Background: Focal adhesion kinase (FAK) functions in cell migration and signaling through activation of the mitogen-activated protein kinase (MAPK) signaling cascade. Neuronal function of FAK has been suggested to control axonal branching; however, the underlying mechanism in this process is not clear. Results: We have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin αPS3βν heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity. Conclusion: We conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes.

Purpose: To investigate whether exposure to static magnetic field (SMF) affects the passive properties of neurons that mediate tail‐flip escape behavior in crayfish. Materials and methods: A permanent magnet was placed under the isolated nerve cord of crayfish to experience SMF at 4.74 to 43.45 mT intensity for various period of time (20 seconds to 3 hours). An intracellular electrode was impaled on the axon of the lateral giant neuron (LG) of the last abdominal ganglion of crayfish to record the evoked action potential (AP) and excitatory postsynaptic potential (EPSP). The amplitudes of evoked AP and EPSPs before and after SMF exposure were measured to study the effect of SMF exposure. Results: The exposure to SMF increased the amplitude of AP in the LG depending upon both the intensity of field and duration of field exposure. The changes in AP by field exposure are likely to be mediated by the increasing level of intracellular Ca²⁺ in the LG because the chelating of intracellular Ca²⁺ would block the effects by SMF exposure, while the injection of Ca²⁺ into the LG could mimic the effects of SMF exposure. SMF exposure also increases the input resistance of the LG membrane. Therefore, the magnitude of the EPSP in LG evoked by electrical shock on the sensory nerves was found to be enhanced after SMF exposure. Conclusion: SMF is usually considered to be safe for the biological issues since no electrical current is induced via the Faraday effect. Our results showed that some passive membrane properties of neurons are affected by SMF exposure. The increase in magnitude of evoked AP and EPSP suggests an increase in the sensitivity of the LG neuron. These changes by SMF exposure may not necessarily to be harmful to animals; however, further study is needed to address the biological effects from SMF exposure, especially in nervous systems.

Our previous studies have shown that early systemic granulocyte colony-stimulating factor (G-CSF) treatment can attenuate neuropathic pain in rats with chronic constriction injury (CCI) by modulating expression of different proinflammatory cytokines, microRNAs, and proteins. Besides the modulation of inflammatory mediators’ expression, previous studies have also reported that G-CSF can modulate autophagic and apoptotic activity. Furthermore, both autophagy and apoptosis play important roles in chronic pain modulation. In this study, we evaluated the temporal interactions of autophagy, and apoptosis in the dorsal root ganglion (DRG) and injured sciatic nerve after G-CSF treatment in CCI rats. We studied the behaviors of CCI rats with or without G-CSF treatment and the various levels of autophagic, proinflammatory, and apoptotic proteins in injured sciatic nerves and DRG neurons at different time points using Western blot analysis and immunohistochemical methods. The results showed that G-CSF treatment upregulated autophagic protein expression in the early phase and suppressed apoptotic protein expression in the late phase after nerve injury. Thus, medication such as G-CSF can modulate autophagy, apoptosis, and different proinflammatory proteins in the injured sciatic nerve and DRG neurons, which have the potential to treat neuropathic pain. However, autophagy-mediated regulation of neuropathic pain is a time-dependent process. An increase in autophagic activity in the early phase before proinflammatory cytokines reach the threshold level to induce neuropathic pain can effectively alleviate further neuropathic pain development.

To investigate the effects of static magnetic field (SMF) exposure on the synaptic transmission in a tail-flip circuit of crayfish. An O-shaped permanent magnet (35 mT intensity) was placed under the isolated nerve cord of crayfish to provide static magnetic field exposure. Using electrophysiological methods, the excitatory post synaptic potential (EPSP) before and after field exposure in the lateral giant interneuron were measured and compared. The EPSP produced via electrical and chemical synapses in the lateral giant neuron were enhanced after 30 min of SMF exposure (8.08 mT). Perfusion of field-exposed crayfish bath solution or preloading of Ca(2+) chelator and intracellular Ca(2+) release blocker failed to observe the SMF-induced enhancement on EPSP. Exposure of SMF increases the efficacy of synaptic-transmission in crayfish tail-flip escape circuit and this SMF-induced potentiation is a Ca(2+) dependent phenomenon.