Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Locomotor activity and evoked dopamine release are reduced in mice overexpressing A30P-mutated human alpha-synuclein.

Neurobiology of disease - 1 Nov 2005

Yavich Leonid, Oksman Mari, Tanila Heikki, Kerokoski Petri, Hiltunen Mikko, van Groen Thomas, Puoliväli Jukka, Männistö Pekka T, García-Horsman Arturo, MacDonald Ewen, Beyreuther Konrad, Hartmann Tobias, Jäkälä Pekka

Abstract excerpt

We have generated a transgenic mouse line overexpressing mutated human A30P alpha-synuclein under the control of the prion-related protein promoter. Immunohistology revealed mutated human A30P alpha-synuclein protein in numerous brain areas, but no gross morphological changes, Lewy bodies, or loss of dopaminergic cell bodies. The transgenic mice displayed decreased locomotion, impaired motor coordination, and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dopamine Plasma Membrane Transport Proteins
Share to Electric Stimulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Neurologic Mutants

Share to Neural Pathways

Share to Parkinsonian Disorders

Share to Substantia Nigra

Share to Synaptic Transmission

Share to Synaptic Vesicles

Source

Identifiers

PMID: 16242637
DOI: 10.1016/j.nbd.2005.03.010

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Locomotor activity and evoked dopamine release are reduced in mice overexpressing A30P-mutated human alpha-synuclein.PMID 16242637Read ↗

Behavioural and dopaminergic changes in double mutated human A30P*A53T alpha-synuclein transgenic mouse model of Parkinson´s diseaseSemantic proximity Read ↗

SNARE protein redistribution and synaptic failure in a transgenic mouse model of Parkinson’s diseaseSemantic proximity Read ↗

Striatal dopamine transmission is subtly modified in human A53Tα-synuclein overexpressing mice.Semantic proximity Read ↗

Neuronal expression of familial Parkinson's disease A53T α-synuclein causes early motor impairment, reduced anxiety and potential sleep disturbances in mice.Semantic proximity Read ↗

Motor impairment and aberrant production of neurochemicals in human alpha-synuclein A30P+A53T transgenic mice with alpha-synuclein pathology.Semantic proximity Read ↗

Olfactory neuron-specific expression of A30P α-synuclein exacerbates dopamine deficiency and hyperactivity in a novel conditional model of early Parkinson's disease stages.Semantic proximity Read ↗

A Pathologic Cascade Leading to Synaptic Dysfunction in -Synuclein-Induced NeurodegenerationSemantic proximity Read ↗

Locomotor hyperactivity and alterations in dopamine neurotransmission are associated with overexpression of A53T mutant human alpha-synuclein in mice.Semantic proximity Read ↗

Modeling Parkinson's disease‐related symptoms in alpha‐synuclein overexpressing miceSemantic proximity Read ↗

Pathological Changes in Dopaminergic Nerve Cells of the Substantia Nigra and Olfactory Bulb in Mice Transgenic for Truncated Human α-Synuclein(1–120): Implications for Lewy Body DisordersSemantic proximity Read ↗

Alpha-Synuclein transgenic mice, h-α-SynL62, display α-Syn aggregation and a dopaminergic phenotype reminiscent of Parkinson's disease.Semantic proximity Read ↗

Behavioral effects of dopaminergic agonists in transgenic mice overexpressing human wildtype alpha-synuclein.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.