Dendritic Translocation of RC3/Neurogranin mRNA in Normal Aging, Alzheimer Disease and Fronto-Temporal Dementia (original) (raw)

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Departments of Psychiatry and Biobehavioral Sciences, Redwood City, California

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Departments of Psychiatry and Biobehavioral Sciences, Redwood City, California

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Phillip M. Coulter, II, MS

Mental Retardation Research Center, Brain Research Institute,

University of California Los Angeles School of Medicine and Sugen Inc.

, Redwood City, California

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Departments of Pathology and Laboratory Medicine, Redwood City, California

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Departments of Psychiatry and Biobehavioral Sciences, Redwood City, California

Correspondence to: Joseph B. Watson, PhD, Department of Psychiatry and Biobehavioral Sciences, Mental Retardation Research Center, Brain Research Institute, UCLA School of Medicine, 48-241 NPI, 760 Westwood Plaza, Los Angeles, CA 90024.

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This work was supported by NIH grant NS 32521, NICHD Training Grant in Mental Retardation 5T32 HD 07032-18 and the Turken Fellowship of the Los Angeles Chapter of the Alzheimer's Association, and UCLA Alzheimer's Disease Center Grant AG 10123.

Author Notes

Published:

01 October 1997

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Julia W. Chang, Eric Schumacher, Phillip M. Coulter, Harry V. Vinters, Joseph B. Watson, Dendritic Translocation of RC3/Neurogranin mRNA in Normal Aging, Alzheimer Disease and Fronto-Temporal Dementia, Journal of Neuropathology & Experimental Neurology, Volume 56, Issue 10, October 1997, Pages 1105–1118, https://doi.org/10.1097/00005072-199710000-00004
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Abstract

RC3/neurogranin is a postsynaptic protein kinase C (PKC)-/calmodulin-binding substrate implicated in long-term potentiation (LTP) forms of synaptic plasticity. Our previous digoxigenin in situ hybridization (DIG-ISH) studies detected RC3 mRNA in apical dendrites and cell bodies of neurons in the rat cerebral cortex and hippocampus. This observation suggested that RC3 mRNA is selectively translocated to dendrites, where it may be translated locally in response to synaptic activity. To test this hypothesis further, we isolated a full-length cDNA clone of the homologous human RC3 mRNA from a human cortex λGT11 library, determined its nucleotide and predicted amino acid sequences, and performed mRNA expression studies in cerebral cortex from normal human patients and from patients with Alzheimer disease (AD) and fronto-temporal dementia (FTD). The human cDNA clone detects a single ≈1.3 kb mRNA whose nucleotide sequence is 73% similar to the rat nucleotide sequence and 96% similar to its amino acid sequence. DIG-ISH studies detect robust staining of RC3 mRNA in cell bodies of numerous neurons throughout Layers II-VI and in both apical and basal dendrites of pyramidal neurons in human neocortex (temporal/frontal). We conclude that dendritic targeting of RC3 mRNA is conserved in human brain. In AD neocortex tissue, there is little or no evidence for RC3 mRNA translocation to dendrites, while in FTD neocortex, targeting of RC3 mRNA to apical dendrites is preserved. Comparative studies in AD and FTD point to the potential importance of synapse integrity and the dendritic cytoskeleton in RC3 mRNA targeting in the human neocortex.

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Author notes

This work was supported by NIH grant NS 32521, NICHD Training Grant in Mental Retardation 5T32 HD 07032-18 and the Turken Fellowship of the Los Angeles Chapter of the Alzheimer's Association, and UCLA Alzheimer's Disease Center Grant AG 10123.

© 1997 by the American Association of Neuropathologists, Inc.

Topic:

• aging
• protein kinase c
• alzheimer's disease
• in situ hybridization
• cerebral cortex
• dementia
• frontotemporal dementia
• amino acid sequence
• base sequence
• calmodulin
• clone cells
• cytoskeleton
• dendrites
• digoxigenin
• dna, complementary
• hippocampus
• libraries
• long-term potentiation
• neocortex
• neuronal plasticity
• neurons
• nucleotides
• rna, messenger
• synapses
• translocation (genetics)
• brain
• rats
• personal integrity
• cell body

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