Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis

Riederer, Peter; Lange, Klaus W.; Kornhuber, Johannes; Jellinger, K. A.

doi:10.1007/978-3-7091-9175-0_26

Cited by 8 publications

(5 citation statements)

References 19 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such poor effectiveness may be connected with their relatively low doses. However, higher doses of memantine and amantadine induce psychoses (Riederer et al, 1991(Riederer et al, , 1992. The above-mentioned conclusion is also supported by the observation that MK-801 was reported not only to be ineffective in reducing parkinsonian symptoms in MPTP-treated monkeys, but even to potentiate the MPTP-induced akinesia and diminish the therapeutic action of levodopa, as well Crossman et al, 1989;Rupniak et al, 1992).…”

Section: Discussionmentioning

confidence: 98%

“…However, it has been recently postulated that the primary loss of dopamine in the striatum leads to hyperactivity of the glutamatergic neurotransmission (Carlsson and Calsson, 1990;Klockgether and Turski, 1989;Riederer et al, 1991Riederer et al, , 1992Schmidt et al, 1990Schmidt et al, , 1992. This concept stems mainly from the finding that antagonists of excitatory amino acid receptors (NMDA and AMPA) exhibited "antiparkinsonian properties" in different animal models of Parkinson's disease.…”

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: A mechanomyographic analysis

Ossowska

Lorenc‐Koci

Wolfarth

1994

J Neural Transm Gen Sect

View full text Add to dashboard Cite

MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action in many animal models of Parkinson's disease. The aim of this study was to examine the influence of MK-801 on the reserpine-induced muscle rigidity. The rigidity was estimated by a direct mechanomyographic method. This method consists in successive bending and straightening of a rat's hind foot in the ankle joint and measuring the resistance of the foot to passive movements. Reserpine in doses of 5-10 mg/kg ip, given alone or in combination with alpha-methyl-p-tyrosine (alpha MT, 250 mg/kg ip), induced rigidity. The strongest muscle rigidity was induced by 10 mg/kg of reserpine 1 hour after administration. MK-801 (0.32-1.28 mg/kg sc) injected 70 min after reserpine (10 mg/kg ip) decreased the rigidity induced by the latter compound. Similarly, MK-801 (1.28 mg/kg sc), administered 27 h 40' after joint treatment with reserpine (10 mg/kg ip) and alpha MT (250 mg/kg ip), strongly inhibited the reserpine-induced muscle rigidity. The obtained results show that the glutamatergic hyperactivity plays a significant role in the reserpine-induced rigidity. As the reserpine-induced motor disturbances are commonly accepted to be an animal model of parkinsonian symptoms, it may be assumed that the NMDA receptor blocking component may contribute substantially to the therapeutic action of antiparkinsonian drugs.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 96%

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: A mechanomyographic analysis

Ossowska

Lorenc‐Koci

Wolfarth

1994

J Neural Transm Gen Sect

View full text Add to dashboard Cite

show abstract

“…This imbalance appears in the basal ganglia and related brain structures. Administration of dopaminominetics (L-DOPA), as well as of NMDA receptor antagonists, restores the balance (Riederer et al, 1991b(Riederer et al, , 1992. Figure 1 presents a hypothesis concerning alterations in the neuronal chain, which might constitute a basis for Parkinson's disease, and about the role of the glutamatergic neurotransmission in these changes (Klockgether and Turski, 1989;Carlsson and Carlsson, 1990;Schmidt et al, 1990Schmidt et al, , 1992Greenamyre, 1993).…”

Section: The Dopaminergic-glutamatergic Imbalance In Parkinson's Disementioning

confidence: 98%

“…The finding that an enhancement of glutamatergic neurotransmission could be responsible for parkinsonian symptoms has led to a hypothesis that, apart from the already known dopaminergic-cholinergic imbalance, in Parkinson's disease there also occur disturbances in the dopaminergic-glutamatergic balance (Riederer et al, 1991b(Riederer et al, , 1992. This imbalance appears in the basal ganglia and related brain structures.…”

Section: The Dopaminergic-glutamatergic Imbalance In Parkinson's Disementioning

confidence: 98%

The role of excitatory amino acids in experimental models of Parkinson's disease

Ossowska

1994

J Neural Transm Gen Sect

View full text Add to dashboard Cite

The aim of this article was to review the recent literature on the role of excitatory amino acids in Parkinson's disease and in animal equivalents of parkinsonian symptoms. Effects of NMDA and AMPA antagonists on the reserpine-induced akinesia, catalepsy and rigidity, on the neuroleptic-induced catalepsy, on the turning behaviour of 6-OHDA-lesioned rats, as well as on the parkinsonian symptoms evoked by MPTP in monkeys were analysed. Moreover, the role of NMDA antagonists in Parkinson's disease was discussed. Data concerning the protective influence of these drugs on degenerative properties of methamphetamine, MPTP and 6-OHDOPA were also presented. On the basis of the above findings, the following conclusions may be drawn: (1) disturbances in the glutamatergic transmission in various brain structures seem to play a significant role in the development of symptoms of Parkinson's disease; (2) the NMDA-receptor blocking component may make a substantial contribution to the therapeutic effect of antiparkinsonian drugs; a similar contribution of AMPA-receptor blocking component has not been sufficiently documented, so far; (3) compounds blocking NMDA receptors may possibly prevent the development of Parkinson's disease; this presumption needs, however further studies; (4) side effects of NMDA receptor antagonists may be a limiting factor in the use of these compounds in humans.

show abstract

“…Among the diverse transmitters in the mammalian central nervous system, glutamate is the major excitatory neurotransmitter and plays a critical role in the development of AD, PD and stroke [40,41,42,43]. To date, every glutamate receptor subtype discovered has been proven to mediate neurotoxicity [44,45,46]. An obvious phenomenon in glutamate-induced excitotoxicity is delayed calcium deregulation (DCD).…”

Section: The Role Of the Mcu In Excitotoxicitymentioning

confidence: 99%

The Function of the Mitochondrial Calcium Uniporter in Neurodegenerative Disorders

Liao

Dong

Cheng

2017

IJMS

View full text Add to dashboard Cite

The mitochondrial calcium uniporter (MCU)—a calcium uniporter on the inner membrane of mitochondria—controls the mitochondrial calcium uptake in normal and abnormal situations. Mitochondrial calcium is essential for the production of adenosine triphosphate (ATP); however, excessive calcium will induce mitochondrial dysfunction. Calcium homeostasis disruption and mitochondrial dysfunction is observed in many neurodegenerative disorders. However, the role and regulatory mechanism of the MCU in the development of these diseases are obscure. In this review, we summarize the role of the MCU in controlling oxidative stress-elevated mitochondrial calcium and its function in neurodegenerative disorders. Inhibition of the MCU signaling pathway might be a new target for the treatment of neurodegenerative disorders.

show abstract

Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis

Cited by 8 publications

References 19 publications

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: A mechanomyographic analysis

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: A mechanomyographic analysis

The role of excitatory amino acids in experimental models of Parkinson's disease

The Function of the Mitochondrial Calcium Uniporter in Neurodegenerative Disorders

Contact Info

Product

Resources

About