Animal models of tremor

Wilms, Hendrik; Sievers, Jobst; Deuschl, Günther

doi:10.1002/1531-8257(199907)14:4<557::aid-mds1004>3.0.co;2-g

Cited by 164 publications

(123 citation statements)

References 205 publications

(203 reference statements)

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“…Current tremor models utilize drug-or lesion-induced tremors or arise from mutant strains. The only model sharing some features of essential tremor uses the γ-aminobutyric acid A (GABA A ) receptor inverse agonist harmaline to induce a temporary tremor in animals (8) through its action at the inferior olive. However, animals develop rapid tolerance to harmaline, enhanced physiological tremor, and locomotor deficits due to Purkinje cell degeneration and do not respond to propranolol (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Genetic essential tremor in γ-aminobutyric acidA receptor α1 subunit knockout mice

Kralic¹,

Criswell²,

Osterman³

et al. 2005

J. Clin. Invest.

102

104

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Essential tremor is the most common movement disorder and has an unknown etiology. Here we report that γ-aminobutyric acid A (GABA A ) receptor α1 -/-mice exhibit postural and kinetic tremor and motor incoordination that is characteristic of essential tremor disease. We tested mice with essential-like tremor using current drug therapies that alleviate symptoms in essential tremor patients (primidone, propranolol, and gabapentin) and several candidates hypothesized to reduce tremor, including ethanol; the noncompetitive N-methyl-Daspartate receptor antagonist MK-801; the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA); the GABA A receptor modulators diazepam, allopregnanolone, and Ro15-4513; and the L-type Ca 2+ channel antagonist nitrendipine. Primidone, propranolol, and gabapentin reduced the amplitude (power) of the pathologic tremor. Nonsedative doses of ethanol eliminated tremor in mice. Diazepam, allopregnanolone, Ro15-4513, and nitrendipine had no effect or enhanced tremor, whereas MK-801 and CCPA reduced tremor. To understand the etiology of tremor in these mice, we studied the electrophysiological properties of cerebellar Purkinje cells. Cerebellar Purkinje cells in GABA A receptor α1 -/-mice exhibited a profound loss of all responses to synaptic or exogenous GABA, but no differences in abundance, gross morphology, or spontaneous synaptic activity were observed. This genetic animal model elucidates a mechanism of GABAergic dysfunction in the major motor pathway and potential targets for pharmacotherapy of essential tremor.

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Section: Introductionmentioning

confidence: 99%

Genetic essential tremor in γ-aminobutyric acidA receptor α1 subunit knockout mice

Kralic¹,

Criswell²,

Osterman³

et al. 2005

J. Clin. Invest.

102

104

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“…Estudos em modelo animal observaram quadros de tremor postural após a estimulação do núcleo olivar inferior 15 . Em indivíduos portadores de tremor essencial, foram observadas alterações histopatológicas na região cerebelar, caracterizada por perda e edema axonal das células de Purkinje (célu-las torpedo) e no tronco cerebral, incluindo a presença de corpúsculos de Lewy 16 .…”

Section: Cad Saúde Pública 2017; 33(8):e00194915unclassified

Tremor essencial em guardas de endemias expostos a agrotóxicos: estudo caso-controle

Azevedo

Meyer

2017

Cad. Saúde Pública

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Resumo: Tremor é o distúrbio do movimento mais frequente na população, e pode estar associado a exposição a agrotóxicos. O objetivo foi avaliar a chance de tremor essencial em 442 guardas de endemias do Estado do Rio de Janeiro, Brasil, expostos a agrotóxicos. Foram selecionados 51 casos e 204 controles (1:4). Todos os participantes responderam a um questionário sobre aspectos sociodemográficos, ocupacionais e toxicológicos. A influência da exposição a agrotóxicos sobre o desenvolvimento do tremor foi estimada por regressão logística não condicional, ajustada por covariáveis selecionadas. A idade média da população estudada foi de 49 (DP = 7) anos, sendo a diferença entre casos (média = 50,8; DP = 6,9) e controles (média = 48,5; DP = 6,9) estatisticamente significativa (p = 0,03). Além disso, aqueles com 16 a 16,9 anos de aplicação de agrotóxicos foram os que estiveram sob maior chance de apresentar a doença (OR ajustada = 4,60; IC95%: 1,29-16,41). Nossos resultados sugerem que o período entre 16 e 16,9 anos de aplicação de agrotóxicos teve impacto importante para o desenvolvimento dessa doença.

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“…At least 3 approaches have been used to produce tremor in animals: (a) administration of tremorgenic drugs such as harmaline; (b) lesioning of different subcortical structures; and (c) use of various inbred strains (13). However, only the single mutant gene models pinpoint potentially heritable causes of the disorder.…”

Section: Animal Models Of Etmentioning

confidence: 99%

Genetic mouse models of essential tremor: are they essential?

Jankovic¹

2005

Journal of Clinical Investigation

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The causative genes for essential tremor (ET), one of the most common genetic neurological disorders, have eluded scientists despite intensive search. Two gene loci linked to ET, one on chromosome 3q13 and another on chromosome 2p24.1, have been identified, and a missense mutation in the HS1-BP3 gene on the 2p has been suggested as the cause of the disorder in about 10% of American ET patients. Therefore, the genetic basis for the vast majority of familial ET is still unknown. In this issue of the JCI, the gene coding for the γ-aminobutyric acid A (GABA A ) receptor α1 subunit is suggested as a potential candidate gene for ET, as mice lacking the gene express a phenotype that overlaps with some clinical characteristics of the human condition (see the related article beginning on page 774).

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Animal models of tremor

Cited by 164 publications

References 205 publications

Genetic essential tremor in γ-aminobutyric acidA receptor α1 subunit knockout mice

Genetic essential tremor in γ-aminobutyric acidA receptor α1 subunit knockout mice

Tremor essencial em guardas de endemias expostos a agrotóxicos: estudo caso-controle

Genetic mouse models of essential tremor: are they essential?

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