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Differential dendritic targeting of AMPA receptor subunit mRNAs in adult rat hippocampal principal neurons and interneurons

Lookup NU author(s): Dr David Cox, Dr Claudia Racca

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Abstract

In hippocampal neurons, AMPA receptors (AMPARs) mediate fast excitatory postsynaptic responses at glutamatergic synapses, and are involved in various forms of synaptic plasticity. Dendritic local protein synthesis of selected AMPAR subunit mRNAs is considered an additional mechanism to independently and rapidly control the strength of individual synapses. We have used fluorescent in situ hybridisation and immunocytochemistry to analyse the localisation of AMPAR subunit (GluA1-4) mRNAs and their relationship with the translation machinery in principal cells and interneurons of the adult rat hippocampus. The mRNAs encoding all four AMPAR subunits were detected in the somata and dendrites of CA3 and CA1 pyramidal cells and those of six classes of CA1 GABAergic interneurons. GluA1-4 subunit mRNAs were highly localised to the apical dendrites of pyramidal cells, while in interneurons they were present in multiple dendrites. In contrast, in dentate gyrus, GluA1-4 subunit mRNAs were virtually restricted to the somata and absent from the dendrites of granule cells. These different regional and cell type-specific labelling patterns also correlated with the localisation of markers for components of the protein synthesis machinery. Our results support the local translation of GluA1-4 mRNAs in dendrites of hippocampal pyramidal cells and CA1 interneurons but not in granule cells of the dendate gyrus. Furthermore, the regional and cell type-specific differences we observed suggest that each cell type uses distinct ways of regulating the local translation of AMPA receptor subunits


Publication metadata

Author(s): Cox DJ, Racca C

Publication type: Article

Publication status: Published

Journal: Journal of Comparative Neurology

Year: 2013

Volume: 521

Issue: 9

Pages: 1954-2007

Print publication date: 18/04/2013

ISSN (print): 0021-9967

ISSN (electronic): 1096-9861

Publisher: John Wiley & Sons, Inc.

URL: http://dx.doi.org/10.1002/cne.23292

DOI: 10.1002/cne.23292


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