Morphological and molecular changes in aging rat prelimbic prefrontal cortical synapses

Erik B. Bloss, Rishi Puri, Frank Yuk, Michael Punsoni, Yuko Hara, William G. Janssen, Bruce S. McEwen, John Morrison

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Age-related impairments of executive functions appear to be related to reductions of the number and plasticity of dendritic spine synapses in the prefrontal cortex (PFC). Experimental evidence suggests that synaptic plasticity is mediated by the spine actin cytoskeleton, and a major pathway regulating actin-based plasticity is controlled by phosphorylated LIM kinase (pLIMK). We asked whether aging resulted in altered synaptic density, morphology, and pLIMK expression in the rat prelimbic region of the PFC. Using unbiased electron microscopy, we found an approximate 50% decrease in the density of small synapses with aging, while the density of large synapses remained unchanged. Postembedding immunogold revealed that pLIMK localized predominantly to the postsynaptic density where it was increased in aging synapses by approximately 50%. Furthermore, the age-related increase in pLIMK occurred selectively within the largest subset of prelimbic PFC synapses. Because pLIMK is known to inhibit actin filament plasticity, these data support the hypothesis that age-related increases in pLIMK may explain the stability of large synapses at the expense of their plasticity.

Original languageEnglish (US)
Pages (from-to)200-210
Number of pages11
JournalNeurobiology of Aging
Volume34
Issue number1
DOIs
StatePublished - Jan 1 2013
Externally publishedYes

Fingerprint

Lim Kinases
Synapses
Prefrontal Cortex
Actin Cytoskeleton
Post-Synaptic Density
Dendritic Spines
Neuronal Plasticity
Executive Function
Actins
Electron Microscopy
Spine

Keywords

  • Actin
  • Aging
  • Electron microscopy
  • Perforated synapse
  • Postembedding immunogold
  • Postsynaptic density
  • Prefrontal cortex
  • Structural plasticity
  • Synapse

ASJC Scopus subject areas

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

Cite this

Morphological and molecular changes in aging rat prelimbic prefrontal cortical synapses. / Bloss, Erik B.; Puri, Rishi; Yuk, Frank; Punsoni, Michael; Hara, Yuko; Janssen, William G.; McEwen, Bruce S.; Morrison, John.

In: Neurobiology of Aging, Vol. 34, No. 1, 01.01.2013, p. 200-210.

Research output: Contribution to journalArticle

Bloss, Erik B. ; Puri, Rishi ; Yuk, Frank ; Punsoni, Michael ; Hara, Yuko ; Janssen, William G. ; McEwen, Bruce S. ; Morrison, John. / Morphological and molecular changes in aging rat prelimbic prefrontal cortical synapses. In: Neurobiology of Aging. 2013 ; Vol. 34, No. 1. pp. 200-210.
@article{13a55726d3c3455c9190056490e654b3,
title = "Morphological and molecular changes in aging rat prelimbic prefrontal cortical synapses",
abstract = "Age-related impairments of executive functions appear to be related to reductions of the number and plasticity of dendritic spine synapses in the prefrontal cortex (PFC). Experimental evidence suggests that synaptic plasticity is mediated by the spine actin cytoskeleton, and a major pathway regulating actin-based plasticity is controlled by phosphorylated LIM kinase (pLIMK). We asked whether aging resulted in altered synaptic density, morphology, and pLIMK expression in the rat prelimbic region of the PFC. Using unbiased electron microscopy, we found an approximate 50{\%} decrease in the density of small synapses with aging, while the density of large synapses remained unchanged. Postembedding immunogold revealed that pLIMK localized predominantly to the postsynaptic density where it was increased in aging synapses by approximately 50{\%}. Furthermore, the age-related increase in pLIMK occurred selectively within the largest subset of prelimbic PFC synapses. Because pLIMK is known to inhibit actin filament plasticity, these data support the hypothesis that age-related increases in pLIMK may explain the stability of large synapses at the expense of their plasticity.",
keywords = "Actin, Aging, Electron microscopy, Perforated synapse, Postembedding immunogold, Postsynaptic density, Prefrontal cortex, Structural plasticity, Synapse",
author = "Bloss, {Erik B.} and Rishi Puri and Frank Yuk and Michael Punsoni and Yuko Hara and Janssen, {William G.} and McEwen, {Bruce S.} and John Morrison",
year = "2013",
month = "1",
day = "1",
doi = "10.1016/j.neurobiolaging.2012.05.014",
language = "English (US)",
volume = "34",
pages = "200--210",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Morphological and molecular changes in aging rat prelimbic prefrontal cortical synapses

AU - Bloss, Erik B.

AU - Puri, Rishi

AU - Yuk, Frank

AU - Punsoni, Michael

AU - Hara, Yuko

AU - Janssen, William G.

AU - McEwen, Bruce S.

AU - Morrison, John

PY - 2013/1/1

Y1 - 2013/1/1

N2 - Age-related impairments of executive functions appear to be related to reductions of the number and plasticity of dendritic spine synapses in the prefrontal cortex (PFC). Experimental evidence suggests that synaptic plasticity is mediated by the spine actin cytoskeleton, and a major pathway regulating actin-based plasticity is controlled by phosphorylated LIM kinase (pLIMK). We asked whether aging resulted in altered synaptic density, morphology, and pLIMK expression in the rat prelimbic region of the PFC. Using unbiased electron microscopy, we found an approximate 50% decrease in the density of small synapses with aging, while the density of large synapses remained unchanged. Postembedding immunogold revealed that pLIMK localized predominantly to the postsynaptic density where it was increased in aging synapses by approximately 50%. Furthermore, the age-related increase in pLIMK occurred selectively within the largest subset of prelimbic PFC synapses. Because pLIMK is known to inhibit actin filament plasticity, these data support the hypothesis that age-related increases in pLIMK may explain the stability of large synapses at the expense of their plasticity.

AB - Age-related impairments of executive functions appear to be related to reductions of the number and plasticity of dendritic spine synapses in the prefrontal cortex (PFC). Experimental evidence suggests that synaptic plasticity is mediated by the spine actin cytoskeleton, and a major pathway regulating actin-based plasticity is controlled by phosphorylated LIM kinase (pLIMK). We asked whether aging resulted in altered synaptic density, morphology, and pLIMK expression in the rat prelimbic region of the PFC. Using unbiased electron microscopy, we found an approximate 50% decrease in the density of small synapses with aging, while the density of large synapses remained unchanged. Postembedding immunogold revealed that pLIMK localized predominantly to the postsynaptic density where it was increased in aging synapses by approximately 50%. Furthermore, the age-related increase in pLIMK occurred selectively within the largest subset of prelimbic PFC synapses. Because pLIMK is known to inhibit actin filament plasticity, these data support the hypothesis that age-related increases in pLIMK may explain the stability of large synapses at the expense of their plasticity.

KW - Actin

KW - Aging

KW - Electron microscopy

KW - Perforated synapse

KW - Postembedding immunogold

KW - Postsynaptic density

KW - Prefrontal cortex

KW - Structural plasticity

KW - Synapse

UR - http://www.scopus.com/inward/record.url?scp=84868139334&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84868139334&partnerID=8YFLogxK

U2 - 10.1016/j.neurobiolaging.2012.05.014

DO - 10.1016/j.neurobiolaging.2012.05.014

M3 - Article

VL - 34

SP - 200

EP - 210

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 1

ER -