Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Comparison of the structure, function and autophagic maintenance of mitochondria in nigrostriatal and tuberoinfundibular dopamine neurons.

Authors: Hawong, Hae-Young; Patterson, Joseph R; Winner, Brittany M; Goudreau, John L; Lookingland, Keith J

Published In Brain Res, (2015 Oct 05)

Abstract: A pathological hallmark of Parkinson׳s disease (PD) is progressive degeneration of nigrostriatal dopamine (NSDA) neurons, which underlies the motor symptoms of PD. While there is severe loss of midbrain NSDA neurons, tuberoinfundibular (TI) DA neurons in the mediobasal hypothalamus (MBH) remain intact. In the present study, confocal microscopic analysis revealed that mitochondrial content and numbers of mitophagosomes were lower in NSDA neuronal cell bodies in the substantia nigra pars compacta (SNpc) compared to TIDA neuronal cell bodies in the arcuate nucleus (ARC) of C57BL/6J male mice. Mitochondrial respiration, mass, membrane potential and morphology were determined using bioenergetic, flow cytometric and transmission electron microscopic analyses of synaptosomes isolated from discrete brain regions containing axon terminals of NSDA and TIDA neurons. Maximum and spare respiratory capacities, and mitochondrial mass were lower in synaptosomal mitochondria derived from the striatum (ST) as compared with the MBH, which correlated with lower numbers of mitochondria per synaptosome in these brain regions. In contrast, there was no regional difference in mitochondrial basal, maximum or spare respirations following inhibition of Complex I activity with rotenone. These results reveal that higher numbers of viable mitochondria are correlated with more extensive autophagic mitochondrial quality maintenance in TIDA neurons as compared with NSDA neurons.

PubMed ID: 26141374 Exiting the NIEHS site

MeSH Terms: Animals; Arcuate Nucleus of Hypothalamus/cytology; Arcuate Nucleus of Hypothalamus/metabolism*; Autophagy/physiology*; Cell Respiration/physiology; Corpus Striatum/cytology; Corpus Striatum/metabolism*; Dopaminergic Neurons/cytology; Dopaminergic Neurons/metabolism*; Electron Transport Complex I/antagonists & inhibitors; Electron Transport Complex I/metabolism; Male; Membrane Potentials/physiology; Mice, Inbred C57BL; Mitochondria/drug effects; Mitochondria/metabolism*; Mitochondria/ultrastructure; Neural Pathways/cytology; Neural Pathways/metabolism; Pars Compacta/cytology; Pars Compacta/metabolism*; Rotenone/pharmacology; Synaptosomes/metabolism; Tyrosine 3-Monooxygenase/metabolism; Uncoupling Agents/pharmacology

Back
to Top