Mechanisms of response homeostasis during retinocollicular map formation.

The mechanisms of Hebbian synaptic plasticity have been widely hypothesized to play a role in the activity-dependent development of neural circuits. However, these mechanisms are inherently unstable and would lead to the runaway excitation or depression of circuits if left unchecked. In the last decade, a number of elegant studies have demonstrated that homeostatic plasticity mechanisms exist to stabilize neural networks and maintain the constancy of neuronal output in response to changes in activity levels.

Retinocollicular synapse maturation and plasticity are regulated by correlated retinal waves.

During development, spontaneous retinal waves are thought to provide an instructive signal for retinotopic map formation in the superior colliculus. In mice lacking the beta2 subunit of nicotinic ACh receptors (beta2-/-), correlated retinal waves are absent during the first postnatal week, but return during the second postnatal week. In control retinocollicular synapses, in vitro analysis reveals that AMPA/NMDA ratios and AMPA quantal amplitudes increase during the first postnatal week while the prevalence of silent synapses decreases.

Developmental homeostasis of mouse retinocollicular synapses.

Spontaneous retinal waves during development are thought to provide an instructive signal for precise retinotopic mapping by correlating the activity of neighboring retinal ganglion cells. In mutant mice (beta2-/-) that lack correlated waves, retinocollicular map refinement is impaired. In vivo recordings reveal that neurons in the superior colliculus of beta2-/- mice have large receptive fields and low peak visual responses, resulting in a conservation of total integrated response.

Estrogen-induced changes in the microtubular system correlate with a decreased susceptibility of aging neurons to beta amyloid neurotoxicity.

A growing body of evidence suggests that estrogen has beneficial effects on Alzheimer's disease. However, the mechanisms underlying estrogen's neuroprotective effects are not completely understood. In the present study, we analyzed first whether estrogen protects mature hippocampal neurons against fibrillar Abeta-induced neurotoxicity.

Membrane topology of a metabotropic glutamate receptor.

The metabotropic glutamate receptors (mGluRs) have been predicted to have a classical seven transmembrane domain structure similar to that seen for members of the G-protein-coupled receptor (GPCR) superfamily. However, the mGluRs (and other members of the family C GPCRs) show no sequence homology to the rhodopsin-like GPCRs, for which this seven transmembrane domain structure has been experimentally confirmed. Furthermore, several transmembrane domain prediction algorithms suggest that the mGluRs have a topology that is distinct from these receptors.