fm1-43 and Parkinsonian-Disorders

fm1-43 has been researched along with Parkinsonian-Disorders* in 1 studies

Other Studies

1 other study(ies) available for fm1-43 and Parkinsonian-Disorders

Article	Year
Loss of Striatonigral GABAergic Presynaptic Inhibition Enables Motor Sensitization in Parkinsonian Mice. Neuron, 2015, Sep-02, Volume: 87, Issue:5 Degeneration of dopamine (DA) neurons in Parkinson's disease (PD) causes hypokinesia, but DA replacement therapy can elicit exaggerated voluntary and involuntary behaviors that have been attributed to enhanced DA receptor sensitivity in striatal projection neurons. Here we reveal that in hemiparkinsonian mice, striatal D1 receptor-expressing medium spiny neurons (MSNs) directly projecting to the substantia nigra reticulata (SNr) lose tonic presynaptic inhibition by GABAB receptors. The absence of presynaptic GABAB response potentiates evoked GABA release from MSN efferents to the SNr and drives motor sensitization. This alternative mechanism of sensitization suggests a synaptic target for PD pharmacotherapy. Topics: Adrenergic Agents; Animals; Bacterial Proteins; Channelrhodopsins; Corpus Striatum; Disease Models, Animal; Dopamine; Excitatory Amino Acid Antagonists; GABA Agents; GABAergic Neurons; gamma-Aminobutyric Acid; Humans; Inhibitory Postsynaptic Potentials; Luminescent Proteins; Medial Forebrain Bundle; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Activity; Oxidopamine; Parkinsonian Disorders; Presynaptic Terminals; Pyridinium Compounds; Quaternary Ammonium Compounds; Quinoxalines; Substantia Nigra	2015

Article

Year

Loss of Striatonigral GABAergic Presynaptic Inhibition Enables Motor Sensitization in Parkinsonian Mice.

Neuron, 2015, Sep-02, Volume: 87, Issue:5

Degeneration of dopamine (DA) neurons in Parkinson's disease (PD) causes hypokinesia, but DA replacement therapy can elicit exaggerated voluntary and involuntary behaviors that have been attributed to enhanced DA receptor sensitivity in striatal projection neurons. Here we reveal that in hemiparkinsonian mice, striatal D1 receptor-expressing medium spiny neurons (MSNs) directly projecting to the substantia nigra reticulata (SNr) lose tonic presynaptic inhibition by GABAB receptors. The absence of presynaptic GABAB response potentiates evoked GABA release from MSN efferents to the SNr and drives motor sensitization. This alternative mechanism of sensitization suggests a synaptic target for PD pharmacotherapy.

Topics: Adrenergic Agents; Animals; Bacterial Proteins; Channelrhodopsins; Corpus Striatum; Disease Models, Animal; Dopamine; Excitatory Amino Acid Antagonists; GABA Agents; GABAergic Neurons; gamma-Aminobutyric Acid; Humans; Inhibitory Postsynaptic Potentials; Luminescent Proteins; Medial Forebrain Bundle; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Activity; Oxidopamine; Parkinsonian Disorders; Presynaptic Terminals; Pyridinium Compounds; Quaternary Ammonium Compounds; Quinoxalines; Substantia Nigra

2015