Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

2.7K
Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
2.7K
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

1.6K
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
1.6K
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

2.0K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.0K
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

905
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
905
Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists01:28

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists

1.1K
Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
1.1K
Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

1.0K
Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...
1.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Protocol to count the number of noradrenergic neurons in mouse locus coeruleus by unbiased stereology.

STAR protocols·2025
Same author

Phenotypic characterization of an Atp13a2 knockout rat model of Parkinson's disease.

NPJ Parkinson's disease·2025
Same author

Viral mediated α-synuclein overexpression results in greater transgene levels and α-synuclein overload in mice bearing kinase dead mutation of LRRK2.

Scientific reports·2025
Same author

Enhancement of D1 dopaminergic responses in aged LRRK2 G2019S knock-in mice.

Neurobiology of disease·2025
Same author

Dopamine neuron dysfunction and loss in the PrknR275W mouse model of juvenile parkinsonism.

Brain : a journal of neurology·2024
Same author

Alpha-synuclein-induced nigrostriatal degeneration and pramipexole treatment disrupt frontostriatal plasticity.

NPJ Parkinson's disease·2024

Related Experiment Video

Updated: Jan 3, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
06:45

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

3.2K

NR2B subunit blockade does not affect motor symptoms induced by 3-nitropropionic acid.

Martina Fantin1, Michele Morari, François Tison

  • 1Department of Experimental and Clinical Medicine, Section of Pharmacology, University of Ferrara, Italy. martina.fantin@epfl.ch

Neurological Research
|May 4, 2011
PubMed
Summary

Selective NR2B antagonists, investigated for Huntington's disease (HD) therapy, did not alleviate motor or sensorimotor deficits in a mouse model of HD. This suggests NR2B blockade may not be an effective symptomatic treatment for HD-related motor impairments.

More Related Videos

Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents
06:51

Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents

Published on: August 10, 2018

8.1K
Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector
08:33

Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector

Published on: February 28, 2016

13.7K

Related Experiment Videos

Last Updated: Jan 3, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
06:45

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

3.2K
Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents
06:51

Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents

Published on: August 10, 2018

8.1K
Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector
08:33

Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector

Published on: February 28, 2016

13.7K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Neurodegenerative Diseases

Background:

  • N-methyl D-aspartate (NMDA) receptor antagonists are explored for Huntington's disease (HD) but cause side effects.
  • Overactivation of NR2B-containing NMDA receptors is implicated in HD pathogenesis.
  • Selective NR2B antagonism offers a potential therapeutic strategy with fewer side effects.

Purpose of the Study:

  • To evaluate the symptomatic effects of a selective NR2B antagonist on motor and sensorimotor deficits in a mouse model of HD.
  • To determine if blocking NR2B subunits can ameliorate HD-like symptoms.

Main Methods:

  • Utilized 3-nitropropionic acid (3-NP) intoxication in mice to create a phenotypic model of HD.
  • Administered a selective NR2B receptor antagonist (R-(R*,S*)-alpha-(4-hydroxyphenyl)-beta-methyl-4-(phenylmethyl)-1-piperidinepropanol).
  • Assessed spontaneous activity, clinical HD-like symptoms, and sensorimotor performance using the beam task.

Main Results:

  • Acute blockade of NR2B subunits did not alter spontaneous activity in 3-NP intoxicated mice.
  • The selective NR2B antagonist showed no effect on clinical HD-like symptoms.
  • Sensorimotor performance, assessed via the beam task, remained unaffected by NR2B antagonism.

Conclusions:

  • Selective NR2B antagonism does not acutely improve motor or sensorimotor impairments in a 3-NP-induced mouse model of striatal injury.
  • These findings suggest that NR2B subunit blockade alone may not be sufficient for symptomatic treatment of motor deficits in HD.