Regional localization of the regulatory subunit (RIIβ) of the type II cAMP-dependent protein kinase in human brain

Viola Licameli, Linda A. Mattiace, Jack Erlichman, Peter Davies, Dennis Dickson, Bridget Shafit-Zagardo

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The distribution of the regulatory (RIIβ) subunits of type II cAMP-dependent protein kinase in cortical and subcortical areas was examined in human control and Alzheimer's disease (AD) brains. Four monoclonal antibodies generated against bovine brain RII, which crossreacted with human brain RIIβ, detected RII-immunoreactivity in pyramidal neurons of the hippocampus and frontal, occipital, parietal and superior temporal cortices and in non-pyramidal neurons of the amygdala and putamen. RIIβ immunoreactivity was localized to neuronal perikarya, proximal dendrites and cell processes. With the exception of rare processes in the ventroposterior lateral nucleus, RII-immunoreactivity was not seen in the thalamus. Other areas lacking RII-immunoreactivity included the midbrain, caudate nucleus and globus pallidus. RII-immunoreactivity was not detected in endothelia or glia. Except for the neocortex, the distribution of RIIβ immunoreactivity was the same in AD and non-demented control brains; however, cell bodies and their processes stained more intensely and uniformly in the neocortical regions of non-demented controls compared to AD. In the neocortex of AD, RIIβ immunoreactivity was substantially decreased in the superior temporal and occipital cortices, but not in the frontal cortex. Our data suggest that RII subunits are regionally distributed in the human brain. RII-immunoreactivity was decreased in some regions of neocortex in AD, but it did not preferentially colocalize with neurofibrillary tangles (NFT), senile plaques, or neuropil threads.

Original languageEnglish (US)
Pages (from-to)61-68
Number of pages8
JournalBrain Research
Volume578
Issue number1-2
DOIs
StatePublished - Apr 24 1992

Fingerprint

Cyclic AMP-Dependent Protein Kinases
Alzheimer Disease
Neocortex
Brain
Temporal Lobe
Neuropil Threads
Occipital Lobe
Neurofibrillary Tangles
Globus Pallidus
Pyramidal Cells
Caudate Nucleus
Putamen
Amyloid Plaques
Frontal Lobe
Dendrites
Mesencephalon
Amygdala
Thalamus
Neuroglia
Endothelium

Keywords

  • Alzheimer's disease
  • cAMP-dependent protein kinase
  • Human brain
  • Protein kinase
  • Regulatory subunit of type II cAMP-dependent protein kinase

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Regional localization of the regulatory subunit (RIIβ) of the type II cAMP-dependent protein kinase in human brain. / Licameli, Viola; A. Mattiace, Linda; Erlichman, Jack; Davies, Peter; Dickson, Dennis; Shafit-Zagardo, Bridget.

In: Brain Research, Vol. 578, No. 1-2, 24.04.1992, p. 61-68.

Research output: Contribution to journalArticle

Licameli, Viola ; A. Mattiace, Linda ; Erlichman, Jack ; Davies, Peter ; Dickson, Dennis ; Shafit-Zagardo, Bridget. / Regional localization of the regulatory subunit (RIIβ) of the type II cAMP-dependent protein kinase in human brain. In: Brain Research. 1992 ; Vol. 578, No. 1-2. pp. 61-68.
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AB - The distribution of the regulatory (RIIβ) subunits of type II cAMP-dependent protein kinase in cortical and subcortical areas was examined in human control and Alzheimer's disease (AD) brains. Four monoclonal antibodies generated against bovine brain RII, which crossreacted with human brain RIIβ, detected RII-immunoreactivity in pyramidal neurons of the hippocampus and frontal, occipital, parietal and superior temporal cortices and in non-pyramidal neurons of the amygdala and putamen. RIIβ immunoreactivity was localized to neuronal perikarya, proximal dendrites and cell processes. With the exception of rare processes in the ventroposterior lateral nucleus, RII-immunoreactivity was not seen in the thalamus. Other areas lacking RII-immunoreactivity included the midbrain, caudate nucleus and globus pallidus. RII-immunoreactivity was not detected in endothelia or glia. Except for the neocortex, the distribution of RIIβ immunoreactivity was the same in AD and non-demented control brains; however, cell bodies and their processes stained more intensely and uniformly in the neocortical regions of non-demented controls compared to AD. In the neocortex of AD, RIIβ immunoreactivity was substantially decreased in the superior temporal and occipital cortices, but not in the frontal cortex. Our data suggest that RII subunits are regionally distributed in the human brain. RII-immunoreactivity was decreased in some regions of neocortex in AD, but it did not preferentially colocalize with neurofibrillary tangles (NFT), senile plaques, or neuropil threads.

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