This study examined the effects of nicotine and endogenous acetylcholine on retrogradely labelled, functionally identified inspiratory-activated AVPNs (IA-AVPNs) using the patch-clamp technique. Nicotine (10 mu mol l(-1)) significantly increased the frequency and amplitude of the spontaneous EPSCs of IA-AVPNs, and these effects were insensitive to methyllycaconitine (MLA, 100 nmol l(-1)), an antagonist A-769662 clinical trial of the alpha 7 type of nAChR, but was prevented by dihydro-beta-erythroidine (DH beta E, 3 mu mol l(-1)), an antagonist of the alpha 4 beta 2 type of nAChR. Nicotine caused a tonic inward

current in IA-AVPNs, which was reduced by MLA or DH beta E alone, but was not abolished by co-application of MLA and DH beta E. Nicotine caused a significant increase in the frequency of GABAergic and glycinergic spontaneous IPSCs and significantly increased the amplitude of glycinergic spontaneous IPSCs, all of which were prevented by DH beta E. Nicotine had no effects on the miniature EPSCs or miniature IPSCs following pretreatment with TTX. Under Raf inhibitor current clamp, nicotine caused depolarization and increased

the firing rate of IA-AVPNs during inspiratory intervals. Neostigmine (10 mu mol l(-1)), an acetylcholinesterase inhibitor, mimicked the effects of nicotine. These results demonstrate that nicotine and endogenous ACh enhance the excitatory and inhibitory synaptic inputs of IA-AVPNs and cause a postsynaptic selleck inhibitor excitatory current and that the nicotinic effects are mediated presynaptically by activation of the alpha 4 beta 2 type of nAChR and postsynaptically by activation of multiple nAChRs, including alpha 7 and alpha 4 beta 2 types.”
“Inflammation plays a significant role in Alzheimer’s disease (AD) pathogenesis. Studies have shown that systemic, peripheral infections affect AD patients. Cognitive dysfunction is a consistent finding in AD and periodontal disease is a chronic, peripheral infection often resulting in tooth loss. We hypothesized that older adults with periodontal inflammation (PI) or many missing teeth would show impaired cognition compared to subjects

without PI or with few missing teeth, and among subjects with PI, those with many missing teeth would show impaired cognition compared to those with few missing teeth. The effect of PI/tooth loss on cognitive function [measured by Digit Symbol (DST) and Block Design (BDT) tests] was assessed in 70-year old Danish subjects. We found: 1) subjects with PI obtained lower mean DST scores compared to subjects without PI (p < 0.05); 2) subjects with many missing teeth had lower mean DST and BDT scores compared to subjects with few missing teeth (p < 0.05); 3) the association of PI with DST and BDT scores was dependant on the number of missing teeth (interaction: p = 0.03 and p = 0.06); and 4) education and previous cognitive scores (age 50) were important covariates.