Rho GTPase activity in the honey bee mushroom bodies is correlated with age and foraging experience

Neuroscience Program, Wake Forest University, Graduate School of Arts and Sciences, Winston-Salem, NC 27157, USA.
Journal of insect physiology (Impact Factor: 2.47). 11/2011; 58(2):228-34. DOI: 10.1016/j.jinsphys.2011.11.009
Source: PubMed


Foraging experience is correlated with structural plasticity of the mushroom bodies of the honey bee brain. While several neurotransmitter and intracellular signaling pathways have been previously implicated as mediators of these structural changes, none interact directly with the cytoskeleton, the ultimate effector of changes in neuronal morphology. The Rho family of GTPases are small, monomeric G proteins that, when activated, initiate a signaling cascade that reorganizes the neuronal cytoskeleton. In this study, we measured activity of two members of the Rho family of GTPases, Rac and RhoA, in the mushroom bodies of bees with different durations of foraging experience. A transient increase in Rac activity coupled with a transient decrease in RhoA activity was found in honey bees with 4 days foraging experience compared with same-aged new foragers. These observations are in accord with previous reports based on studies of other species of a growth supporting role for Rac and a growth opposing role for RhoA. This is the first report of Rho GTPase activation in the honey bee brain.

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Available from: Susan E Fahrbach, Jan 06, 2014
    • "On the other hand, precocious light exposure triggers an increase in JH levels in the hemolymph of young bees suggesting a dual effect of light exposure (Scholl et al., 2014). Activation of muscarinic receptors in the honeybee caused an increase in MB volume and KC dendritic complexity (Ismail et al., 2006;Dobrin et al., 2011), and rho-GTPase activation mediates growth of KC dendrites (Dobrin and Fahrbach, 2012) giving first hints on potential molecular pathways involved in the remarkable activitydependent structural plasticity in the MBs. Regarding long-term memory (LTM)-associated structural plasticity in the MB calyx, the calcium-dependent protein kinase II (CamKII) was suggested to play a role in LTM-induced KC dendritic plasticity (Pasch et al., 2011;Scholl et al., 2015). "
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