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Objective: The sympathetic–parasympathetic (or axo–axonal) interaction mechanism mediated that neurogenic relaxation, which was dependent on norepinephrine (NE) releases from sympathetic nerve terminal and acts on β2‐adrenoceptor of parasympathetic nerve terminal, has been reported. As NE is a weak β2‐adrenoceptor agonist, there is a possibility that synaptic NE is converted to epinephrine by phenylethanolamine‐N‐methyltransferase (PNMT) and then acts on the β2‐adrenoceptors to induce neurogenic vasodilation. Methods: Blood vessel myography technique was used to measure relaxation and contraction responses of isolated basilar arterial rings of rats. Results: Nicotine‐induced relaxation was sensitive to propranolol, guanethidine (an adrenergic neuronal blocker), and Nω‐nitro‐l‐arginine. Nicotine‐ and exogenous NE‐induced vasorelaxation was partially inhibited by LY‐78335 (a PNMT inhibitor), and transmural nerve stimulation depolarized the nitrergic nerve terminal directly and was not inhibited by LY‐78335; it then induced the release of nitric oxide (NO). Epinephrine‐induced vasorelaxation was not affected by LY‐78335. However, these vasorelaxations were completely inhibited by atenolol (a β1‐adrenoceptor antagonist) combined with ICI‐118,551 (a β2‐adrenoceptor antagonist). Conclusions: These results suggest that NE may be methylated by PNMT to form epinephrine and cause the release of NO and vasodilation. These results provide further evidence supporting the physiological significance of the axo–axonal interaction mechanism in regulating brainstem vascular tone. [ABSTRACT FROM AUTHOR]

Heat Shock Protein BAP1 (heat shock 27-kDa-associated protein 1, HSPBAP1) inhibits the function of heat shock protein 27, which has a neuroprotective effect during experimentally induced epileptic neuropathology. In our study, fluorescence quantitative polymerase chain reaction, immunohistochemistry, immunofluorescence, western blot were used to test the levels of HSPBAP1 mRNA and protein in surgical samples of the anterior temporal neocortex of patients with intractable epilepsy (IE) and normal controls samples. HSPBAP1 mRNA was abnormally expressed in the anterior temporal neocortex of patients with IE. Moreover, HSPBAP1 was found extensively in the cytoplasm of neurons and glial cells in all epilepsy specimens. Western blot showed a clear immunoreactive band of HSPBAP1 in IE specimens whereas it was absent in control specimens. The expression of HSPBAP1 mRNA and protein in the anterior temporal neocortex from patients with IE may play a role in the development of epileptic seizures in patients with cell loss in this brain region. Additional studies will be required to elucidate the mechanism by which HSPBAP1 affects brain function in IE. Synapse 61:741-747, 2007. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]