Arginine vasopressin differentially modulates GABAergic synaptic transmission onto temperature-sensitive and temperature-insensitive neurons in the rat preoptic area.

The preoptic area (POA) of the hypothalamus, containing temperature-sensitive and temperature-insensitive neurons, plays a key role in specific thermoregulatory responses. Although arginine vasopressin (AVP) has been shown to induce hypothermia by increasing the firing activities of warm-sensitive neurons and decreasing those of cold-sensitive and temperature-insensitive neurons, the effects of AVP on POA GABAergic transmission remain unknown. Herein, inhibitory postsynaptic currents (IPSCs) of temperature-sensitive and temperature-insensitive neurons in POA slices were recorded using whole-cell patch clamp. By monitoring changes in GABAergic transmission during AVP treatment, we showed that AVP decreased the amplitudes and frequencies of spontaneous IPSCs in mostly warm-sensitive neurons and in some temperature-insensitive neurons but increased these parameters in other temperature-insensitive neurons. The IPSC amplitude was reduced for only cold-sensitive neurons. RT-PCR and Western blot analyses further confirmed the POA expression of V1a receptors and GABAA receptors, including the subunits α1, α2, α3, ß2, ß3 and γ2. The effects of AVP on IPSCs in temperature-sensitive and temperature-insensitive neurons were dependent on G proteins and intracellular Ca2+ . AVP-mediated modulation was associated with changes in the kinetic parameters (decay time, 10-90% rise time, half-width). Together, these results suggest that AVP, acting via V1a receptors but not V1b receptors, differentially modulates GABAergic synaptic transmission and fine-tunes the firing activities of temperature-sensitive and temperature-insensitive neurons in the rat POA.

Increased serum amyloid A and its association with autoantibodies, acute phase reactants and disease activity in patients with rheumatoid arthritis.

Determination of disease activity in patients with rheumatoid arthritis (RA) has become an important component for RA management. The aim of the present study was to investigate the association between circulating levels of serum amyloid A (SAA) and disease activity in RA patients. The types of disease and the respective number of patients enrolled in the present study were as follows: RA, 88; osteoarthritis (OA), 54; systemic lupus erythematosus (SLE), 43; and other autoimmune diseases, 30, as well as 50 healthy controls (HC). SAA levels were measured using an ELISA assay and western blot analysis was used to detect serum SAA levels. The correlations between SAA levels and disease activity score for 28 joints (DAS28), erythrocyte sedimentation rate (ESR) and C­reactive protein (CRP), respectively, were evaluated; in addition, the presence and absence of rheumatoid factor (RF) and anti­cyclic citrullinated peptide antibody (anti­CCP) were detected in respect to SAA levels. The results of the present study demonstrated that serum levels of SAA in RA patients were significantly increased compared to those of the OA, SLE, others and HC patients (P<0.05). SAA levels were found to be positively correlated with DAS28, ESR and CRP levels (R2=0.6174, 0.4422 and 0.3919, respectively). In addition, anti­CCP was not correlated with DAS28 (R2=0.0154). Furthermore, increased SAA levels were detected in patients with positive anti­CCP compared with those in anti­CCP negative subjects (P<0.01). In conclusion, the results of the present study provided further evidence for possible roles of SAA in RA, which indicated that it may be a useful biomarker for assessing disease severity and may provide additional information about disease activity.