Synapse最新文献

Traumatic brain injury (TBI) is a world-wide leading health problem with high morbidity and mortality rates. Emerging studies have demonstrated that TBI is the consequence of a series of inflammatory responses in the body. The alteration of Cystatin C (Cys C) was reported in a variety of chronic inflammatory diseases and was also recommended as a biomarker for predicting renal diseases. In this study, we aimed to investigate the relationship between serum Cys C and TBI, and to evaluate the prognostic role of Cys C in TBI prediction. One hundred and seventy-six patients with TBI were recruited and 102 patients were finally analyzed, with 30 healthy control subjects. The concentrations of Cys C were significantly reduced in the healthy control group compared to the TBI group, and correlated with high GCS scores. The levels of hsCRP, counts of white blood cells, and levels of IL-6 and TNF-α were remarkably elevated in the TBI patients compared with the control group in a severity-dependent manner. Moreover, the concentration of Cys C was negatively correlated with TBI severity and positively correlated with inflammatory factors. In conclusion, serum Cys is an inflammatory cytokine-related factor and might indicate the severity of TBI thus serving as a prognostic biomarker.

Animals appoint incentive value and learn to approach otherwise behaviorally inert stimuli if these stimuli come to predict the delivery of reward. Interestingly, this adaptive Pavlovian learning process has been implicated in behavioral control disorders, such as drug addiction. One brain region implicated in directing conditioned approach behavior is the prelimbic region of the prefrontal cortex. The present study employed in vivo electrophysiology in the prelimbic cortex to characterize the distribution of neural responses to the presence of a cue that had acquired incentive value after being associated with a primary reward. Male rats were trained in a Pavlovian autoshaping task in which a lever was presented prior to reward delivery. Following repeated pairings of lever availability and reward delivery, rats pressed the lever even though reward delivery was not contingent on any interaction with the lever. Neurons in the prelimbic cortex selectively encoded the presentation of the reward-predicting lever. Although the response was heterogeneous, most responsive neurons decreased their firing rate in response to the presence of the lever. These findings characterize the varied responses of prelimbic cortical neurons to reward cues and are consistent with evidence that the role of the prelimbic cortex in reward learning depends on the downstream target.

Information from the entorhinal cortex arrives to the hippocampal CA1 microcircuit directly through the temporoammonic path (TA) that terminates in the stratum lacunosum-moleculare (SLM), and indirectly through Schaffer collateral pathway (SC) that terminates in the stratum radiatum (SR). By virtue of this input convergence, CA1 circuitry may act to compare and integrate incoming cortical information. Although a remarkable dorsal-ventral difference in short-term plasticity (STP) has been recently described at SC-CA1 synapses, the corresponding properties at TA-CA1 synapses have not been examined. Here, we report that stimulation of TA in the dorsal hippocampus produces significant facilitation of all conditioned responses evoked by 1-30 Hz, peaking at 20-30 Hz, and significant depression of steady-state responses to 50-100 Hz. Dorsal SC-CA1 synapses display a similar pattern of responses, yet, facilitation peaked at 10 Hz and depression (at 75-100 Hz) is weaker. Strikingly, stimulation of TA in the ventral hippocampus produces facilitation of steady-state responses to 1-30 Hz and highly contrasts with the depression of SC-CA1 synapses. Steady-state responses to 40-100 Hz in the ventral hippocampus depress in both layers similarly. High-frequency TA input (40-100 Hz) to the dorsal hippocampus depresses more in proximal than in distal SLM, while low-frequency (1-3 Hz) TA input to the ventral hippocampus facilitates more in distal than in proximal SLM. The present evidence suggests that direct and indirect entorhinal cortical inputs across the septotemporal extent of hippocampal CA1 field display frequency selectivity both in the radial and transverse axes, and that a rapid information processing may take place through direct ventral hippocampal CA1-EC circuit interactions independently of trisynaptic circuit.

Severe voluntary food restriction is the defining symptom of anorexia nervosa (AN), but anxiety and excessive exercise are maladaptive symptoms that contribute significantly to the severity of AN and which individuals with AN have difficulty suppressing. We hypothesized that the excitability of hippocampal pyramidal neurons, known to contribute to anxiety, leads to the maladaptive behavior of excessive exercise. Conversely, since glutamate transporter GLT-1 dampens the excitability of hippocampal pyramidal neurons through the uptake of ambient glutamate and suppression of the GluN2B-subunit containing NMDA receptors (GluN2B-NMDARs), GLT-1 may contribute toward dampening excessive exercise. This hypothesis was tested using the mouse model of AN, called activity-based anorexia (ABA), whereby food restriction evokes the maladaptive behavior of excessive wheel running (food restriction-evoked running, FRER). We tested whether individual differences in ABA vulnerability of mice, quantified based on FRER, correlated with individual differences in the levels of GLT-1 at excitatory synapses of the hippocampus. Electron microscopic immunocytochemistry (EM-ICC) was used to quantify GLT-1 levels at the excitatory synapses of the hippocampus. The FRER seen in individual mice varied more than 10-fold, and Pearson correlation analyses revealed a strong negative correlation (p = .02) between FRER and GLT-1 levels at the axon terminals of excitatory synapses and at the surrounding astrocytic plasma membranes. Moreover, synaptic levels of GluN2B-NMDARs correlated strongly with GLT-1 levels at perisynaptic astrocytic plasma membranes. There is at present no accepted pharmacotherapy for AN, and little is known about the etiology of this deadly illness. Current findings suggest that drugs increasing GLT-1 expression may reduce AN severity through the reduction of GluN2B-NMDAR activity.