Striatal Microinjection of Sydenham Chorea Antibodies: Using a Rat Model to Examine the Dopamine Hypothesis

Ben‐Pazi, Hilla; Sadan, Ofer; Offen, Daniel

doi:10.1007/s12031-011-9559-6

Cited by 13 publications

(13 citation statements)

References 36 publications

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“…In one in vivo study antibodies from patients with SC infused in the basal ganglia of rodents did not induce behavioural changes. Interestingly, though, the antibodies bound to a ∼50-kDa molecule in the striatum extract 25. These results are at odds with another study of our own group that lends support to the molecular mimicry hypothesis.…”

Section: Sydenham's Choreacontrasting

confidence: 72%

Autoimmune choreas

Cardoso

2016

J Neurol Neurosurg Psychiatry

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Chorea, a movement disorder characterised by a continuous flow of unpredictable muscle contractions, has a myriad of genetic and non-genetic causes. Although autoimmune processes are rare aetiology of chorea, they are relevant both for researchers and clinicians. The aim of this article is to provide a review of the epidemiology, clinical and laboratory features, pathogenesis and management of the most common autoimmune causes of chorea. Emphasis is given particularly to Sydenham's chorea, systemic lupus erythematosus, primary antiphospolipid antibody syndrome, paraneoplastic chorea and anti--methyl-d-aspartate receptor encephalitis.

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Section: Sydenham's Choreacontrasting

confidence: 72%

Autoimmune choreas

Cardoso

2016

J Neurol Neurosurg Psychiatry

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“…Several studies reported the presence of autoantibodies in the sera and CSF of GAS-related neuropsychiatric disorders patients (Bronze and Dale, 1993; Church et al, 2002; Gause et al, 2009; Husby et al, 1976; Kotby et al, 1998; Singer et al, 1998), and plasma exchange treatment has been reported to alleviate symptoms in these patients (Garvey et al, 2005; Perlmutter et al, 1999), fulfilling criteria A and B. We (Brimberg et al, 2012) and others (Hoffman et al, 2004) have found that exposure of rodents to GAS antigen leads to behavioral alterations, fulfilling Criterion D. Others (Ben-Pazi et al, 2012; Doyle et al, 2012; Hallett et al, 2000; Loiselle et al, 2004; Singer et al, 2005; Taylor et al, 2002; Yaddanapudi et al, 2010) have attempted to demonstrate that passive transfer of Immunoglobulin G (IgG) alters behavior (Criterion E). Some have been successful (Doyle et al, 2012; Hallett et al, 2000; Taylor et al, 2002; Yaddanapudi et al, 2010) while others have not (Ben-Pazi et al, 2012; Loiselle et al, 2004; Singer et al, 2005).…”

Section: Introductionmentioning

confidence: 87%

“…We (Brimberg et al, 2012) and others (Hoffman et al, 2004) have found that exposure of rodents to GAS antigen leads to behavioral alterations, fulfilling Criterion D. Others (Ben-Pazi et al, 2012; Doyle et al, 2012; Hallett et al, 2000; Loiselle et al, 2004; Singer et al, 2005; Taylor et al, 2002; Yaddanapudi et al, 2010) have attempted to demonstrate that passive transfer of Immunoglobulin G (IgG) alters behavior (Criterion E). Some have been successful (Doyle et al, 2012; Hallett et al, 2000; Taylor et al, 2002; Yaddanapudi et al, 2010) while others have not (Ben-Pazi et al, 2012; Loiselle et al, 2004; Singer et al, 2005). The aim of the present study was to extend our previous findings (Brimberg et al, 2012) and test whether intra-striatal passive transfer of antibodies to animals would lead to the induction of a behavioral syndrome similar to those reported (Criterion E).…”

Section: Introductionmentioning

confidence: 90%

Behavioral and neural effects of intra-striatal infusion of anti-streptococcal antibodies in rats

Lotan

Benhar

Alvarez

et al. 2014

Brain, Behavior, and Immunity

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Group A β-hemolytic streptococcal (GAS) infection is associated with a spectrum of neuropsychiatric disorders. The leading hypothesis regarding this association proposes that a GAS infection induces the production of auto-antibodies, which cross-react with neuronal determinants in the brain through the process of molecular mimicry. We have recently shown that exposure of rats to GAS antigen leads to the production of anti-neuronal antibodies concomitant with the development of behavioral alterations. The present study tested the causal role of the antibodies by assessing the behavior of naïve rats following passive transfer of purified antibodies from GAS-exposed rats. Immunoglobulin G (IgG) purified from the sera of GAS-exposed rats was infused directly into the striatum of naïve rats over a 21-day period. Their behavior in the induced-grooming, marble burying, food manipulation and beam walking assays was compared to that of naïve rats infused with IgG purified from adjuvant-exposed rats as well as of naïve rats. The pattern of in vivo antibody deposition in rat brain was evaluated using immunofluorescence and colocalization. Infusion of IgG from GAS-exposed rats to naïve rats led to behavioral and motor alterations partially mimicking those seen in GAS-exposed rats. IgG from GAS-exposed rats reacted with D1 and D2 dopamine receptors and 5HT-2A and 5HT-2C serotonin receptors in vitro. In vivo, IgG deposits in the striatum of infused rats colocalized with specific brain proteins such as dopamine receptors, the serotonin transporter and other neuronal proteins. Our results demonstrate the potential pathogenic role of autoantibodies produced following exposure to GAS in the induction of behavioral and motor alterations, and support a causal role for autoantibodies in GAS-related neuropsychiatric disorders.

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“…These studies, using serum from PANDAS or Sydenham's chorea patients, failed to demonstrate motor or behavioral abnormalities in the injected rats (211, 212). In studies in which mice were immunized with a GAS homogenate, some of the immunized animals developed motor and behavioral disturbances that were correlated with immunoreactivity to the deep cerebellar nuclei (213, 214).…”

Section: Induction Of Brain-reactive Antibodies By Microbial Pathogensmentioning

confidence: 99%

Brain-Reactive Antibodies and Disease

Diamond

Honig

Mader

et al. 2013

Annu. Rev. Immunol.

117

102

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Autoimmune diseases currently affect 5–7% of the world's population; in most diseases there are circulating autoantibodies. Brain-reactive antibodies are present in approximately 2–3% of the general population but do not usually contribute to brain pathology. These antibodies penetrate brain tissue only early in development or under pathologic conditions. This restriction on their pathogenicity and the lack of correlation between serum titers and brain pathology have, no doubt, contributed to a delayed appreciation of the contribution of autoantibodies in diseases of the central nervous system. Nonetheless, it is increasingly clear that antibodies can cause damage in the brain and likely initiate or aggravate multiple neurologic conditions; brain-reactive antibodies contribute to symptomatology in autoimmune disease, infectious disease, and malignancy.

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Striatal Microinjection of Sydenham Chorea Antibodies: Using a Rat Model to Examine the Dopamine Hypothesis

Cited by 13 publications

References 36 publications

Autoimmune choreas

Autoimmune choreas

Behavioral and neural effects of intra-striatal infusion of anti-streptococcal antibodies in rats

Brain-Reactive Antibodies and Disease

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