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Differential mitochondrial morphology in ventral striatal projection neuron subtypes
Author(s) -
Chandra Ramesh,
Calarco Cali A.,
Lobo Mary Kay
Publication year - 2019
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.24511
Subject(s) - medium spiny neuron , mitochondrion , mitochondrial fusion , biology , mitochondrial fission , microbiology and biotechnology , transcriptome , dopamine , neuroscience , biophysics , mitochondrial dna , striatum , genetics , gene expression , gene
Abstract The two striatal projection neuron subtypes (medium spiny neurons‐ MSNs), those enriched in dopamine receptor 1 versus 2 (D1‐MSNs and D2‐MSNs), display dichotomous properties at the level of the transcriptome, projections, morphology, and electrophysiology. Recent work illustrates dichotomous mitochondrial length in NAc MSN subtype dendrites after cocaine self‐administration, with a shift toward smaller mitochondria, due to enhanced fission, occurring in D1‐MSN dendrites and a shift toward larger mitochondria in D2‐MSN dendrites. However, to date there has been no comparison of mitochondrial morphological properties between MSN subtypes. In this study, we examine mitochondrial morphology in NAc D1‐MSNs versus D2‐MSNs. We observe an increase in the frequency of smaller length mitochondria in D2‐MSN dendrites relative to D1‐MSN dendrites, while D1‐MSN dendrites display an increase in larger length mitochondria. The differences in mitochondrial length occur in both NAc core and shell, although to a greater extent in NAc core. Finally, we demonstrate that the mitochondrial fusion molecule, Opa1, is differentially expressed in NAc MSN subtypes, with D1‐MSNs displaying higher expression of Opa1 ribosome‐associated mRNA. The difference in Opa1 levels may account for the bias toward enhanced smaller mitochondria in D2‐MSNs and enhanced larger mitochondria in D1‐MSNs. Collectively, our study demonstrates differential mitochondrial size and a potential molecular mediator of these mitochondrial differences in NAc MSN subtypes.