Abstract：
:The purpose of the present studies was to investigate the behavioral and convulsant effects produced by the group I metabotropic glutamate receptor agonist (S)-3,5-dihydroxyphenylglycine (DHPG). Administered i.c.v. to mice, (S)-3,5-DHPG produced a behavioral syndrome consisting of scratching and/or facial grooming, tremors, slow forelimb clonus, rearing, and falling that increased over the dose range of 10-400 nmol. The full syndrome, produced by 400 nmol of (S)-3,5-DHPG, was antagonized by the selective mGlu1 receptor antagonist LY456236 but not by the mGlu5 receptor antagonist MPEP or the mGlu2/3 receptor antagonist LY341495. The behaviors induced by the 400 nmol dose were not blocked by the NMDA receptor antagonist MK-801, but were attenuated by the non-NMDA receptor antagonists GYKI 52466 and NBQX, and the Ca2+ mobilization inhibitor dantrolene, but at motor-impairing doses. The scratching behaviors produced by 30 nmol of (S)-3,5-DHPG were antagonized by LY456236 but not by MPEP, LY341495 or MK-801. GYKI 52466 and dantrolene, but not NBQX, inhibited scratching at motor-impairing doses. Both 400 and 30 nmol of (S)-3,5-DHPG produced a generalized seizure as recorded by surface EEG electrodes. LY456236 blocked the seizures produced by 30 nmol but not by 400 nmol; dantrolene was ineffective in blocking seizures produced by either dose. The present findings suggest that (S)-3,5-DHPG produces an increase in excitation that is mediated by mGlu1 and non-NMDA receptors.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Barton ME,Shannon HEdoi
10.1016/j.neuropharm.2005.01.017subject
Has Abstractpub_date
2005-05-01 00:00:00pages
779-87issue
6eissn
0028-3908issn
1873-7064pii
S0028-3908(05)00035-3journal_volume
48pub_type
杂志文章abstract：:Understanding the natural history of and factors associated with pharmacoresistant epilepsy provides the foundation for formulating mechanistic hypotheses that can be evaluated to drive the development of novel treatments. This article reviews the modern definition of drug-resistant epilepsy, its prevalence and incide...
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doi：10.1016/j.neuropharm.2011.08.025
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pub_type： 杂志文章
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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pub_type： 杂志文章
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更新日期：1984-02-01 00:00:00
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pub_type： 杂志文章
doi：10.1016/s0028-3908(02)00180-6
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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journal_title：Neuropharmacology
pub_type： 杂志文章
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2009.04.017
更新日期：2009-08-01 00:00:00
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更新日期：1994-11-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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journal_title：Neuropharmacology
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更新日期：2006-03-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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更新日期：2011-04-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2007.06.023
更新日期：2008-01-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2019.05.017
更新日期：2019-09-01 00:00:00
abstract：:In general, N-methyl-D-aspartate (NMDA) receptor antagonists inhibit learning and long term potentiation (LTP). However, it has been suggested that direct tonic, i.e. non-temporal, activation of NMDA receptors, in contrast to learning, may lead to an increase in synaptic "noise" and, in turn, to a loss of association ...
journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：1997-07-01 00:00:00
