Dopaminergic Neuronal Loss, Reduced Neurite Complexity and Autophagic Abnormalities in Transgenic Mice Expressing G2019S Mutant LRRK2 methods
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Normal Locomotor Activity and Prepulse Inhibition in G2019S LRRK2 Transgenic Mice
To investigate whether G2019S mutant LRRK2 expression influences motor performance, we measured locomotor activity in the open field quadrant ( ). G2019S-LRRK2 mice display normal locomotor activity in the open field at 6 and 15 months of age ( ). In contrast, R1441C-LRRK2 mice exhibit a significant reduction in horizontal and vertical locomotor activity at 15 months compared to their non-transgenic littermate mice that is not evident at 6 months ( ). We also assessed prepulse inhibition of the acoustic startle reflex, a measure of sensorimotor gating that can be modulated in part by dopaminergic neurotransmission. However, G2019S- and R1441C-LRRK2 transgenic mice do not perform differently from their non-transgenic littermates when tested at 6 months (data not shown) and 15 months of age ( ). Our data demonstrate that G2019S-LRRK2 expression does not influence locomotor activity or...
Normal Locomotor Activity and Prepulse Inhibition in G2019S LRRK2 Transgenic Mice
A-D, In the open field G2019S LRRK2 TG mice (line 340) exhibit normal horizontal ( A ) and vertical ( B ) locomotor activity compared to NTG littermates at 6 and 15 months ( n = 7-9 mice/genotype). R1441C LRRK2 TG mice (line 574) reveal normal locomotor activity at 6 months but deficits at 15 months ( C and D ) compared to NTG mice ( n = 6-9 mice/genotype). Data represent the number of beam breaks during the first 15 min period. E-F, Normal pre-pulse inhibition (PPI) of the acoustic startle response in LRRK2 transgenic mice. E and F, G2019S and R1441C LRRK2 TG mice display normal PPI of the acoustic startle reflex at 15 months compared to their NTG littermates, with increasing pre-pulse tones of 74-90 dB ( n = 6-8 mice/genotype). Data are expressed as % PPI relative to no pre-pulse tone. Bars present the mean ...
Reduced Complexity of Dopaminergic Neurites in Primary Midbrain Cultures from G2019S LRRK2 Transgenic Mice
LRRK2 has been shown to regulate the morphology of neuronal processes in cultured primary cortical neurons,. To further explore this phenotype in our LRRK2 transgenic mice, primary midbrain cultures were prepared from the ventral mesencephalon of G2019S-LRRK2 transgenic mice (line 340) and their non-transgenic littermates. These cultures typically contain 5-10% of TH+ dopaminergic neurons (unpublished observation). Sholl analysis was conducted to provide a measure of neuritic complexity ( and ). At days-in-vitro (DIV) 3, developing dopaminergic neurons from G2019S-LRRK2 mice exhibit significantly reduced overall neurite complexity manifesting as shorter neurites but with modestly increased neurite branching compared to non-transgenic neurons ( and ). However, at DIV 7 when dopaminergic neurite outgrowth is fully established, G2019S-LRRK2 dopaminergic neurons reveal a dramatic...
Western blot analysis
Protein extracts were prepared from hemi-brains of 2-4 month-old mice as previously described by homogenization in TNE buffer (10 mM Tris-HCl pH 7.4, 150 mM NaCl, 5 mM EDTA, 0.5% NP-40, 1 X Complete protease inhibitor cocktail [Roche], 1 X phosphatase inhibitor cocktail I and II [Sigma-Aldrich, St. Louis, MO, USA]). Protein concentration was determined by BCA method (Pierce Biotechnology, Rockford, IL, USA) and 75 µg of protein was resolved by SDS-PAGE, transferred to nitrocellulose and probed with rabbit anti-LRRK2 antibodies recognizing human/mouse (JH5514 or monoclonal c81-8, Epitomics, Inc, Burlingame, CA) or human-specific (NB300-267, Novus Biologicals, Littleton, CO, USA ) epitopes, or mouse β-tubulin (TUB 2.1, Sigma-Aldrich) antibody. Refer to www.pdonlineresearch.org for detailed characterization of rabbit monoclonal LRRK2 antibody (clone c81-8, Epitomics, Inc). Quan...
Measurement of biogenic amines by HPLC
HPLC with electrochemical detection was employed to measure the concentration of the biogenic amines, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE) as previously described. Samples were prepared from dissected brain regions and injected onto a C-18 80 × 4.6 mm column (ESA Inc., Chelmsford, MA, USA) with detection using a 2-channel Coulochem II electrochemical detector (ES Inc.). Data were processed on an EZChrome Elite Client Workstation (ESA Inc.) with biogenic amine concentration expressed as ng per mg protein.
TH immunohistochemistry and stereological assessments
Mice were anesthetized with sodium pentobarbital (150 mg/kg) before intracardial perfusion with cold PBS and 4% paraformaldehyde (PFA). Brains were removed, post-fixed with PFA overnight and cryopreserved in 30% sucrose in PBS at 4°C for 48 h. Coronal midbrain sections (40-µm) were prepared and processed for immunohistochemistry with rabbit anti-TH antibody (Novus Biologicals) and Nissl counterstain as previously described.
Transmission electron microscopy (TEM)
For TEM analysis, mice were perfused with fixative (3% PFA, 1.5% glutaraldehyde, 100 mM cacodylate, 2.5% sucrose, pH 7.4) and post-fixed for 1 h. Cortex and striatal sections were processed as described. Sections were post-fixed in Palade's OsO 4, en bloc stained in Kellenberger's uranyl acetate, dehydrated, and flat-embedded in epon. 80 nm en face sections were prepared on a Leica UCT ultramicrotome, collected onto 400 mesh high transmission nickel grids, and post-stained with lead and uranyl acetate. Images were collected on a Philips EM 410 TEM equipped with a Soft Imaging System Megaview III digital camera.
Primary midbrain cultures and analysis of neuritic complexity
Cultures were fixed with 4% PFA and processed for immunocytochemistry with rabbit anti-TH (Novus Biologicals) and mouse anti-MAP2 (Sigma-Aldrich) antibodies and anti-rabbit IgG-AlexaFluor-546 and anti-mouse IgG-AlexaFluor-488 antibodies (Invitrogen). Fluorescent images were captured using a Leica DMI 4000 inverted fluorescence microscope (Leica) at 10x magnification. Sholl analysis was performed on TH+/MAP+ neurons using NIH ImageJ software with a Sholl analysis plug-in (v1.0) developed by the laboratory of Anirvan Ghosh ( http://www.biology.ucsd.edu/labs/ghosh/software/index.html ) to quantify neuritic complexity. Briefly, we constructed continuous concentric circles centered upon the neuronal soma to measure the number of intersections of dendrites with circles of increasing radii. Sholl analysis was performed using the semi-log method and measurements are shown in.
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Evidence quotes (8)
To investigate whether G2019S mutant LRRK2 expression influences motor performance, we measured locomotor activity in the open field quadrant ( ). G2019S-LRRK2 mice display normal locomotor activity in the open field at 6 and 15 months of age ( ). In contrast, R1441C-LRRK2 mice exhibit a significant reduction in horizontal and vertical locomotor activity at 15 months compared to their non-transgenic littermate mice that is not evident at 6 months ( ). We also assessed prepulse inhibition of the acoustic startle reflex, a measure of sensorimotor gating that can be modulated in part by dopaminergic neurotransmission. However, G2019S- and R1441C-LRRK2 transgenic mice do not perform differently from their non-transgenic littermates when tested at 6 months (data not shown) and 15 months of age ( ). Our data demonstrate that G2019S-LRRK2 expression does not influence locomotor activity or prepulse inhibition of the acoustic startle reflex in aged mice. Furthermore, our data suggests that R1441C-LRRK2 mice exhibit a progressive impairment of locomotor activity.
A-D, In the open field G2019S LRRK2 TG mice (line 340) exhibit normal horizontal ( A ) and vertical ( B ) locomotor activity compared to NTG littermates at 6 and 15 months ( n = 7-9 mice/genotype). R1441C LRRK2 TG mice (line 574) reveal normal locomotor activity at 6 months but deficits at 15 months ( C and D ) compared to NTG mice ( n = 6-9 mice/genotype). Data represent the number of beam breaks during the first 15 min period. E-F, Normal pre-pulse inhibition (PPI) of the acoustic startle response in LRRK2 transgenic mice. E and F, G2019S and R1441C LRRK2 TG mice display normal PPI of the acoustic startle reflex at 15 months compared to their NTG littermates, with increasing pre-pulse tones of 74-90 dB ( n = 6-8 mice/genotype). Data are expressed as % PPI relative to no pre-pulse tone. Bars present the mean ± SEM. * P <0.05 comparing TG with NTG as indicated.
LRRK2 has been shown to regulate the morphology of neuronal processes in cultured primary cortical neurons,. To further explore this phenotype in our LRRK2 transgenic mice, primary midbrain cultures were prepared from the ventral mesencephalon of G2019S-LRRK2 transgenic mice (line 340) and their non-transgenic littermates. These cultures typically contain 5-10% of TH+ dopaminergic neurons (unpublished observation). Sholl analysis was conducted to provide a measure of neuritic complexity ( and ). At days-in-vitro (DIV) 3, developing dopaminergic neurons from G2019S-LRRK2 mice exhibit significantly reduced overall neurite complexity manifesting as shorter neurites but with modestly increased neurite branching compared to non-transgenic neurons ( and ). However, at DIV 7 when dopaminergic neurite outgrowth is fully established, G2019S-LRRK2 dopaminergic neurons reveal a dramatic reduction of neurite length and branching with an overall reduction in neurite complexity (, ). We did not perform similar measurements on cultured dopaminergic neurons derived from R1441C-LRRK2 mice (line 574) since these transgenic mice do not exhibit transgene expression within the nigrostriatal...
Protein extracts were prepared from hemi-brains of 2-4 month-old mice as previously described by homogenization in TNE buffer (10 mM Tris-HCl pH 7.4, 150 mM NaCl, 5 mM EDTA, 0.5% NP-40, 1 X Complete protease inhibitor cocktail [Roche], 1 X phosphatase inhibitor cocktail I and II [Sigma-Aldrich, St. Louis, MO, USA]). Protein concentration was determined by BCA method (Pierce Biotechnology, Rockford, IL, USA) and 75 µg of protein was resolved by SDS-PAGE, transferred to nitrocellulose and probed with rabbit anti-LRRK2 antibodies recognizing human/mouse (JH5514 or monoclonal c81-8, Epitomics, Inc, Burlingame, CA) or human-specific (NB300-267, Novus Biologicals, Littleton, CO, USA ) epitopes, or mouse β-tubulin (TUB 2.1, Sigma-Aldrich) antibody. Refer to www.pdonlineresearch.org for detailed characterization of rabbit monoclonal LRRK2 antibody (clone c81-8, Epitomics, Inc). Quantitation of total LRRK2 and β-tubulin protein levels by densitometry was conducted using LabImage 1D software (Kapelan Bio-Imaging Solutions, Leipzig, Germany) on Western blot images captured using a FujiFilm LAS-4000 Luminescent Image Analysis system.
HPLC with electrochemical detection was employed to measure the concentration of the biogenic amines, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE) as previously described. Samples were prepared from dissected brain regions and injected onto a C-18 80 × 4.6 mm column (ESA Inc., Chelmsford, MA, USA) with detection using a 2-channel Coulochem II electrochemical detector (ES Inc.). Data were processed on an EZChrome Elite Client Workstation (ESA Inc.) with biogenic amine concentration expressed as ng per mg protein.
Mice were anesthetized with sodium pentobarbital (150 mg/kg) before intracardial perfusion with cold PBS and 4% paraformaldehyde (PFA). Brains were removed, post-fixed with PFA overnight and cryopreserved in 30% sucrose in PBS at 4°C for 48 h. Coronal midbrain sections (40-µm) were prepared and processed for immunohistochemistry with rabbit anti-TH antibody (Novus Biologicals) and Nissl counterstain as previously described.
For TEM analysis, mice were perfused with fixative (3% PFA, 1.5% glutaraldehyde, 100 mM cacodylate, 2.5% sucrose, pH 7.4) and post-fixed for 1 h. Cortex and striatal sections were processed as described. Sections were post-fixed in Palade's OsO 4, en bloc stained in Kellenberger's uranyl acetate, dehydrated, and flat-embedded in epon. 80 nm en face sections were prepared on a Leica UCT ultramicrotome, collected onto 400 mesh high transmission nickel grids, and post-stained with lead and uranyl acetate. Images were collected on a Philips EM 410 TEM equipped with a Soft Imaging System Megaview III digital camera.
Cultures were fixed with 4% PFA and processed for immunocytochemistry with rabbit anti-TH (Novus Biologicals) and mouse anti-MAP2 (Sigma-Aldrich) antibodies and anti-rabbit IgG-AlexaFluor-546 and anti-mouse IgG-AlexaFluor-488 antibodies (Invitrogen). Fluorescent images were captured using a Leica DMI 4000 inverted fluorescence microscope (Leica) at 10x magnification. Sholl analysis was performed on TH+/MAP+ neurons using NIH ImageJ software with a Sholl analysis plug-in (v1.0) developed by the laboratory of Anirvan Ghosh ( http://www.biology.ucsd.edu/labs/ghosh/software/index.html ) to quantify neuritic complexity. Briefly, we constructed continuous concentric circles centered upon the neuronal soma to measure the number of intersections of dendrites with circles of increasing radii. Sholl analysis was performed using the semi-log method and measurements are shown in.
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