Immune response to gut escherichia coli and susceptibility to adjuvant arthritis in the rats

We have investigated the humoral immune response to antigens of predominant gut aerobic bacterial strains (i.e. Escherichia coli) over the course of adjuvant arthritis and oil-induced arthritis in two inbred rat strains: Dark Agouti (DA) and Albino Oxford (AO). We report the presence of antibodies specific to proteins of Escherichia coli in molecular weight range between 20-30 kDa in sera of diseased DA rats, and the absence of these antibodies in the sera of AO rats. In DA rats, CFA and IFA provoked a stronger antibody response to Escherichia coli, especially of the IgG2b antibody class. Intramuscular administration of Escherichia coli preceding the adjuvant arthritis induction had no effect on the development and course of disease, as well as on the activation of T cells in the draining inguinal lymph nodes. Higher serum levels of natural and induced IgA antibodies, combined with a higher CD3(+)CD26(+) cell percentage were found in AO rats. The observed correlation between the serologic response to commensal flora and rats' genetic background as a defining factor for arthritis susceptibility may contribute to the process of creating a favorable (or less favorable) milieu for arthritis development

High and low responders to novelty and mesolimbic noradrenaline: effects of noradrenergic agents on radial-maze performance

Contains fulltext : 62286.pdf (publisher's version ) (Closed access)The authors used high and low responders to novelty (HRs and LRs, respectively) to examine the effects of noradrenergic injections into the nucleus accumbens using a special radial-maze task. During the 5 successive test days, solvent-treated HRs acquired this task faster than LRs. Isoproterenol ([beta]-agonist) combined with phenylephrine ([alpha]-agonist) improved acquisition in LRs but not in HRs; this effect was counteracted by propranolol ([beta]-antagonist) and phentolamine ([alpha]-antagonist). Propranolol combined with phentolamine, as well as phentolamine alone, disrupted acquisition in HRs but not in LRs. Data show that the effects of noradrenergic agents in HRs and LRs are due to differences in acquisition directed by type-specific differences in functional mesolimbic noradrenaline