Using an identified LPeD1 neuron from Lymnaea
stagnalis, we sought to determine how lidocaine affects these factors and how lidocaine is related to damage of the cell membrane.
Cell size and morphological form were measured by a micrograph and imaging analysis system. Membrane potential and survival rate were obtained by intracellular recording. Membrane resistance and capacitance were measured by whole-cell patch clamp. Phosphatidyl serine and nucleic acid were double stained and simultaneously measured by annexin V and propidium iodide.
Lidocaine at a clinical dose (5-20 mM) induced morphological change (bulla Autophagy inhibitor and bleb) in the neuron and increased cell size in a concentration-dependent manner. Membrane potential was depolarized in a concentration-dependent manner. At perfusion of more than 5 mM lidocaine, the depolarized membrane potential was irreversible. Lidocaine decreased membrane resistance and increased membrane capacitance in a concentration-dependent manner. Both phosphatidyl serine and nucleic acid were stained under lidocaine exposure in a concentration-dependent manner.
A clinical dose of lidocaine greater than 5 mM destroys the cell
membrane and induces both necrosis and apoptosis in an identified NU7441 nmr Lymnaea neuron.”
“Aims: To report the conclusions of the Think Tank on mechanisms of incontinence and surgical cure in female and male SUI: surgical research initiatives during the ICI-RS meeting in 2010. Methods: The sub-group considered five areas for future research in stress urinary incontinence (SUI); (i) epidemiology and public health efforts in
SUI, (ii) the basic sciences examining the physiology and pathophysiology of the continence mechanism, (iii) diagnostic techniques and clinical assessment of SUI, (iv) the future of treatment and surgical cure, and (v) the separate issue of male SUI. Results: Roadblocks to progress were identified for each of the five DZNeP clinical trial directions. Conclusions: Future research directions are suggested for each of these areas. Neurourol. Urodynam 30:704-707, 2011. (C) 2011 Wiley-Liss, Inc.”
“Drug addiction is thought to result from an intractable and aberrant learning and memory in response to drug-related stimulation, and cholinergic neurotransmission plays an important role in this process. Phosphatidylethanolamine-binding protein (PEBP) is the precursor of the hippocampal cholinergic neurostimulating peptide (HCNP), an 11 amino acid peptide that enhances the production of choline acetyltransferase (ChAT) and assists in the development of cholinergic projections from the medial septal nuclei to the hippocampus. However, whether PEBP is involved in drug addiction remains unclear. In the present study, PEBP expression in the hippocampus, as detected by proteomics analysis, was found to be dramatically up-regulated after rats received chronic morphine treatment.