similar findings in other strains of rat and in mouse and human. Nucleolar size increased between 3 and 12 months of age, due, in part, to nucleolar fusion, and was unchanged between 12 and 32 months of age, indicating maintenance of general cellular function in old age. Dendritic extent quantified in Golgi-stained tissue increased between 3 and 12 months of age, was stable between 12 and 20 months, and decreased between 20 and 27 months. We interpret the increase between 3 and 12 months as a late maturational change. Dendritic regression between 20 and 27 months was probably the result of deafferentation due to the preceding age-related loss of the noradrenergic input to the SON from the ventral medulla.",
keywords = "Aging, Dendrites, Fischer 344, Golgi, Hypothalamus, Neuronal number, Nucleoli, Rat, Supraoptic nucleus",
author = "Flood, {Dorothy G.} and Paul Coleman",
year = "1993",
month = "1",
day = "1",
doi = "10.1016/0197-4580(93)90042-A",
language = "English (US)",
volume = "14",
pages = "575--587",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier Inc.",
number = "6",

}

TY - JOUR

T1 - Dendritic regression dissociated from neuronal death but associated with partial deafferentation in aging rat supraoptic nucleus

AU - Flood, Dorothy G.

AU - Coleman, Paul

PY - 1993/1/1

Y1 - 1993/1/1

N2 - As neurons are lost in normal aging, the dendrites of surviving neighbor neurons may proliferate, regress, or remain unchanged. In the case of age-related dendritic regression, it has been difficult to distinguish whether the regression precedes neuronal death or whether it is a consequence of loss of afferent supply. The rat supraoptic nucleus (SON) represents a model system in which there is no age-related loss of neurons, but in which there is an age-related loss of afferents. The magnocellular neurosecretory neurons of the SON, that produce vasopressin and oxytocin for release in the posterior pituitary, were studied in male Fischer 344 rats at 3, 12, 20, 27, 30, and 32 months of age. Counts in Nissl-stained sections showed no neuronal loss with age, and confirmed similar findings in other strains of rat and in mouse and human. Nucleolar size increased between 3 and 12 months of age, due, in part, to nucleolar fusion, and was unchanged between 12 and 32 months of age, indicating maintenance of general cellular function in old age. Dendritic extent quantified in Golgi-stained tissue increased between 3 and 12 months of age, was stable between 12 and 20 months, and decreased between 20 and 27 months. We interpret the increase between 3 and 12 months as a late maturational change. Dendritic regression between 20 and 27 months was probably the result of deafferentation due to the preceding age-related loss of the noradrenergic input to the SON from the ventral medulla.

AB - As neurons are lost in normal aging, the dendrites of surviving neighbor neurons may proliferate, regress, or remain unchanged. In the case of age-related dendritic regression, it has been difficult to distinguish whether the regression precedes neuronal death or whether it is a consequence of loss of afferent supply. The rat supraoptic nucleus (SON) represents a model system in which there is no age-related loss of neurons, but in which there is an age-related loss of afferents. The magnocellular neurosecretory neurons of the SON, that produce vasopressin and oxytocin for release in the posterior pituitary, were studied in male Fischer 344 rats at 3, 12, 20, 27, 30, and 32 months of age. Counts in Nissl-stained sections showed no neuronal loss with age, and confirmed similar findings in other strains of rat and in mouse and human. Nucleolar size increased between 3 and 12 months of age, due, in part, to nucleolar fusion, and was unchanged between 12 and 32 months of age, indicating maintenance of general cellular function in old age. Dendritic extent quantified in Golgi-stained tissue increased between 3 and 12 months of age, was stable between 12 and 20 months, and decreased between 20 and 27 months. We interpret the increase between 3 and 12 months as a late maturational change. Dendritic regression between 20 and 27 months was probably the result of deafferentation due to the preceding age-related loss of the noradrenergic input to the SON from the ventral medulla.

KW - Aging

KW - Dendrites

KW - Fischer 344

KW - Golgi

KW - Hypothalamus

KW - Neuronal number

KW - Nucleoli

KW - Rat

KW - Supraoptic nucleus

UR - http://www.scopus.com/inward/record.url?scp=0027130922&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027130922&partnerID=8YFLogxK

U2 - 10.1016/0197-4580(93)90042-A

DO - 10.1016/0197-4580(93)90042-A

M3 - Article

VL - 14

SP - 575

EP - 587

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 6

ER -