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Distribution of metabotropic glutamate receptor mGluR5 immunoreactivity in rat brain
TLDR
Light and electron microscopic evidence indicates that some mGLUR5 immunoreactivity is located in presynaptic axon terminals, suggesting that mGluR5 may function as a Presynaptic receptor.
Metabotropic Glutamate Receptor 5 Is a Disulfide-linked Dimer*
TLDR
mGluR5, as well as other mGluRs, behave as species approximately twice as large as expected from their sequence, but reducing conditions cause a decrease to the predicted molecular mass, due to specific, disulfide-dependent dimerization of the receptor.
Ultrastructural Localization Suggests that Retinal and Cortical Inputs Access Different Metabotropic Glutamate Receptors in the Lateral Geniculate Nucleus
TLDR
It is concluded that mGLUR1 appears to have a dominant role in corticogeniculate control of response mode through the feedback glutamatergic pathway from layer VI, whereas mGluR5 is positioned to affect retinogeniculate activation of relay cells through feed forward glomerular interactions.
Selective abolition of the NMDA component of long-term potentiation in mice lacking mGluR5.
TLDR
Results suggest that PKC may couple the postsynaptic mGluR5 to the NMDA-receptor potentiation during LTP, and that this signaling mechanism is distinct from LTP(AMPA).
Distinct Roles for Sodium, Chloride, and Calcium in Excitotoxic Dendritic Injury and Recovery
TLDR
Despite marked structural changes affecting virtually all neurons, dendrite shape returned to normal within 2 h of terminating glutamate receptor agonist application and varicosity formation was attenuated in sucrose-supplemented hypertonic media.
Growth factor upregulation of a phosphoinositide-coupled metabotropic glutamate receptor in cortical astrocytes
TLDR
It is demonstrated that expression of mGluRs in astrocytes is plastic, and a novel pathway through which specific growth factors may selectively modulate neurotransmitter action is indicated.
Excitotoxic Cell Death Dependent on Inhibitory Receptor Activation
TLDR
The results indicate that, paradoxically, excitotoxic cell death is completely dependent on activation of inhibitory receptors, in at least some neuronal systems, and this pathological process may contribute to disease.
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