L-701,324, a selective antagonist at the glycine site of the NMDA receptor, counteracts haloperidol-induced muscle rigidity in rats

Konieczny, Jolanta; Ossowska, Krystyna; Schulze, G.; Coper, H.; Wolfarth, S

doi:10.1007/s002130050942

Cited by 20 publications

(8 citation statements)

References 39 publications

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“…(Trevitt et al., 2009; Maj et al., 1990; Juszkiewicz et al., 1994; Juszkiewicz et al., 1995; Mandhane et al., 1997; Konieczny et al., 1999; Jagtap & Inamdar, 2001; Ossowska et al., 2001; Breysse et al., 2002; Moo‐Puc et al., 2003; Ossowska et al., 2003; Rukoyatkina et al., 2003; Wardas et al., 2003; Tanganelli et al., 2004; Ossowska et al., 2005; Zazpe et al., 2006; Lopez et al., 2007; Sibille et al., 2007; Ahemad et al., 2009; Beurrier et al., 2009; Góngora‐Alfaro et al., 2009; Konieczny et al., 2009; Ardashov et al., 2011; Joshi et al., 2011; Trevizol et al., 2011; Lopez et al., 2012; Shyamjith et al., 2012; Goudet et al., 2012; Acuña‐Lizama et al., 2013; Konieczny & Lenda, 2013; Atack et al., 2014; Ittiyavira & Ruby, 2014; Azam, et al., 2009; Zheng et al., 2014; Gmiro et al., 2015; Maurice et al., 2015; Nade et al., 2015; Bhangale & Acharya, 2016; Dhingra & Gahalain, 2016; Basu et al., 2017; Chitra et al., 2017; Gupta et al., 2017; Kumari et al., 2017; Kronbauer et al., 2017; Tian et al., 2017; Yang et al., 2016; Engelhardt et al., 2018; Slee et al., 2008; Saleem et al., 2019; Kabra et al., 2020; Łażewska et al., 2020; Chiu et al., 1981; Schmidt & Bubser, 1989; Schmidt et al., 1991; Kretschmer, 1994; Kretschmer et al.,…”

Section: Resultsmentioning

confidence: 99%

Haloperidol‐induced catalepsy as an animal model for parkinsonism: A systematic review of experimental studies

Waku

Magalhães

Alves

et al. 2021

Eur J of Neuroscience

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Several useful animal models for parkinsonism have been developed so far. Haloperidol‐induced catalepsy is often used as a rodent model for the study of motor impairments observed in Parkinson's disease and related disorders and for the screening of potential antiparkinsonian compounds. The objective of this systematic review is to identify publications that used the haloperidol‐induced catalepsy model for parkinsonism and to explore the methodological characteristics and the main questions addressed in these studies. A careful systematic search of the literature was carried out by accessing articles in three different databases: Web of Science, PubMed and SCOPUS. The selection and inclusion of studies were performed based on the abstract and, subsequently, on full‐text analysis. Data extraction included the objective of the study, study design and outcome of interest. Two hundred and fifty‐five articles were included in the review. Publication years ranged from 1981 to 2020. Most studies used the model to explore the effects of potential treatments for parkinsonism. Although the methodological characteristics used are quite varied, most studies used Wistar rats as experimental subjects. The most frequent dose of haloperidol used was 1.0 mg/kg, and the horizontal bar test was the most used to assess catalepsy. The data presented here provide a framework for an evidence‐based approach to the design of preclinical research on parkinsonism using the haloperidol‐induced catalepsy model. This model has been used routinely and successfully and is likely to continue to play a critical role in the ongoing search for the next generation of therapeutic interventions for parkinsonism.

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Section: Resultsmentioning

confidence: 99%

Haloperidol‐induced catalepsy as an animal model for parkinsonism: A systematic review of experimental studies

Waku

Magalhães

Alves

et al. 2021

Eur J of Neuroscience

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“…The antagonists of NMDA reporters include competitive antagonists (e.g., SDZ 220–581, MDL 100, 453), noncompetitive antagonists (e.g., MK-801, dextrorphan, PD 174494, CP-101, 606) as well as glycine site antagonists (e.g., MRZ 2/570, L-701,324, 7-chlorokynurenate, (R)-HA-966) [60]. Plenty of studies have demonstrated that NMDA receptor antagonists can attenuate catalepsy and counteract Parkinsonian rigidity induced by dopamine receptor antagonists in rats as well as akinesia and other motor complications in monoamine-depleted rodents [61,62,63,64]. Similar effects were also shown in an ifenprodil-treated MPTP-lesioned marmoset model [65].…”

Section: Key Targets Of Glutamate Receptors In Pd Treatmentmentioning

confidence: 99%

Roles of Glutamate Receptors in Parkinson’s Disease

Zhang

et al. 2019

IJMS

119

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Parkinson’s disease is a progressive neurodegenerative disorder resulting from the degeneration of pigmented dopaminergic neurons in the substantia nigra pars compacta. It induces a series of functional modifications in the circuitry of the basal ganglia nuclei and leads to severe motor disturbances. The amino acid glutamate, as an excitatory neurotransmitter, plays a key role in the disruption of normal basal ganglia function regulated through the interaction with its receptor proteins. It has been proven that glutamate receptors participate in the modulation of neuronal excitability, transmitter release, and long-term synaptic plasticity, in addition to being related to the altered neurotransmission in Parkinson’s disease. Therefore, they are considered new targets for improving the therapeutic strategies used to treat Parkinson’s disease. In this review, we discuss the biological characteristics of these receptors and demonstrate the receptor-mediated neuroprotection in Parkinson’s disease. Pharmacological manipulation of these receptors during anti-Parkinsonian processes in both experimental studies and clinical trials are also summarized.

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“…Several NMDA antagonists have been shown to reverse haloperidol-induced catalepsy and muscle rigidity (Mehta and Ticku, 1990; McAllister, 1996; Kaur et al, 1997; Konieczny et al, 1999) and also to reverse akinesia and other motor disturbances in reserpine-treated rodents (Carlsson and Carlsson, 1989; Kaur and Starr, 1995; Dutra et al, 2002). These effects have also been replicated in primate and rodent models of PD.…”

Section: Introductionmentioning

confidence: 99%

Advances in non-dopaminergic treatments for Parkinson's disease

Stayte

2014

Front. Neurosci.

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Since the 1960's treatments for Parkinson's disease (PD) have traditionally been directed to restore or replace dopamine, with L-Dopa being the gold standard. However, chronic L-Dopa use is associated with debilitating dyskinesias, limiting its effectiveness. This has resulted in extensive efforts to develop new therapies that work in ways other than restoring or replacing dopamine. Here we describe newly emerging non-dopaminergic therapeutic strategies for PD, including drugs targeting adenosine, glutamate, adrenergic, and serotonin receptors, as well as GLP-1 agonists, calcium channel blockers, iron chelators, anti-inflammatories, neurotrophic factors, and gene therapies. We provide a detailed account of their success in animal models and their translation to human clinical trials. We then consider how advances in understanding the mechanisms of PD, genetics, the possibility that PD may consist of multiple disease states, understanding of the etiology of PD in non-dopaminergic regions as well as advances in clinical trial design will be essential for ongoing advances. We conclude that despite the challenges ahead, patients have much cause for optimism that novel therapeutics that offer better disease management and/or which slow disease progression are inevitable.

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L-701,324, a selective antagonist at the glycine site of the NMDA receptor, counteracts haloperidol-induced muscle rigidity in rats

Abstract: The present study suggests that L-701,324 exhibits a beneficial action in the animal model of parkinsonian rigidity, but not that of parkinsonian akinesia. Nonetheless, this compound is not devoid of motor side-effects.

Cited by 20 publications

References 39 publications

Haloperidol‐induced catalepsy as an animal model for parkinsonism: A systematic review of experimental studies

Haloperidol‐induced catalepsy as an animal model for parkinsonism: A systematic review of experimental studies

Roles of Glutamate Receptors in Parkinson’s Disease

Advances in non-dopaminergic treatments for Parkinson's disease

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