PubMed · 13917334
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J STOFFREGEN, W THUERIGEN, H G FISCHER. 1962. [Halothane-controlled respiration anesthesia].. https://pubmed.ncbi.nlm.nih.gov/13917334/
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OBJECTIVES: The peripheral administration of granulocyte macrophage colony-stimulating factor (GM-CSF), widely used for the treatment of cytopenias, is often associated with neurological effects [Lieschke et al., N Engl J Med 1992;327:28-34]. This cytokine has recently been reported to affect neurotransmitter metabolism in the nervous system [Bianchi, Neuroreport 1997;8:3587-3590]. To further investigate the neuromodulatory effect of GM-CSF we studied the influence of GM-CSF on the efferent electric activity in the splenic nerve and the integral neuronal activity in medullary gigantocellular reticular formation (MGRF) in rats. METHODS: Anaesthetized (sodium thiopental 70 mg/kg, i.p.) Wistar rats were injected subcutaneously with 1 microg/kg of hr GM-CSF. Efferent electric activity in the splenic nerve and integral electric activity in MGRF were analyzed. The effectiveness of the applied dose of GM-CSF was verified by determining the elevation of the white blood cell count in peripheral blood 60 min after injection. RESULTS: We found that GM-CSF increases efferent electric activity in the splenic nerve and decreases that of MGRF as is evident by the frequency of electric discharges. The latency of both effects was 5-15 min. CONCLUSIONS: This data support the view that GM-CSF exerts a neuromodulatory effect and may provide a new link of neuroimmune communication.
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Neuroactive steroids modulate the function of gamma-aminobutyric acid type A (GABA(A)) receptors in brain; this is the presumed basis of their action as anesthetics. In a previous study using the neuroactive steroid analog, (3alpha,5beta)-6-azi-3-hydroxypregnan-20-one (6-AziP), as a photoaffinity-labeling reagent, we showed that voltage-dependent anion channel-1 (VDAC-1) was the predominant protein labeled in brain. Antisera to VDAC-1 were shown to coimmunoprecipitate GABA(A) receptors, suggesting a functional relationship between steroid binding to VDAC-1 and modulation of GABA(A) receptor function. This study examines the contribution of steroid binding to VDAC proteins to modulation of GABA(A) receptor function and anesthesia. Photolabeling of 35-kDa protein with [(3)H]6-AziP was reduced 85% in brain membranes prepared from VDAC-1-deficient mice but was unaffected by deficiency of VDAC-3. The photolabeled 35-kDa protein in membranes from VDAC-1-deficient mice was identified by two-dimensional electrophoresis and electrospray ionization-tandem mass spectrometry as VDAC-2. The absence of VDAC-1 or VDAC-3 had no effect on the ability of neuroactive steroids to modulate GABA(A) receptor function as evidenced by radioligand ([(35)S] t-butylbicyclophosphorothionate) binding or by electrophysiological studies. Electrophysiological studies also showed that neuroactive steroids modulate GABA(A) receptor function normally in VDAC-2-deficient fibroblasts transfected with alpha(1)beta(2)gamma(2) GABA(A) receptor subunits. Finally, the neuroactive steroid pregnanolone [(3alpha,5beta)-3-hydroxypregnan-20-one] produced anesthesia (loss of righting reflex) in VDAC-1- and VDAC-3-deficient mice, and there was no difference in the recovery time between the VDAC-deficient mice and wild-type controls. These data indicate that neuroactive steroid binding to VDAC-1, -2, or -3 is unlikely to mediate GABA(A) receptor modulation or anesthesia.