Behavioural neuroscienceExogenous corticosterone reduces l-DOPA-induced dyskinesia in the hemi-parkinsonian rat: Role for interleukin-1β
Section snippets
Animals
Adult male Sprague–Dawley rats were used (225–250 g upon arrival; Taconic Farms, Hudson, NY, USA). Animals were housed in plastic cages (22 cm high, 45 cm deep and 23 cm wide) and had free access to standard laboratory chow (Rodent Diet 5001; Laboratory Diet, Brentwood, MO, USA) and water. The colony room was maintained on a 12-h light/dark cycle (lights on at 07:00 h) at a temperature of 22–23 °C. Animals and all experiments were maintained and conformed to international and local
Monoamine and metabolite levels
The effects of the 6-OHDA lesion on concentrations of monoamine and metabolite levels and turnover ratios (metabolite/monoamine) in the intact (right) versus lesioned (left) striata were examined using HPLC across all experiments (see Table 2). Unilateral 6-OHDA injection into the medial forebrain bundle produced significant reductions in striatal DOPAC and DA levels (P<0.05), 88% and 96% respectively, compared with intact striatum. The denervated side also showed an increased DOPAC/DA turnover
Discussion
Convergent evidence supports the hypothesis that neuroinflammation contributes to the progressive loss of DA neurons in PD by direct recruitment of apoptotic pathways or through increased production of reactive oxygen species (Schulz et al 1995, He et al 2000, Anderson 2001). While DA replacement therapy with l-DOPA provides unique symptomatic relief of PD-related movement disability, repeated administration leads to the development of LID (Jankovic, 2005). Traditional investigations of LID
Acknowledgments
This work was supported by grants from the American Parkinson Disease Association (C. Bishop), NIH NS059600 (C. Bishop), National Science Foundation grant No. 0549987 (T. Deak), and Center for Development and Behavioral Neuroscience at Binghamton University (C. Bishop and T. Deak). The authors would especially like to thank Sheri Zola for her excellent technical assistance during the running of these studies. We would also like to thank Kayla Wilt, Amy Steiniger, and Anna Klioueva for their
References (75)
- et al.
Up-regulation of inducible nitric oxide synthase in the substantia nigra by lipopolysaccharide causes microglial activation and neurodegeneration
Neurobiol Dis
(2003) - et al.
Combined blockade of AMPA and NMDA glutamate receptors reduces levodopa-induced motor complications in animals models of PD
Exp Neurol
(2005) A rapid and sensitive method for quantitation of microgram quantities of protein utilizing the principle of protein dye binding
Anal Biochem
(1976)Dopamine dysregulation of movement control in l-DOPA-induced dyskinesia
Trends Neurosci
(2007)- et al.
Biochemical and anatomical characterization of forepaw adjusting steps in rats models of Parkinson's disease: studies on medial forebrain bundle and striatal lesions
Neuroscience
(1999) - et al.
Parkinson's disease: Mechanisms and models
Neuron
(2003) - et al.
Stress-induced increases in hypothalamic IL-1: a systematic analysis of multiple stressor paradigms
Brain Res Bull
(2005) - et al.
The differential effects of 5-HT1A receptor stimulation on dopamine receptor-mediated abnormal involuntary movements and rotations in the primed hemiparkinsonian rat
Brain Res
(2007) - et al.
The partial 5-HT1A agonist buspirone reduces the expression and development of l-DOPA-induced dyskinesia in rats and improves l-DOPA efficacy
Pharmacol Biochem Behav
(2007) - et al.
Physiology of microglial cells
Brain Res Rev
(2005)
Progressive neurodegeneration and motor disabilities induced by chronic expression of IL-1 beta in the substantia nigra
Neurobiol Dis
Glucocorticoid ligands specify different interactions with NF-KB by allosteric effects on the glucocorticoid receptor DNA binding domain
J Biol Chem
6-Hydroxydopamine induced apoptosis of dopaminergic cells in the rat substantia nigra
Brain Res
Temporal control of NF-kB activation by ERK differentially regulates interleukin-1beta-induced gene expression
J Biol Chem
Transcriptome analysis in a rat model of L-DOPA-induced dyskinesia
Neurobiol Dis
Dexamethasone protects against dopaminergic neurons in a mouse model of Parkinson's disease
Int Immunopharmacol
The repeated immobilization stress increases IL-1beta immunoreactivities in only neuron, but not astrocyte or microglia in hippocampal CA1 region, striatum and paraventricular nucleus
Neurosci Lett
The “motor complication syndrome” in rats with 6-OHDA lesions treated chronically with l-DOPA: relation to dose and route of administration
Behav Brain Res
Analysis of relative gene expression data using real-time quantitative PCR and the 2(-delta delta C(T)) method
Methods
Interleukin-1 beta growth factor and transforming growth factor-alpha are elevated in the brain from parkinsonian patients
Neurosci Lett
Behavioral and anatomical effects of long-term l-dihydroxyphenylalanine (l-DOPA) administration in rats with unilateral lesions of the nigrostriatal system
Exp Neurol
Glucocorticoid regulation of glial responses during hippocampal neurodegeneration and regeneration
Brain Res Rev
Pathological synaptic plasticity in the striatum: implications of Parkinson's disease
Neurotoxicology
Acute and repeated treatment with L-DOPA increase c-jun expression in the 6-hydroxydopamine-lesioned forebrain of rats and common marmosets
Brain Res
Dopamine D1 and D2 receptor contributions to l-DOPA-induced dyskinesia in the dopamine-depleted rat
Pharmacol Biochem Behav
Alterations in striatal neuropeptide mRNA produced by repeated administration of l-DOPA, ropinirole or bromocriptine correlate with dyskinesia induction in MPTP-treated common marmosets
Neuroscience
Cytokines role in neurodegenerative events
Toxicol Lett
L-DOPA-induced dyskinesia in the intrastriatal 6-hydroxydopamine model of Parkinson's disease: relation to motor and cellular parameters of nigrostriatal function
Neurobiol Dis
Prospective controlled studies of the behavioral and biological effects of exogenous corticosteroids
Psychoneuroendocrinology
Differential effects of corticosterone and dexamethasone on hippocampal neurogenesis in vitro
Biochem Biophys Res Commun
Chronic corticosterone administration dose-dependently modulates Abeta(1–42)-and NMDA-induced neurodegeneration in rat magnocellular nucleus basalis
J Neuroendocrinol
Frequency of levodopa-related dyskinesias and motor fluctuations as estimated from the cumulative literature
Mov Disord
Varied actions of proinflammatory cytokines on excitotoxic cell death in the rat central nervous system
J Neurosci Res
Does neuronal loss in Parkinson's disease involve programmed cell death?
Bioessays
Adaptation in the corticosterone and hyperthermic responses to stress following repeated stressor exposure
J Neuroendocrinol
Mechanisms of cell signaling in immune-mediated inflammation
Cytokines Cell Mol Ther
Glucocorticoids enhance oxidative stress-induced cell death in hippocampal neurones in vitro
Endocrinology
Cited by (82)
Effects of hydrogen gas inhalation on L-DOPA-induced dyskinesia
2023, Brain, Behavior, and Immunity - HealthPregnenolone for the treatment of L-DOPA-induced dyskinesia in Parkinson's disease
2023, Experimental NeurologyCirculating corticosterone levels mediate the relationship between acute ethanol intoxication and markers of NF-κB activation in male rats
2022, NeuropharmacologyCitation Excerpt :The injection timeline was the same as for Experiment 1, with the addition of a CORT (or vehicle) injection being given immediately after the i.p. injection of ethanol or saline. This CORT dose was predicted to approximate blood CORT concentration induced by a challenge with 3.5 g/kg ethanol at 3 h post-injection (Barnum et al., 2008). All rats received a total of 3 s.c. injections and 1 i.p. injection (see Fig. 3).
New insights into pathogenesis of L-DOPA-induced dyskinesia
2021, NeuroToxicologyCitation Excerpt :There is evidence that IL-10 can down-regulate the expression of TNF-α and other pro-inflammatory cytokines and growth factors (John et al., 2003; Majumder et al., 2012), which may promote the occurrence of LID. Also, it was found that the development of LID was accompanied by an increase in interleukin-1β (IL-1β), cyclooxygenase 2 (COX2), neuronal NOS (nNOS), and NF-κB levels in the dorsolateral striatum (Barnum et al., 2008; Bortolanza et al., 2015a, b; Dos-Santos-Pereira et al., 2016). Reducing the expression of various inflammatory factors was reported beneficial to improve the symptoms of dyskinesia (Boi et al., 2019; Del-Bel et al., 2015; Dos-Santos-Pereira et al., 2016).
Chronic restraint stress induces serotonin transporter expression in the rat adrenal glands
2020, Molecular and Cellular Endocrinology