The Experts below are selected from a list of 339 Experts worldwide ranked by ideXlab platform
Johannes Kornhuber - One of the best experts on this subject based on the ideXlab platform.
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Aminoadamantanes as NMDA receptor antagonists and Antiparkinsonian Agents - Preclinical studies
Neuroscience and Biobehavioral Reviews, 1997Co-Authors: Wojciech Danysz, C. G. Parsons, W J Schmidt, Johannes Kornhuber, Günter QuackAbstract:Aminoadamantanes such as 1-aminoadamantane (amantadine) and 1-amino- 3,5-dimethyladamantane (memantine) are N-methyl-D-aspartate (NMDA) receptor antagonists which show Antiparkinsonian-like activity in animal models and in Parkinson's patients. The issue of whether NMDA antagonism plays a role in the symptomatological Antiparkinsonian activity of amantadine and memantine is addressed by comparing: behaviourally effective doses, serum/brain levels, and their potency as NMDA receptor antagonists. In the case of memantine, blockade of NMDA receptors is probably the only mechanism responsible for Antiparkinsonian activity, whereas for amantadine the situation is clearly far more complex. There are a number of differences between memantine and amantadine both in vitro and in vivo, and although NMDA receptor antagonism certainly participates in the Antiparkinsonian activity of amantadine, other effects, some of which are elusive, also play a role. Moreover, it has been suggested that the pathomechanism of Parkinson's disease involves excitotoxic processes and that treatment with NMDA receptor antagonists might also slow the progression of neurodegeneration. If this claim is true, such an effect could be achieved with amantadine and memantine which show neuroprotective activity in animals at therapeutically relevant doses.
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amantadine and memantine are nmda receptor antagonists with neuroprotective properties
Journal of Neural Transmission-supplement, 1994Co-Authors: Johannes Kornhuber, M Weller, K Schoppmeyer, P RiedererAbstract:Abstract The pharmacological inhibition of excitatory amino acid neurotransmission has evolved to be a major topic in neuropharmacology since enhanced synaptic action of glutamate and possibly other related neurotransmitters has been suggested to play a role both in acute neurological conditions such as ischemia and epilepsy and in chronic degenerative neurological diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. While antagonists at N-methyl-D-aspartate (NMDA) type glutamate receptors include psychotomimetic and neurotoxic Agents such as phencyclidine and MK-801, the aminoadamantanes represent a class of drugs which may be largely free of such actions and which have already been used clinically as antiviral and Antiparkinsonian Agents. Multiple in vitro studies have recently delineated the neuroprotective properties of amantadine, and of its more potent congener, memantine, which appear to mediate neuroprotection via inhibition of NMDA receptor-dependent glutamate activity. Thus, neuroprotection targeting glutamate receptors does apparently not have to be associated with prominent psychotogenicity, and the development and evaluation of new neuroprotective drugs will have to performed in consideration both of the relative safety and of the good clinical effect of the already known and established aminoadamantanes.
Merce Correa - One of the best experts on this subject based on the ideXlab platform.
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conditional neural knockout of the adenosine a2a receptor and pharmacological a2a antagonism reduce pilocarpine induced tremulous jaw movements studies with a mouse model of parkinsonian tremor
European Neuropsychopharmacology, 2013Co-Authors: John D Salamone, Lyndsey E Collinspraino, Marta Pardo, Samantha J Podurgiel, Younis Baqi, Christa E Muller, Michael A Schwarzschild, Merce CorreaAbstract:Abstract Tremulous jaw movements are rapid vertical deflections of the lower jaw that resemble chewing but are not directed at any particular stimulus. In rats, tremulous jaw movements can be induced by a number of conditions that parallel those seen in human parkinsonism, including dopamine depletion, dopamine antagonism, and cholinomimetic drugs. Moreover, tremulous jaw movements in rats can be attenuated using Antiparkinsonian Agents such as L-DOPA, dopamine agonists, muscarinic antagonists, and adenosine A 2A antagonists. In the present studies, a mouse model of tremulous jaw movements was established to investigate the effects of adenosine A 2A antagonism, and a conditional neuronal knockout of adenosine A 2A receptors, on cholinomimetic-induced tremulous jaw movements. The muscarinic agonist pilocarpine significantly induced tremulous jaw movements in a dose-dependent manner (0.25–1.0 mg/kg IP). These movements occurred largely in the 3–7.5 Hz local frequency range. Administration of the adenosine A 2A antagonist MSX-3 (2.5–10.0 mg/kg IP) significantly attenuated pilocarpine-induced tremulous jaw movements. Furthermore, adenosine A 2A receptor knockout mice showed a significant reduction in pilocarpine-induced tremulous jaw movements compared to littermate controls. These results demonstrate the feasibility of using the tremulous jaw movement model in mice, and indicate that adenosine A 2A receptor antagonism and deletion are capable of reducing cholinomimetic-induced tremulous jaw movements in mice. Future studies should investigate the effects of additional genetic manipulations using the mouse tremulous jaw movement model.
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dopamine agonists suppress cholinomimetic induced tremulous jaw movements in an animal model of parkinsonism tremorolytic effects of pergolide ropinirole and cy 208 243
Behavioural Brain Research, 2005Co-Authors: John D Salamone, B B Carlson, Clifford G Rios, Elizabeth Lentini, Merce Correa, Ania Wisniecki, Adrienne J BetzAbstract:Abstract Considerable evidence indicates that cholinomimetic-induced tremulous jaw movements in rats share many characteristics with human Parkinsonian tremor, and several Antiparkinsonian drugs suppress cholinomimetic-induced tremulous jaw movements. The present study investigated three different types of dopamine agonists, which have known Antiparkinsonian characteristics, for their ability to suppress the tremulous jaw movements induced by tacrine (5.0 mg/kg). The non-selective dopamine agonist pergolide, a widely used Antiparkinsonian drug, was highly potent at suppressing tacrine-induced jaw movements (e.g. 0.125–1.0 mg/kg). The selective D2 agonist ropinirole, which also is used clinically as an Antiparkinsonian drug, suppressed jaw movements in the dose range of 2.5–20.0 mg/kg. The D1 agonist CY 208–243, which has been reported to suppress tremor, also reduced jaw movement activity (4.0 mg/kg). Across several studies, the rank order of potency for suppressing cholinomimetic-induced jaw movements in rats is related to the potency for producing Antiparkinsonian effects in humans. Together with previous studies, the present results suggest that cholinomimetic-induced jaw movements in rats can be used to characterize dopaminergic Antiparkinsonian Agents and to investigate the basal ganglia circuits involved in the generation of tremulous movements.
Günter Quack - One of the best experts on this subject based on the ideXlab platform.
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Aminoadamantanes as NMDA receptor antagonists and Antiparkinsonian Agents - Preclinical studies
Neuroscience and Biobehavioral Reviews, 1997Co-Authors: Wojciech Danysz, C. G. Parsons, W J Schmidt, Johannes Kornhuber, Günter QuackAbstract:Aminoadamantanes such as 1-aminoadamantane (amantadine) and 1-amino- 3,5-dimethyladamantane (memantine) are N-methyl-D-aspartate (NMDA) receptor antagonists which show Antiparkinsonian-like activity in animal models and in Parkinson's patients. The issue of whether NMDA antagonism plays a role in the symptomatological Antiparkinsonian activity of amantadine and memantine is addressed by comparing: behaviourally effective doses, serum/brain levels, and their potency as NMDA receptor antagonists. In the case of memantine, blockade of NMDA receptors is probably the only mechanism responsible for Antiparkinsonian activity, whereas for amantadine the situation is clearly far more complex. There are a number of differences between memantine and amantadine both in vitro and in vivo, and although NMDA receptor antagonism certainly participates in the Antiparkinsonian activity of amantadine, other effects, some of which are elusive, also play a role. Moreover, it has been suggested that the pathomechanism of Parkinson's disease involves excitotoxic processes and that treatment with NMDA receptor antagonists might also slow the progression of neurodegeneration. If this claim is true, such an effect could be achieved with amantadine and memantine which show neuroprotective activity in animals at therapeutically relevant doses.
Rita A. Gangwani - One of the best experts on this subject based on the ideXlab platform.
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Medication-induced acute angle closure attack.
Hong Kong medical journal = Xianggang yi xue za zhi, 2012Co-Authors: Jimmy S. M. Lai, Rita A. GangwaniAbstract:OBJECTIVE To review acute angle closure attacks induced by local and systemic medications. DATA SOURCES PubMed literature searches up to August 2011. STUDY SELECTION The following key words were used for the search: "drug", "iatrogenic", "acute angle closure glaucoma". DATA EXTRACTION A total of 86 articles were retrieved using the key words. Only those concerning acute angle closure attack triggered by local or systemic drug administration were included. For articles on the same or related topics, those published at later or more recent dates were selected. As a result, 44 articles were included and formed the basis of this review. DATA SYNTHESIS An acute attack of angle closure can be triggered by dilatation of the pupil, by anatomical changes in the ciliary body and iris, or by movement of the iris-lens diaphragm. Local and systemic medications that cause these changes have the potential to precipitate an attack of acute angle closure. The risk is higher in subjects who are predisposed to the development of angle closure. Many pharmaceutical Agents including ophthalmic eyedrops and systemic drugs prescribed by general practitioners and various specialists (in psychiatry, otorhinolaryngology, ophthalmology, medicine, and anaesthesia) can precipitate an acute angle closure attack. The medications include: anti-histamines, anti-epileptics, Antiparkinsonian Agents, antispasmolytic drugs, mydriatic Agents, sympathetic Agents, and botulinum toxin. CONCLUSION Since acute angle closure attack is a potentially blinding eye disease, it is extremely important to be vigilant and aware of ophthalmic and systemic medications that can lead to such attacks in predisposed subjects and to diagnose the condition when it occurs.
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Medication-induced acute angle closure attack
'The University of Hong Kong Libraries', 2012Co-Authors: Lai Jsm, Rita A. GangwaniAbstract:OBJECTIVE: To review acute angle closure attacks induced by local and systemic medications. DATA SOURCES: PubMed literature searches up to August 2011. STUDY SELECTION: The following key words were used for the search: 'drug', 'iatrogenic', 'acute angle closure glaucoma'. DATA EXTRACTION: A total of 86 articles were retrieved using the key words. Only those concerning acute angle closure attack triggered by local or systemic drug administration were included. For articles on the same or related topics, those published at later or more recent dates were selected. As a result, 44 articles were included and formed the basis of this review. DATA SYNTHESIS: An acute attack of angle closure can be triggered by dilatation of the pupil, by anatomical changes in the ciliary body and iris, or by movement of the iris-lens diaphragm. Local and systemic medications that cause these changes have the potential to precipitate an attack of acute angle closure. The risk is higher in subjects who are predisposed to the development of angle closure. Many pharmaceutical Agents including ophthalmic eyedrops and systemic drugs prescribed by general practitioners and various specialists (in psychiatry, otorhinolaryngology, ophthalmology, medicine, and anaesthesia) can precipitate an acute angle closure attack. The medications include: anti-histamines, anti-epileptics, Antiparkinsonian Agents, antispasmolytic drugs, mydriatic Agents, sympathetic Agents, and botulinum toxin. CONCLUSION: Since acute angle closure attack is a potentially blinding eye disease, it is extremely important to be vigilant and aware of ophthalmic and systemic medications that can lead to such attacks in predisposed subjects and to diagnose the condition when it occurs.published_or_final_versio
John D Salamone - One of the best experts on this subject based on the ideXlab platform.
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conditional neural knockout of the adenosine a2a receptor and pharmacological a2a antagonism reduce pilocarpine induced tremulous jaw movements studies with a mouse model of parkinsonian tremor
European Neuropsychopharmacology, 2013Co-Authors: John D Salamone, Lyndsey E Collinspraino, Marta Pardo, Samantha J Podurgiel, Younis Baqi, Christa E Muller, Michael A Schwarzschild, Merce CorreaAbstract:Abstract Tremulous jaw movements are rapid vertical deflections of the lower jaw that resemble chewing but are not directed at any particular stimulus. In rats, tremulous jaw movements can be induced by a number of conditions that parallel those seen in human parkinsonism, including dopamine depletion, dopamine antagonism, and cholinomimetic drugs. Moreover, tremulous jaw movements in rats can be attenuated using Antiparkinsonian Agents such as L-DOPA, dopamine agonists, muscarinic antagonists, and adenosine A 2A antagonists. In the present studies, a mouse model of tremulous jaw movements was established to investigate the effects of adenosine A 2A antagonism, and a conditional neuronal knockout of adenosine A 2A receptors, on cholinomimetic-induced tremulous jaw movements. The muscarinic agonist pilocarpine significantly induced tremulous jaw movements in a dose-dependent manner (0.25–1.0 mg/kg IP). These movements occurred largely in the 3–7.5 Hz local frequency range. Administration of the adenosine A 2A antagonist MSX-3 (2.5–10.0 mg/kg IP) significantly attenuated pilocarpine-induced tremulous jaw movements. Furthermore, adenosine A 2A receptor knockout mice showed a significant reduction in pilocarpine-induced tremulous jaw movements compared to littermate controls. These results demonstrate the feasibility of using the tremulous jaw movement model in mice, and indicate that adenosine A 2A receptor antagonism and deletion are capable of reducing cholinomimetic-induced tremulous jaw movements in mice. Future studies should investigate the effects of additional genetic manipulations using the mouse tremulous jaw movement model.
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dopamine agonists suppress cholinomimetic induced tremulous jaw movements in an animal model of parkinsonism tremorolytic effects of pergolide ropinirole and cy 208 243
Behavioural Brain Research, 2005Co-Authors: John D Salamone, B B Carlson, Clifford G Rios, Elizabeth Lentini, Merce Correa, Ania Wisniecki, Adrienne J BetzAbstract:Abstract Considerable evidence indicates that cholinomimetic-induced tremulous jaw movements in rats share many characteristics with human Parkinsonian tremor, and several Antiparkinsonian drugs suppress cholinomimetic-induced tremulous jaw movements. The present study investigated three different types of dopamine agonists, which have known Antiparkinsonian characteristics, for their ability to suppress the tremulous jaw movements induced by tacrine (5.0 mg/kg). The non-selective dopamine agonist pergolide, a widely used Antiparkinsonian drug, was highly potent at suppressing tacrine-induced jaw movements (e.g. 0.125–1.0 mg/kg). The selective D2 agonist ropinirole, which also is used clinically as an Antiparkinsonian drug, suppressed jaw movements in the dose range of 2.5–20.0 mg/kg. The D1 agonist CY 208–243, which has been reported to suppress tremor, also reduced jaw movement activity (4.0 mg/kg). Across several studies, the rank order of potency for suppressing cholinomimetic-induced jaw movements in rats is related to the potency for producing Antiparkinsonian effects in humans. Together with previous studies, the present results suggest that cholinomimetic-induced jaw movements in rats can be used to characterize dopaminergic Antiparkinsonian Agents and to investigate the basal ganglia circuits involved in the generation of tremulous movements.