These data suggest that ApoEr2 does not alter dendritic complexity; however, it may regulate dendritic spine formation.
However, it is still possible that extracellular stimuli, particularly those such as ephrins that acutely regulate spine dynamics via PAK (Penzes et al., 2003), may dynamically alter LIMK1 palmitoylation.
Recently, AMPA and NMDA subunits have been reported to regulate spine density and size [48] [50].
This demonstrates that PICK1 can regulate spine size independently of GluA2 trafficking, strongly suggesting that PICK1-induced spine shrinkage occurs via downregulation of structural F-actin in spines.
As actin regulation is involved in both processes, there is the intriguing possibility that specific regulators of actin polymerisation may regulate both receptor trafficking and spine morphology.
These diverse forms of structural plasticity may be important for regulating spine function and synaptic plasticity.
Phytophagous insects may regulate primary production.
Alternatively, FruM may regulate dopamine neuronal activities.
Different oncogenic pathways may regulate common genes.
RA may regulate neurogenesis via several mechanisms.
