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Attenuated sensitivity to neuroactive steroids in gamma-aminobutyrate type A receptor delta subunit knockout mice.
TLDR
The results begin to illuminate the novel contributions of the delta subunit to GABA pharmacology and sedative/hypnotic responses and behavior and provide insights into the physiology of neurosteroids.
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Memantine Improves Spatial Learning in a Transgenic Mouse Model of Alzheimer's Disease
TLDR
It is indicated that memantine improves hippocampus-based spatial learning in a transgenic mouse model of AD without producing nonspecific effects on locomotion/exploratory activity.
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Memantine improves cognition and reduces Alzheimer's-like neuropathology in transgenic mice.
TLDR
The results suggest that the effects of memantine treatment on AD brain include disease modification and prevention of synaptic dysfunction.
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Memantine leads to behavioral improvement and amyloid reduction in Alzheimer's‐disease‐model transgenic mice shown as by micromagnetic resonance imaging
TLDR
These findings provide further evidence of the potential role of NMDA receptor antagonists in ameliorating AD‐related pathology and the utility of μMRI in conjunction with gadolinium‐labeled Aβ labeling agents to monitor the therapeutic response to amyloid‐reducing agents is shown.
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Presynaptic gamma-hydroxybutyric acid (GHB) and gamma-aminobutyric acidB (GABAB) receptor-mediated release of GABA and glutamate (GLU) in rat thalamic ventrobasal nucleus (VB): a possible mechanism…
TLDR
By selectively modulating the basal and K(+)-evoked release of GABA and GLU, GHB induces, in the thalamic ventrobasal relay nucleus, an optimal "excitatory" environment conducive to the generation of absence seizures, raising the possibility that a presynaptic GHB/GABAB receptor complex occurs in VB.
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Modulation of Absence Seizures by the GABAA Receptor: A Critical Role for Metabotropic Glutamate Receptor 4 (mGluR4)
TLDR
The resistance of mGLUR4−/− mice to absence seizures induced by GABAAR antagonists was mimicked by bilateral administration of a mGluR4 antagonist into the nucleus reticularis thalami (nRT) of m GluR 4+/+ mice, indicating that the presence of mR4 within nRT is critical to GABAergic modulation of thalamocortical synchronization in normal and pathological states, such as generalized absence epilepsy.
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Age‐related decrease in stimulated glutamate release and vesicular glutamate transporters in APP/PS1 transgenic and wild‐type mice
TLDR
There was an age‐dependent decline in VGLUT1 levels, but not in the levels of V GLUT2, GLT‐1 or synaptophysin, and Astrocyte activation as measured by glial acidic fibrillary protein was increased in middle‐aged APdE9 mice.
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Memantine normalizes several phenotypic features in the Ts65Dn mouse model of Down syndrome.
TLDR
Oral treatment of aged TS mice with a clinically relevant dose of memantine improved spatial learning in the water maze task and slightly reduced brain AbetaPP levels, and data indicate that memantine may normalize several phenotypic abnormalities in TS mice, many of which--such as impaired cognition--are also associated with Down syndrome and Alzheimer's disease.
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Thalamic mediodorsal and intralaminar nuclear lesions disrupt the generation of experimentally induced generalized absence-like seizures in rats
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Behavioral characterization of GLT1 (+/-) mice as a model of mild glutamatergic hyperfunction
TLDR
The results suggest that GLT1 (+/-) mice may serve as a potentially useful model to study neurodegenerative disease conditions with mild hyperglutamatergic activity.
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