Changes in expression of BDNF and its receptors TrkB and p75NTR in the hippocampus of a dog model of chronic alcoholism and abstinence

Chronic ethanol consumption can produce learning and memory deficits. Brain-derived neurotrophic factor (BDNF) and its receptors affect the pathogenesis of alcoholism. In this study, we examined the expression of BDNF, tropomyosin receptor kinase B (TrkB) and p75 neurotrophin receptor (p75NTR) in the hippocampus of a dog model of chronic alcoholism and abstinence. Twenty domestic dogs (9-10 months old, 15-20 kg; 10 males and 10 females) were obtained from Harbin Medical University. A stable alcoholism model was established through ad libitum feeding, and anti-alcohol drug treatment (Zhong Yao Jie Jiu Ling, the main ingredient was the stems of watermelon; developed in our laboratory), at low- and high-doses, was carried out. The Zhong Yao Jie Jiu Ling was effective for the alcoholism in dogs. The morphology of hippocampal neurons was evaluated using hematoxylin-eosin staining. The number and morphological features of BDNF, TrkB and p75NTR-positive neurons in the dentate gyrus (DG), and the CA1, CA3 and CA4 regions of the hippocampus were observed using immunohistochemistry. One-way ANOVA was used to determine differences in BDNF, TrkB and p75NTR expression. BDNF, TrkB and p75NTR-positive cells were mainly localized in the granular cell layer of the DG and in the pyramidal cell layer of the CA1, CA3 and CA4 regions (DG>CA1>CA3>CA4). Expression levels of both BDNF and TrkB were decreased in chronic alcoholism, and increased after abstinence. The CA4 region appeared to show the greatest differences. Changes in p75NTR expression were the opposite of those of BDNF and TrkB, with the greatest differences observed in the DG and CA4 regions.

Identification and pathogenicity analysis of a novel non-tuberculous mycobacterium clinical isolate with nine-antibiotic resistance.

With mycobacteriosis increasing, the study of non-tuberculous mycobacteria is imperative for clinical therapy and management. Non-tuberculous mycobacteria are naturally resistant to most anti-tuberculosis drugs. Accordingly, it is important to decipher the biology of the novel non-tuberculous mycobacteria through complete genomic analysis of novel pathogenic mycobacteria. We describe Mycobacterium sinense JDM601, a novel, slow-growing mycobacterium of the Mycobacterium terrae complex resistant to nine antibiotics, by clinical presentation, cultural and biochemical characteristics, minimal inhibitory concentrations, and genome-sequencing analysis. JDM601 is closest to Mycobacterium nonchromogenicum according to mycolic acid composition, but closest to Mycobacterium algericum sp. nov according to 16S rDNA. JDM601 is resistant to isoniazid, streptomycin, rifampin, euteropas, protionamide, capromycin, ciprofloxacin, amikacin and levofloxacin but not ethambutol. The clinical information, mycolic acid composition, and virulence genes indicate that JDM601 is an opportunistic pathogen.

Functional GABA(B) receptors are expressed at the cone photoreceptor terminals in bullfrog retina.

GABA(B) receptors at the cone terminals in bullfrog retina were characterized by immunocytochemical and whole-cell patch clamp techniques in retinal slice preparations. Somata, axons and synaptic terminals (pedicles) of cones were both GABA(B) receptor (GABA(B)R) 1 and GABA(B)R2 immunoreactive. Physiologically, barium/calcium currents of cones to voltage steps were significantly reduced in size when GABA was puffed to cone terminals in the presence of picrotoxin that is supposed to block both GABA(A) and GABA(C) receptors. Similar reduction in barium currents was obtained with puff application of baclofen to cone terminals. These results suggest the presence of functional GABA(B) receptors at the bullfrog cone terminals. Suppression of barium currents of cones by baclofen was dose-dependent. Moreover, barium currents of cones were potentiated by background illumination, as compared with those recorded in the dark. 6,7-Dinitroquinoxaline-2,3-dione, an antagonist of non-NMDA receptors that hyperpolarizes horizontal cells and reduces GABA release from these cells, and saclofen, a GABA(B) receptor antagonist, both potentiated barium currents of cones in the dark, thereby mimicking the effects of background illumination. It is suggested that changes in calcium influx into the cone synaptic terminals due to activation of GABA(B) receptors may provide a negative feedback mechanism for regulating signal transmission between cones and second-order neurons in the retina by modifying the amount of glutamate released from the cones.