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Biological, Medical
Aging Mouse
Observation Type
Standard Data
Jan 23rd, 2017
Mar 9th, 2017
  • Figure
  • References
  • 1
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    Increased whole cerebellar serotonin in aged C57BL/6 mice


    Mobility and locomotor impairments have high prevalence, morbidity, and significant mortality in older adult populations. Cerebellar functional changes have been implicated in the pathogenesis of these age-related mobility and gait deficits unrelated to stroke, Parkinson’s disease, or degenerative joint disease. We thus examined total cerebellar glutamate, glutamine, GABA, glycine, dopamine, norepinephrine, tryptophan, serotonin, alanine, threonine, and asparagine content from male 2-3-month (young, = 6) and 21-24-month-old (aged, = 6) C57BL/6 mice. Neurotransmitter and amino acid concentrations were determined by high-performance liquid chromatography followed with mass spectroscopy. We found a significant increase in cerebellar serotonin in aged versus young mice, but otherwise no significant phenotypic differences in measured neurotransmitter concentrations. Applying current thought about cerebellar aging and cerebellar serotonergic systems, we consider how this age-related increase in cerebellar serotonin may contribute to gait ataxia.


    Figurea.Age-evoked increase in whole cerebellar serotonin in C57BL/6 mice.

    Boxplots provided for whole cerebellum neurotransmitter concentrations; data points superimposed upon boxplots. Glutamate, GABA, glutamine, tryptophan, and norepinephrine values correspond to the y-axis valued 0-10; dopamine values correspond to the y-axis labeled 0-100; glycine and serotonin values correspond to the y-axis labeled 0-1,000. Neurotransmitter concentration units provided on the x-axis. Blue dots depict measures from the young (2-3 months) cohort; green dots depict measures from the old (21- 24 months) cohort.

    For all comparisons, age df = 1, error df = 10, total df = 11. Respective F and p values are as follows: Glu F1,10 = 1.13, = 0.3131; GABA F1,10 = 1.64, = 0.229; Gln F1,10 = 0.38, = 0.5495; Gly F1,10 = 6.85, = 0.0257; Ala F1,10 = 0.44, = 0.52; Thr F1,10 = 3.8, = 0.0799; Trp F1,10 = 3.13, = 0.1073; Asn F1,10 = 2.9. = 0.1192; DA F1,10 = 0.08, = 0.7863; NE F1,10 = 0.03, = 0.8665; 5-HT (*) F1,10 = 13.53, = 0.0043. Critical = 0.0063 to achieve α = 0.05 for Bonferroni correction over eight comparisons.

    The MATLAB program used to generate the figures as well as to run ANOVA statistics can be found in the supplementary data.


    It is essential to understand how aging affects mobility, and find interventions to prevent or delay mobility, impairments. Mobility impairments often accompany advanced age[1]. They are major causes of morbidity in the “oldest old,” the most rapidly expanding demographic group in the United States[2][3][4]. Gait speed is a sensitive biomarker of overall functional status[5], as well as a powerful predictor of overall mortality[6][7]. Cerebellar dysfunction may be a potential source of age-related mobility impairments. In humans, overall cerebellar volume decreases with age as shown by voxel-based morphometry[8] and is associated with age-related gait impairments including slow gait speed[9]. Aging is accompanied by a marked change in cerebellar gene expression patterns in both rodent models and humans[10][11]. No age-related decrease in cerebellar granule cell number or density has been noted in rodent models[12][13]; small decreases have been described in humans[14]. Aging is also associated with a strain-specific increase in excitatory synaptic puncta in the internal granule cell layer; however, these synapses show deficits in excitatory amino acid neurotransmission[10]. Loss of visualized synaptic boutons on Purkinje cell dendritic networks also accompanies age-related Purkinje cell involution and loss[15]. Aging also evokes deficits in Purkinje cell function, including marked slowing of firing rates[16]and blunted responses to adrenergic stimulation[17]. These changes have been correlated with impairment in mobility-related behaviors, including walking on a runway and dynamic balance[18].


    To further explore potential synaptic deficits underlying age-related gait impairments, we assessed whole-cerebellum neurotransmitter and excitatory amino acid content in cohorts of young and aged C57BL/6 mice using HPLCmass spectroscopy (HPLC-MS). We report a novel finding of increased whole cerebellum serotonin in aged, compared to young, C57BL/6 mice.

    Results & Discussionlink


    All samples were suitable for HPLC-MS determination of cerebellar neurotransmitter and amino acid levels: glutamate, GABA, glycine, glutamine, dopamine, norepinephrine, tryptophan, serotonin, alanine, threonine, and asparagine. Our results suggest a 1.4-fold statistically significant increase in whole-cerebellar serotonin in aged C57BL/6 mice compared to young conspecifics (Figure a). We otherwise found no other differences in whole cerebellum neurotransmitter or amino acid concentrations between the young and old mouse cohorts.

    Serotonin is an ancient regulator of cellular function[19], and has a coordinating role in the performance of movement behaviors across a wide variety of organisms[20][21][22][23]. Aging has a clear impact on cerebellar serotonergic function. The activity of tryptophan hydroxylase, the enzyme catalyzing the rate-limiting conversion of tryptophan to serotonin, is significantly decreased in the midbrain and pons of aged rats[24][25]. Concordantly, age-associated decreases in whole cerebellar serotonin have been reported in rats (assayed by a fluorometric reaction between serotonin and o-phthaldialdehyde[26]) and senescence-accelerated mice (assessed by 3H-tryptophan injection[27]). However, no age-associated differences in cerebellar serotonin content were noted among cohorts of 6-24-month-old BALB mice (assayed by HPLC[28]), and our study is the first to report an age-associated increase in cerebellar serotonin content in a mouse model. Multiple studies have also demonstrated a marked loss of serotonin reuptake transporter function in the cerebellum of older adults[29][30].
    Serotonin has its most profound effect on the Lugaro inhibitory interneurons of the internal granule cell layer. These cells are numerous, have strong inhibitory projections onto Golgi cell inhibitory interneurons, and are typically silent. Lugaro cells respond to serotonin (likely through a 5-HT2 subfamily receptor) with a marked increase in spiking activity leading to increased inhibitory postsynaptic potentials onto Golgi cell membranes[31][32]. Lugaro cell activity also directly inhibits Purkinje neuron firing[33]. A single Lugaro cell makes inhibitory synaptic contact with about 150 nearby Golgi cells[31]; each Golgi cell makes inhibitory synaptic contact with about 3,000-5,000 granule cells[34]. Lugaro cell activity thus has the potential to reduce both the tonic and phasic components of Golgi cell inhibition onto large populations of granule cells. Serotonergic neurotransmission also contributes more subtle effects on cerebellar input signal processing. Serotonin attenuates parallel fiber input onto Purkinje cells (both by increasing activity of inhibitory basket and stellate interneurons and by presynaptic decreases of granule cell glutamate[35][36]). Serotonin also modulates cerebellar deep nuclei function in a complex, incompletely understood manner[37].


    Our results suggest an age-related 1.4-fold increase in whole cerebellar serotonin content. The methods we employed do not allow us to further determine if this difference reflects increased intravesicular serotonin within cerebellar serotonergic projections, and/or increased extracellular serotonin. Similarly, we cannot determine if this increase occurs over the cerebellum as a whole, or preferentially affects either the cerebellar input regions (internal granule cell, molecular, and Purkinje layers) or the cerebellar output nuclei; nor can we determine whether this finding localizes to specific folia.


    The predicted outcome of increasing cerebellar serotonergic activity may thus be to increase granule cell input sensitivity to mossy fiber input, decrease Purkinje cell sensitivity to parallel fiber input, and increase inhibition of Purkinje cell firing. These effects would combine to expand mossy fiber input participating in center-surround inhibition[38][39]. In other words, increased serotonergic activity may allow a larger set of afferent sensory inputs concurrent access to the Purkinje cell network while preserving overall Purkinje cell firing properties. Of note, in normal human volunteers, increased extracellular serotonin (through a single dose of a selective serotonin uptake inhibitor) evoked a significant increase in resting-state fMRI centrality measures across the cerebellum, consistent with the hypothesis that increased serotonergic activity enhances cerebellar functional connectivity[40].

    It is thus interesting to note in this context that inhibition of serotonergic tone (by treatment with the partial 5-HT1AR agonist buspirone) improved cerebellar tremor[41][42]. Further, prominent cerebellar ataxia has been observed in aged (21-24 months old) compared to young (2-3 months old) C57BL/6 mice obtained from the same colony as the mice in this study[10]. Interestingly, this appeared to be strain-specific with no ataxia present in BALB mice of identical ages. Locomotor ataxia thus accompanies the increased cerebellar serotonin content observed in C57BL/6 mice, but not in BALB mice with no age-related changes in cerebellar serotonin content[28]. Gait ataxia may potentially be a behavior evoked by serotonergic increases in cerebellar functional connectivity. Further studies to determine if age-associated increases in cerebellar serotonin content are reflected in extracellular serotonin concentrations, and to determine the specific serotonin receptor subtypes associated with Lugaro cell activation, will better define the mechanisms through which serotonergic activity may influence cerebellar tremor, as well as identify potential therapeutic targets.



    All studies were performed in accordance with the NIH Guide for the Care and Use of Laboratory Animals and were approved by our Institutional Animal Care and Use Committee. Six young male C57BL/6J mice were obtained from Jackson Laboratories at 8 weeks of age. Six old (20 months) male C57BL/6 mice were obtained from the National Institute of Aging rodent facility. Animals were housed in our vivarium for 1 month in microisolator cages (Lab Products Inc., Seaford, DE). Mice experienced a 12:12 lighting cycle (lights on 0600 CST) and were provided with chow (Envigo Teklad #7012) and water ad libitum.

    Tissue processing

    Mice were euthanized with acute CO2 asphyxiation, followed by rapid decapitation. Brain was isolated from the skull and placed into ice-cold PBS (Hyclone SH30256.01). Under a dissecting microscope, cerebellum was separated from brain and flash-frozen in isopentane for 5-10 s. Frozen cerebellums were stored at -80°C in canonical tubes until shipping, at which time the tissues/tubes were packed in dry ice and shipped overnight to Brains Online for further analysis.
    Sample preparation
    Mouse cerebella were homogenized using a Misonix Sonicator 3000 ultrasonic cell disruptor (Qsonica, LLC, Newton, USA). Per mg cerebellum 4 μL of 0.5 M perchloric acid was added as tissue destruction matrix. After homogenization, the samples were spun down and supernatant was processed further for the quantification of glutamate, GABA, glycine, glutamine, tryptophan, dopamine, norepinephrine, serotonin, alanine, asparagine, and threonine.
    Supernatant was further processed and 20 μL of the processed sample was mixed with 4 μL stable labeled internal standards mix of the analytes of interest. The mixture was derivatized with the proprietary SymDAQ reagent (BrainLink, Groningen, NL) in the autosampler part of an integrated LC system (prominence series; Shimadzu, Japan) by addition of 30 μL SymDAQ reagent solution to the sample vial. After the reaction, 45 μL of the mixture was injected onto the HPLC-MS system. Chromatographic separation was performed on a reverse-phase column (100×3.0 mm, 2.5 μm particle size; Synergi MAX-RP, Phenomenex, Torrance, USA) at 30°C. Sample analytes were separated using a 100 to 0% gradient of mobile phase A (ultrapure water/acetonitrile (98/2), 0.1% formic acid) to mobile phase B (ultrapure water/acetonitrile (30/70), 0.1% formic acid) at a flow rate of 300 μl/min. A post-column make-up flow of 150 μL/min consisting of 90% acetonitrile and 10% water, was added to the flow of the HPLC, prior to entering the MS for analyte detection. MS analysis was performed using a system consisting of an API 4000 triple quadropole detector and a Turbo V Ion Spray interface (AB Sciex, Redwood City, USA). The acquisitions were performed in positive ionization mode, with ionization spray voltage set at 3 kV and a probe temperature of 200°C. The instrument was operated in multiple reaction monitoring mode. The collision gas (nitrogen) pressure was held at 2 psig. Data was calibrated and quantified using the Analyst™ version 1.4.2 data system (AB Sciex, Redwood City, USA).
    Statistical analysis
    Neurotransmitter/amino acid concentrations were compared over the two cohorts using one-way analysis of variance, with Bonferroni corrections applied to adjust the critical p value for eight simultaneous comparisons (we did not include alanine or threonine in our calculations since these amino acids are not neurotransmitters or neurotransmitter precursors in the cerebellum). Statistics were calculated using MATLAB R (anova1; Mathworks, Natick, MA).

    Funding Statementlink

    This study was supported by NIH/NIA R01-AG031158 to SJB.


    The authors thank Ms. Tammy Chaudoin for her expert technical support.

    Ethics Statementlink

    Not applicable.

    No fraudulence is committed in performing these experiments or during processing of the data. We understand that in the case of fraudulence, the study can be retracted by Matters.

    1. Luppa Melanie, Undefined, Riedel-Heller Steffi G.,more_horiz, Weyerer Siegfried
      Age-related predictors of institutionalization: results of the German study on ageing, cognition and dementia in primary care patients (AgeCoDe)
      Social Psychiatry and Psychiatric Epidemiology, 47/2010, pages 263-270 DOI: 10.1007/s00127-010-0333-9chrome_reader_mode
    2. Vincent, Grayson K, Velkoff, Victoria Averil
      The next four decades: The older population in the United States: 2010 to 2050
    3. Hobbs, Fb, Damon, Bl
      65+ in the United States (US Bureau of the Census, Current Population Reports, Special Studies, P23-190)
      Washington and DC: US Government Printing Office, 1996 chrome_reader_mode
    4. Ferrer Assumpta, Formiga Francesc, Plana-Ripoll Oleguer,more_horiz, Pujol Ramón
      Risk of falls in 85-year-olds is associated with functional and cognitive status: The Octabaix study
      Archives of Gerontology and Geriatrics, 54/2012, pages 352-356 DOI: 10.1016/j.archger.2011.06.004chrome_reader_mode
    5. Wong W. L., Masters R. S. W., Maxwell J. P., Abernethy A. B.
      Reinvestment and Falls in Community-Dwelling Older Adults
      Neurorehabilitation and Neural Repair, 22/2007, pages 410-414 DOI: 10.1177/1545968307313510chrome_reader_mode
    6. van Kan, Gabor Abellan, Rolland,more_horiz, Vellas
      Gait speed at usual pace as a predictor of adverse outcomes in community-dwelling older people an International Academy on Nutrition and Aging (IANA) Task Force
      JNHA - The Journal of Nutrition and Health and Aging, 13/2009, pages 881-889 chrome_reader_mode
    7. Studenski S, Perera S, Patel K, Rosano C, Faulkner K, Inzitari M, Brach J, Chandler J, Cawthon P, Connor Eb, Nevitt M, Visser M, Kritchevsky S, Badinelli S, Harris T, Newman Ab, Cauley J, Ferrucci L, Guralnik J.
      Gait Speed and Survival in Older Adults
    8. Andersen Birgitte Bo, Gundersen Hans Jørgen G., Pakkenberg Bente
      Aging of the human cerebellum: A stereological study
      The Journal of Comparative Neurology, 466/2003, pages 356-365 DOI: 10.1002/cne.10884chrome_reader_mode
    9. Rosano, Caterina, Aizenstein,more_horiz, Anne B
      A regions-of-interest volumetric analysis of mobility limitations in community-dwelling older adults
      The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 62/2007, pages 1048-1055 chrome_reader_mode
    10. Bonasera Stephen J., Arikkath Jyothi, Boska Michael D.,more_horiz, Volden Tiffany A.
      Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits
      Aging, 8/2016, pages 2153-2181 DOI: 10.18632/aging.101040chrome_reader_mode
    11. Weindruch Richard, Prolla Tomas A., Lee Cheol-Koo
      Gene-expression profile of the ageing brain in mice
      Nature Genetics, 25/2000, pages 294-297 DOI: 10.1038/77046chrome_reader_mode
    12. Sturrock, Rr
      A comparison of quantitative histological changes in different regions of the ageing mouse cerebellum.
      Journal fur Hirnforschung, 31/1989, pages 481-486 chrome_reader_mode
    13. Dlugos, Cynthia A, Pentney, Roberta J
      Morphometric analyses of Purkinje and granule cells in aging F344 rats
      Neurobiology of aging, 15/1994, pages 435-440 chrome_reader_mode
    14. Renovell, Arsenio, Giner,more_horiz, Manual
      Loss of granule neurons in the aging human cerebellar cortex.
      International Journal of Developmental Biology, 40/2001, pages S193-S194 chrome_reader_mode
    15. Chen, Suzanne, Hillman, Dean E
      Dying-back of Purkinje cell dendrites with synapse loss in aging rats
      Journal of neurocytology, 28/1999, pages 187-196 chrome_reader_mode
    16. Rogers, Joseph, Silver,more_horiz, Floyd E
      Senescent changes in a neurobiological model system: Cerebellar Purkinje cell electrophysiology and correlative anatomy
      Neurobiology of aging, 1/1980, pages 3-11 chrome_reader_mode
    17. Gould, Thomas J, Bickford, Paula C
      Age-Related Deficits in the Cerebellar BetaAdrenergic Signal Transduction Cascade in Fischer 344 Rats
      Journal of Pharmacology and Experimental Therapeutics, 281/1997, pages 965-971 chrome_reader_mode
    18. Bickford, Paula C, Gould,more_horiz, James
      Antioxidant-rich diets improve cerebellar physiology and motor learning in aged rats
      Brain research, 866/2000, pages 211-217 chrome_reader_mode
    19. Turlejski, K
      Evolutionary ancient roles of serotonin: long-lasting regulation of activity and development
      Acta Neurobiol Exp (Wars), 56/1996, pages 619-636 chrome_reader_mode
    20. Flavell Steven W., Pokala Navin, Macosko Evan Z.,more_horiz, Bargmann Cornelia I.
      Serotonin and the Neuropeptide PDF Initiate and Extend Opposing Behavioral States in C. elegans
    21. Murakami Hana, Bessinger Karalee, Hellmann Jason, Murakami Shin
      Manipulation of serotonin signal suppresses early phase of behavioral aging in Caenorhabditis elegans
      Neurobiology of Aging, 29/2008, pages 1093-1100 DOI: 10.1016/j.neurobiolaging.2007.01.013chrome_reader_mode
    22. Harris-Warrick Rm, Cohen Ah
      Serotonin modulates the central pattern generator for locomotion in the isolated lamprey spinal cord
      J Exp Biol, 116/1985, pages 27-46 chrome_reader_mode
    23. Yuan Quan, Joiner William J., Sehgal Amita
      A Sleep-Promoting Role for the Drosophila Serotonin Receptor 1A
      Current Biology, 16/2006, pages 1051-1062 DOI: 10.1016/j.cub.2006.04.032chrome_reader_mode
    24. Hussain, Azher M, Mitra, Ashim K
      Effect of aging on tryptophan hydroxylase in rat brain: implications on serotonin level
      Drug metabolism and disposition, 28/2000, pages 1038-1042 chrome_reader_mode
    25. Hussain, Azher M, Mitra, Ashim K
      Effect of reactive oxygen species on the metabolism of tryptophan in rat brain: influence of age
      Molecular and cellular biochemistry, 258/2004, pages 145-153 chrome_reader_mode
    26. Arivazhagan, P, Panneerselvam, C
      Neurochemical changes related to ageing in the rat brain and the effect of DL-α-lipoic acid
      Experimental gerontology, 37/2002, pages 1489-1494 chrome_reader_mode
    27. Kabuto, Hideaki, Yokoi,more_horiz, Shuzo
      Neurochemical changes related to ageing in the senescence-accelerated mouse brain and the effect of chronic administration of nimodipine
      Mechanisms of ageing and development, 80/1995, pages 1-9 chrome_reader_mode
    28. Magnone, Maria Chiara, Rossolini,more_horiz, Paolo
      Neurochemical parameters of the main neurotransmission systems in aging mice
      Archives of gerontology and geriatrics, 30/2000, pages 269-279 chrome_reader_mode
    29. van Dyck, Christopher H, Malison,more_horiz, Robert B
      Age-related decline in central serotonin transporter availability with [123 I] β-CIT SPECT
      Neurobiology of aging, 21/2000, pages 497-501 chrome_reader_mode
    30. Kish Stephen J., Furukawa Yoshiaki, Chang Li-Jan,more_horiz, Meyer Jeffrey H.
      Regional distribution of serotonin transporter protein in postmortem human brain
      Nuclear Medicine and Biology, 32/2005, pages 123-128 DOI: 10.1016/j.nucmedbio.2004.10.001chrome_reader_mode
    31. Dieudonné, Stéphane, Dumoulin, Andréa
      Serotonin-driven long-range inhibitory connections in the cerebellar cortex
      The Journal of Neuroscience, 20/2000, pages 1837-1848 chrome_reader_mode
    32. Dumoulin, Andréa, Triller,more_horiz, Stéphane
      IPSC kinetics at identified GABAergic and mixed GABAergic and glycinergic synapses onto cerebellar Golgi cells
      The Journal of Neuroscience, 21/2001, pages 6045-6057 chrome_reader_mode
    33. Dean, Isabel, Robertson,more_horiz, Frances A
      Serotonin drives a novel GABAergic synaptic current recorded in rat cerebellar Purkinje cells: a Lugaro cell to Purkinje cell synapse
      The Journal of neuroscience, 23/2003, pages 4457-4469 chrome_reader_mode
    34. Li Wen-Ke, Hausknecht Matthew J., Stone Peter, Mauk Michael D.
      Using a million cell simulation of the cerebellum: Network scaling and task generality
      Neural Networks, 47/2013, pages 95-102 DOI: 10.1016/j.neunet.2012.11.005chrome_reader_mode
    35. Mitoma, H, Konishi, S
      Monoaminergic long-term facilitation of GABA-mediated inhibitory transmission at cerebellar synapses
      Neuroscience, 88/1999, pages 871-883 chrome_reader_mode
    36. Maura, Guido, Ricchetti,more_horiz, Maurizio
      Serotonin inhibits the depolarization-evoked release of endogenous glutamate from rat cerebellar nerve endings
      Neuroscience letters, 67/1986, pages 218-222 chrome_reader_mode
    37. Saitow, Fumihito, Hirono,more_horiz, Hidenori
      Serotonin and synaptic transmission in the cerebellum
      Handbook of the Cerebellum and Cerebellar Disorders, 2013, pages 915-926 chrome_reader_mode
    38. Dizon M. J., Khodakhah K.
      The Role of Interneurons in Shaping Purkinje Cell Responses in the Cerebellar Cortex
      Journal of Neuroscience, 31/2011, pages 10463-10473 DOI: 10.1523/jneurosci.1350-11.2011chrome_reader_mode
    39. Solinas Sergio, Nieus Thierry, D‘angelo Egidio
      A realistic large-scale model of the cerebellum granular layer predicts circuit spatio-temporal filtering properties
      Frontiers in Cellular Neuroscience, 4/2010 DOI: 10.3389/fncel.2010.00012chrome_reader_mode
    40. Schaefer Alexander, Burmann Inga, Regenthal Ralf,more_horiz, Sacher Julia
      Serotonergic Modulation of Intrinsic Functional Connectivity
      Current Biology, 24/2014, pages 2314-2318 DOI: 10.1016/j.cub.2014.08.024chrome_reader_mode
    41. Lou, Jau-Shin, Goldfarb,more_horiz, Mark
      Use of buspirone for treatment of cerebellar ataxia: an open-label study
      Archives of neurology, 52/1995, pages 982-988 chrome_reader_mode
    42. Trouillas, Paul, Xie,more_horiz, B
      Buspirone, a 5-hydroxytryptamine1A agonist, is active in cerebellar ataxia: Results of a double-blind drug placebo study in patients with cerebellar cortical atrophy
      Archives of neurology, 54/1997, pages 749-752 chrome_reader_mode

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