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The medial amygdala (MA) plays an important role in the innate fear circuit. However, the electrophysiological mechanism of MA for processing innate fear needs to be further explored. In this study, we fabricated microelectrode arrays (MEAs) with detecting sites arranged to match the location and shape of MA in mice and detected the electrophysiology in freely behaving mice under 2-methyl-2-thiazoline (2MT)-induced fear. The detection performance of MEA is improved by modifying metal nanoparticles and conductive polymers (PtNPs/PEDOT:PSS). After modification, the impedance magnitude and phase of electrodes were decreased to 27.0 ± 2.3 kΩ and −12.30 ± 0.52°, respectively, leading to a signal-to-noise ratio of 10. Its electrochemical stability and mechanical stability were also verified by cyclic voltammetry (CV) sweeping and ultrasonic vibration. MEAs were then implanted into the MA of mice, and the electrophysiology and behavioral characteristics were synchronously recorded and analyzed. The results showed that 2MT induced strong defensive behaviors in mice, accompanied by increases in the average spike firing rate and local field potential (LFP) power of MA neurons. According to principles commonly applied to cortical extracellular recordings, the recorded neurons are divided into two classes based on waveforms. Statistics showed that about 37% of type 1 neurons (putative GABAergic neurons) and 87% of type 2 neurons (putative glutamatergic neurons) were significantly activated under innate fear. At the same time, the firing rate of some activated neurons had a good linear correlation with the freezing rate.

Defense is the basic survival mechanism of animals when facing dangers. Previous studies have shown that the midbrain periaqueduct gray (PAG) was essential for the production of defense responses. However, the correlation between the endogenous neuronal activities of the dorsal PAG (dPAG) and different defense behaviors was still unclear. In this article, we designed and manufactured microelectrode arrays (MEAs) whose detection sites were arranged to match the shape and position of dPAG in rats, and modified it with platinum-black nanoparticles to improve the detection performance. Subsequently, we successfully recorded the electrophysiological activities of dPAG neurons via designed MEAs in freely behaving rats before and after exposure to the potent analog of predator odor 2-methyl-2-thiazoline (2-MT). Results demonstrated that 2-MT could cause strong innate fear and a series of defensive behaviors, accompanied by the significantly increased average firing rate and local field potential (LFP) power of neurons in dPAG. We also observed that dPAG participated in different defense behaviors with different degrees of activation, which was significantly stronger in the flight stage. Further analysis showed that the neuronal activities of dPAG neurons were earlier than flight, and the intensity of activation was inversely proportional to the distance from predator odor. Overall, our results indicate that dPAG neuronal activities play a crucial role in controlling different types of predator odor-evoked innate fear/defensive behaviors, and provide some guidance for the prediction of defense behavior.

Threatened animals respond with appropriate defensive behaviors to survive. It has been accepted that midbrain periaqueductal gray (PAG) plays an essential role in the circuitry system and organizes defensive behavioral responses. However, the role and correlation of different PAG subregions in the expression of different defensive behaviors remain largely unexplored. Here, we designed and manufactured a microelectrode array (MEA) to simultaneously detect the activities of dPAG and vPAG neurons in freely behaving rats. To improve the detection performance of the MEAs, PtNP/PEDOT:PSS nanocomposites were modified onto the MEAs. Subsequently, the predator odor was used to induce the rat’s innate fear, and the changes and information transmission in neuronal activities were detected in the dPAG and vPAG. Our results showed that the dPAG and vPAG participated in innate fear, but the activation degree was distinct in different defense behaviors. During flight, neuronal responses were stronger and earlier in the dPAG than the vPAG, while vPAG neurons responded more strongly during freezing. By applying high-performance MEA, it was revealed that neural information spread from the activated dPAG to the weakly activated vPAG. Our research also revealed that dPAG and vPAG neurons exhibited different defensive discharge characteristics, and dPAG neurons participated in the regulation of defense responses with burst-firing patterns. The slow activation and continuous firing of vPAG neurons cooresponded with the regulation of long-term freezing responses. The results demonstrated the important role of PAG neuronal activities in controlling different aspects of defensive behaviors and provided novel insights for investigating defense from the electrophysiological perspective.

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Grid cells with stable hexagonal firing patterns in the medial entorhinal cortex (MEC) carry the vital function of serving as a metric for the surrounding environment. Whether this mechanism processes only spatial information or involves nonspatial information remains elusive. Here, we fabricated an MEC-shaped microelectrode array (MEA) to detect the variation in neural spikes and local field potentials of the MEC when rats forage in a square enclosure with a planar, three-dimensional object and social landmarks in sequence. The results showed that grid cells exhibited rate remapping under social conditions in which spike firing fields closer to the social landmark had a higher firing rate. Furthermore, global remapping showed that hexagonal firing patterns were rotated and scaled when the planar landmark was replaced with object and social landmarks. In addition, when grid cells were activated, the local field potentials were dominated by the theta band (5–8 Hz), and spike phase locking was observed at troughs of theta oscillations. Our results suggest the pattern separation mechanism of grid cells in which the spatial firing structure and firing rate respond to spatial and social information, respectively, which may provide new insights into how the brain creates a cognitive map.

Background Subchromosomal deletions and duplications are the leading cause of congenital malformations and mental retardation in children. With the recent clinical application of genomic microarrays in the evaluation of patients with developmental delays and congenital malformations, it has led to the discovery of several new microdeletion and microduplication syndromes. However, there are no published reports involving patients with both microduplications in the 9p21.1-p24.3 region and microdeletions in the 7p22.1-p22.3 region. Case presentation We report an infant with an autosomal abnormality confirmed by conventional karyotype combined with copy number variations sequencing (CNV-seq), showing the patient with an unbalanced translocation. The karyotype of the patient was 46, XX, der (7)t (7;9) (p22; p21) and CNV-seq results showed an approximately 32.34-Mb duplication in 9p21.1-p24.3 (200000-32540000) and an approximately 3.3-Mb deletion in 7p22.2-p22.3 (40000-3340000). Conclusions The patient carried an unbalanced translocation 46, XX, der (7)t (7;9) (p22; p21) derived from her mother. The clinical presentation is closely related to the size and position of the missing and duplicated chromosomes. To our knowledge, the simultaneous occurrence of de novo partial trisomy 9p(9p21.1-p24.3) and partial monosomy 7p (7p22.2-p22.3) has not previously been reported up until now. The present study additionally demonstrated that CNV-seq combined with karyotype is able to reliably detect unbalanced submicroscopic chromosomal aberrations.