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Biomedical subjects

Jian Feng

Publications and source records attributed to Jian Feng.

41 records · Page 3Linked to original sources

Regulation of neurotransmitter release by synapsin III.

Synapsin III is the most recently identified member of the synapsin family, a group of synaptic vesicle proteins that play essential roles in neurotransmitter release and neurite outgrowth. Here, through the generation and analysis of synapsin III knock-out mice, we demonstrate that synapsin III regulates neurotransmitter release in a manner that is distinct from that of synapsin I or synapsin II. In mice lacking synapsin III, the size of the recycling pool of synaptic vesicles was increased, and synaptic depression was reduced. The number of vesicles that fuse per action potential was similar between synapsin III knock-out and wild-type mice, and there was no change in the quantal content of EPSCs; however, IPSCs were greatly reduced in synapsin III-deficient neurons. The density and distribution of synaptic vesicles in presynaptic terminals did not appear to be different in synapsin III knock-out mice in comparison to wild-type littermates. In addition to the changes in neurotransmitter release, we observed a specific delay in axon outgrowth in cultured hippocampal neurons from synapsin III knock-out mice. Our data indicate that synapsin III plays unique roles both in early axon outgrowth and in the regulation of synaptic vesicle trafficking.

Action Potentials↗

Activity-dependent bidirectional regulation of GABA(A) receptor channels by the 5-HT(4) receptor-mediated signalling in rat prefrontal cortical pyramidal neurons.

Emerging evidence has implicated a potential role for 5-HT(4) receptors in cognition and anxiolysis. One of the main target structures of 5-HT(4) receptors on 'cognitive and emotional' pathways is the prefrontal cortex (PFC). As GABAergic signalling plays a key role in regulating PFC functions, we examined the effect of 5-HT(4) receptors on GABA(A) receptor channels in PFC pyramidal neurons. Application of 5-HT(4) receptor agonists produced either an enhancement or a reduction of GABA-evoked currents in PFC neurons, which are both mediated by anchored protein kinase A (PKA). Although PKA phosphorylation of GABA(A) receptor beta3 or beta1 subunits leads to current enhancement or reduction respectively in heterologous expression systems, we found that beta3 and beta1 subunits are co-expressed in PFC pyramidal neurons. Interestingly, altering PKA activation levels can change the direction of the dual effect, switching enhancement to reduction and vice versa. In addition, increased neuronal activity in PFC slices elevated the PKA activation level, changing the enhancing effect of 5-HT(4) receptors on the amplitude of GABAergic inhibitory postsynaptic currents (IPSCs) to a reduction. These results suggest that 5-HT(4) receptors can modulate GABAergic signalling bidirectionally, depending on the basal PKA activation levels that are determined by neuronal activity. This modulation provides a unique and flexible mechanism for 5-HT(4) receptors to dynamically regulate synaptic transmission and neuronal excitability in the PFC network.

4-Aminobenzoic Acid↗

Identification, cDNA cloning, and targeted deletion of p70, a novel, ubiquitously expressed SH3 domain-containing protein.

In a screen for proteins that interact with Jak2, we identified a previously uncharacterized 70-kDa protein and cloned the corresponding cDNA. The predicated sequence indicates that p70 contains an SH3 domain and a C-terminal domain with similarities to the catalytic motif of phosphoglycerate mutase. p70 transcripts were found in all tissues examined. Similarly, when an antibody raised against a C-terminal peptide to analyze p70 protein expression was used, all murine tissues examined were found to express p70. To investigate the in vivo role of p70, we generated a p70-deficient mouse strain. Mice lacking p70 are viable, develop normally, and do not display any obvious abnormalities. No differences were detected in various hematological parameters, including bone marrow colony-forming ability, in response to cytokines that utilize Jak2. In addition, no impairment in B- and T-cell development and proliferative ability was detected.

Adaptor Proteins, Signal Transducing↗

The effect of gingival retraction procedures on periodontal indices and crevicular fluid cytokine levels: a pilot study.

PURPOSE: The purpose of this study was to examine the effects of placement of retraction cord subgingivally upon periodontal indices including plaque index (PI), gingival index (GI), pocket depth (PD), bleeding on probing (BOP), and attachment level (AL), as well as gingival crevicular fluid (GCF) and TNF-alpha levels. METHODS: Ten teeth in 6 patients who were periodontally healthy were selected. These teeth had pocket depths of 3 mm or less, no evidence of significant loss of attachment, BOP, or plaque accumulation. The patients each received an oral prophylaxis. The following week, baseline measurements of periodontal indices and TNF-alpha were taken and the retraction cord was placed for 15 minutes. Following removal, the patients were dismissed. The periodontal indices measured included PI, GI, PD, BOP, and AL. In addition, the levels of TNF-alpha in GCF, were investigated. These measurements were made before gingival retraction as a baseline and on the 1st, 3rd, 7th, 14th, and 28th days post retraction. RESULTS: A repeated measures ANOVA showed that TNF-alpha levels in GCF were significantly increased at all five intervals after gingival retraction compared to the baseline. The mean TNF-alpha level peaked at Day 1 (0.90 +/- 0.62), then declined at Days 3 (0.53 +/- 0.16), 7 (0.43 +/- 0.08), 14 (0.47 +/- 0.10), and 28 (0.43 +/- 0.08) but was still elevated 54% above baseline at Day 28, p < 0.01. The GI was significantly elevated at Day 1 (0.9 +/- 0.49), p < 0.01; Day 3 (0.53 +/- 0.32); and Day 7 (0.33 +/- 0.33), p < 0.05. Unlike TNF-alpha, GI recovered to the baseline by day 14. Other periodontal parameters, PI, PD, BOP, and AL were not significantly altered by the gingival retraction procedure. CONCLUSION: This pilot study supports the previous research that gingival retraction causes an acute injury that heals clinically in 2 weeks as is indicated by the GI. It also provides the first evidence that gingival retraction results in an elevation of the proinflammatory cytokine, TNF-alpha, in GCF.

Adult↗