时间：11月20日 (周四)  18:00-20:00

地点：恕园28号楼205室

主题：文献报告

1、文献汇报：B-SNIP精神病生物亚型差异性生物标志物及家族性特征

主讲：徐涌轩 同学

2、文献汇报：外侧下丘脑脑啡肽原神经元调控负性情绪相关的威胁诱发的暴食行为

主讲：朱慧榕 同学

3、文献汇报： 满足性反应的大脑中枢

主讲：邱舒琦 同学

4、文献汇报：表达胆囊收缩素的GABA能神经元诱导皮层抑制性突触长时程增强并损害声音-电击联想记忆

主讲：闫航天 同学

欢迎老师与同学们踊跃出席！

脑科学研究所

文献详细信息

1、Differentiating biomarker features and familial characteristics of B-SNIP psychosis Biotypes

期刊信息：Translational Psychiatry；IF: 6.2；SCI: Q1；中科院：二区

摘要：

Idiopathic psychosis shows considerable biological heterogeneity across cases. The Bipolar-Schizophrenia Network for Intermediate Phenotypes (B-SNIP) used psychosis-relevant biomarkers to identify psychosis Biotypes, which will aid etiological and targeted treatment investigations. Here, our previous approach (Clementz et al. 2022) is updated, which supports the development of an efficient psychosis Biotype diagnostic procedure called ADEPT. Psychosis probands (n = 1907), their first-degree biological relatives (n = 705), and healthy participants (n = 895) completed a biomarker battery composed of cognitive performance, saccades, and auditory EEG/ERP measurements. EEG and ERP quantifications were modified from previous Biotypes iterations. Multivariate integration using multiple approaches reduced biomarker outcomes to 11 “bio-factors.” Twenty-four different approaches indicated bio-factor data among probands were best described by three subgroups. Numerical taxonomy with k-means clustering yielded psychosis Biotypes; Rand Indices evaluated individual-case consistency of Biotype assignments. Psychosis subgroups, their non-psychotic first-degree relatives, and healthy individuals were compared across bio-factors. The three psychosis Biotypes differed significantly on all 11 bio-factors, especially prominent for general cognition, antisaccades, ERP magnitude, and intrinsic neural activity. Rand Indices showed excellent individual-case consistency of Biotype membership when samples included more than 1000 subjects. Canonical discriminant analysis described composite bio-factors that simplified group comparisons: “Pattern-2” (high antisaccade errors, low BACS, high ongoing EEG) captured Biotype-2, “Pattern-1” (low ERP amplitudes, low intrinsic EEG) captured Biotype-1, and “Pattern-3” (low frontal P3 complex, accentuated S2 ERP, faster saccadic reaction times) captured Biotype-3. First-degree relatives had patterns like their proband for general cognition, antisaccades, ERP magnitudes, and intrinsic brain activity. These outcomes refine and extend operations for characterizing biologically distinct psychosis Biotypes. They also show that over 1000 observations are useful for achieving consistent individual-case diagnostic assignments. First-degree relative data implicate specific bio-factors as familial within idiopathic psychosis which may inform genetic studies.

2、Lateral hypothalamic proenkephalin neurons drive threat-induced overeating associated with a negative emotional state

期刊信息：nature communications；IF：15.7；SCI：Q1；中科院：一区

摘要：

Psychological stressors, like the nearby presence of a predator, can be strong enough to induce physiological/hormonal alterations, leading to appetite changes. However, little is known about how threats can alter feeding-related hypothalamic circuit functions. Here, we found that proenkephalin (Penk)-expressing lateral hypothalamic (LHPenk) neurons of mice exposed to predator scent stimulus (PSS) show sensitized responses to high-fat diet (HFD) eating, whereas silencing of the same neurons normalizes PSS-induced HFD overconsumption associated with a negative emotional state. Downregulation of endogenous enkephalin peptides in the LH is crucial for inhibiting the neuronal and behavioral changes developed after PSS exposure. Furthermore, elevated corticosterone after PSS contributes to enhance the reactivity of glucocorticoid receptor (GR)-containing LHPenk neurons to HFD, whereas pharmacological inhibition of GR in the LH suppresses PSS-induced maladaptive behavioral responses. We have thus identified the LHPenk neurons as a critical component in the threat-induced neuronal adaptation that leads to emotional overconsumption.

3、A brain center that consummatory responses

期刊信息：Cell；IF：42.5；SCI：Q1；中科院：一区

摘要：

The innate attraction to sweet mediates appetitive and consummatory responses. Here, we dissected the circuit driving responses to sweet and showed that amygdala neurons tuned to sweet connect to the bed nucleus of the stria-terminalis (BNST) to promote sweet-evoked consumption. Next, we demonstrate that the BNST functions as a central hub, transforming appetitive signals into consumption and linking sensory inputs to the internal state, not only for sweet but also for other stimuli such as salt or food, to flexibly regulate consummatory behaviors. Using single-cell functional imaging, we show that ensemble activity in the BNST encodes stimulus identity and the animal’s internal state. Finally, we demonstrate that manipulating BNST activity can bidirectionally transform consummatory responses. Together, these findings illustrate how the internal state modulates sensory responses, characterize a general brain dial for consumption, and provide fresh insights into sites of action of GLP1R agonists and a strategy to help promote weight gain in pathological states.

4、Cholecystokinin-expressing GABA neurons elicit long-term potentiation in the cortical inhibitory synapses and attenuate sound-shock associative memory

期刊信息：scientific reports；IF: 3.9；SCI: Q1；中科院：二区

摘要：

Neuronal interactions between inhibitory and excitatory neurons play a pivotal role in regulating the balance of excitation and inhibition in the central nervous system (CNS). Consequently, the efficacy of inhibitory/excitatory synapses profoundly affects neural network processing and overall neuronal functions. Here, we describe a novel form of long-term potentiation (LTP) induced at cortical inhibitory synapses and its behavioral consequences. We show that high-frequency laser stimulation (HFLS) of GABAergic neurons elicit inhibitory LTP (i-LTP) in pyramidal neurons of the auditory cortex (AC). The selective activation of cholecystokinin-expressing GABA (GABA CCK) neurons is essential for the formation of HFLS-induced i-LTP, rather than the classical parvalbumin (PV) neurons and somatostatin (SST) neurons. Intriguingly, i-LTP can be evoked in the AC by adding the exogenous neuropeptide CCK when PV neurons and SST neurons are selectively activated in PV-Cre and SST-Cre mice, respectively. Additionally, we discovered that low-frequency laser stimulation (LFLS) of PV neurons paired with HFLS of GABA CCK neurons potentiates the inhibitory effect of PV interneurons on pyramidal neurons, thereby generating heterosynaptic i-LTP in the AC. Notably, light activation of GABA CCK neurons in CCK-Cre mice significantly attenuates sound- shock associative memory, while stimulation of PV neurons does not affect this memory in PV-Cre mice. In conclusion, these results demonstrate a critical mechanism regulating the excitation-inhibition balance and modulating learning and memory in cortical circuits. This mechanism might serve as a potential target for the treatment of neurological disorders, including epilepsy and Alzheimer’s disease.