ABSTRACT
The development of the olfactory system is influenced by sensory inputs, and it maintains neuronal generation and plasticity throughout the lifespan. The olfactory bulb contains a higher proportion of interneurons than other brain regions, particularly during the early postnatal period of neurogenesis. Although the relationship between sensory stimulation and olfactory bulb development during the postnatal period has been well studied, the molecular mechanisms have yet to be identified. In this study, we used western blotting and immunohistochemistry to analyze the expression of the transcription factor Npas4, a neuron-specific immediate-early gene that acts as a developmental regulator in many brain regions.We found that Npas4 is highly expressed in olfactory bulb interneurons during the early postnatal stages and gradually decreases toward the late postnatal stages. Npas4 expression was observed in all olfactory bulb layers, including the rostral migratory stream, where newborn neurons are generated and migrate to the olfactory bulb. Under sensory deprivation, the olfactory bulb size and the number of olfactory bulb interneurons were reduced. Furthermore, Npas4 expression and the expression of putative Npas4 downstream molecules were decreased. Collectively, these findings indicate that Npas4 expression induced by sensory input plays a role in the formation of neural circuits with excitatory mitral/tufted cells by regulating the survival of olfactory bulb interneurons during the early stages of postnatal development.
ABSTRACT
Gender differences in aggression viewed from an evolutionary and sociocultural perspective have traditionally explained why men engage in more direct and physical aggression, and women engage in more indirect and relational aggression. However, psychological and behavioral studies offer inconsistent support for this theory due to personal or social factors, and little is known about the gender-based neurobiological mechanisms of aggression. This study investigates gender differences in aggression through an analysis of electroencephalography (EEG) and electrocardiography (ECG) based neurobiological responses to commonly encountered stimuli, as well as psychological approaches in healthy Korean youth. Our results from self-reports indicate that overall aggression indices, including physical and reactive/overt aggression, were stronger in men. This agrees with the results of previous studies. Furthermore, our study reveals prominent gender-related patterns in γ signals from the right ventrolateral frontal cortex and changes in heart rate through stimulation by aggressive videos. In particular, gender differences in EEG and ECG responses were observed in response to different scenes, as simple aversion and situation-dependent aggression, respectively. In addition, we discovered decisive gender-distinct EEG signals during stimulation of the situation-dependent aggression regions within the right ventromedial prefrontal and ventrolateral frontal regions. Our findings provide evidence of a psychological propensity for aggression and neurobiological mechanisms of oscillation underlying gender differences in aggression. Further studies of oscillatory responses to aggression and provocation will expand the objective understanding of the different emotional worlds between men and women.
Subject(s)
Adolescent , Female , Humans , Male , Aggression , Electrocardiography , Electroencephalography , Frontal Lobe , Heart RateABSTRACT
The olfactory system can detect many odorants with high sensitivity and selectivity based on the expression of nearly a thousand types of olfactory receptors (ORs) in olfactory receptor neurons (ORNs). These ORs have a dynamic odorant detection range and contribute to signal encoding processes in the olfactory bulb (OB). To harness the capabilities of the olfactory system and develop a biomimetic sensor, stable culture and maintenance of ORNs are required. However, in vitro monolayer culture models have several key limitations: i) short available period of cultured neurons, ii) low cultural efficiency, and iii) long-term storage challenges. This study aims to develop a technique: i) to support the spheroid culture of primary ORN precursors facilitating stable maintenance and long-term storage, and ii) to demonstrate the viability of ORN spheroid culture in developing an olfactory system mimetic bioelectronic nose. Recombinant protein (REP; TGPG[VGRGD(VGVPG)₆]₂₀WPC) was used to form the ORN spheroids. Spheroid formation enabled preservation of primary cultured ORNs without a significant decrease in viability or the expression of stemness markers for ten days. Physiological characteristics of the ORNs were verified by monitoring intracellular calcium concentration upon odorant mixture stimulation; response upon odorant stimulation were observed at least for ten days in these cultivated ORNs differentiated from spheroids. Coupling ORNs with multi electrode array (MEA) enabled the detection and discrimination of odorants by analyzing the electrical signal patterns generated following odorant stimulation. Taken together, the ORN spheroid culture process is a promising technique for the development of a bioelectronic nose and high-throughput odorant screening device.
Subject(s)
Biomimetics , Calcium , Discrimination, Psychological , Electrodes , In Vitro Techniques , Mass Screening , Neurons , Nose , Odorants , Olfactory Bulb , Olfactory Receptor NeuronsABSTRACT
BACKGROUND: Reperfusion in ischemia is believed to generate cytotoxic oxidative stress, which mediates reperfusion injury. These stress conditions can initiate lipid peroxidation and damage to proteins, as well as promote DNA strand breaks. As biliverdin and bilirubin produced by heme oxygenase isoform 1 (HO-1) have antioxidant properties, the production of both antioxidants by HO-1 may help increase the resistance of the ischemic brain to oxidative stress. In the present study, the survival effect of HO-1 was confirmed using hemin. METHODS: To confirm the roles of HO-1, carbon monoxide, and cyclic guanosine monophosphate further in the antioxidant effect of HO-1 and bilirubin, cells were treated with cycloheximide, desferoxamine, and zinc deuteroporphyrin IX 2,4 bis glycol, respectively. RESULTS: HO-1 itself acted as an antioxidant. Furthermore, iron, rather than carbon monoxide, was involved in the HO-1-mediated survival effect. HO-1 activity was also important in providing bilirubin as an antioxidant. CONCLUSION: Our results suggested that HO-1 helped to increase the resistance of the ischemic brain to oxidative stress.
Subject(s)
Animals , Rats , Antioxidants , Bilirubin , Biliverdine , Brain , Carbon Monoxide , Cycloheximide , DNA , Guanosine Monophosphate , Heme , Heme Oxygenase (Decyclizing) , Hemin , Iron , Ischemia , Lipid Peroxidation , Microvessels , Oxidative Stress , Oxygen , Oxygenases , Reperfusion , Reperfusion Injury , ZincABSTRACT
Apoptosis inducing factor (AIF) has been proposed to act as a putative reactive oxygen species scavenger in mitochondria. When apoptotic cell death is triggered, AIF translocates to the nucleus, where it leads to nuclear chromatin condensation and large-scale DNA fragmentation which result in caspase-independent neuronal death. We performed this study to investigate the possibility that, in addition to caspase-dependent neuronal death, AIF induced neuronal death could be a cause of neuronal death in Alzheimer's disease (AD). We have found that AIF immunoreactivity was increased in the hippocampal pyramidal neurons in the Alzheimer brains compared to those of healthy, age-matched control brains. Nuclear AIF immunoreactivity was detected in the apoptotic pyramidal CA1 neurons at the early stage of AD and CA2 at the advanced stage. Nuclear AIF positive neurons were also observed in the amygdala and cholinergic neurons of the basal forebrain (BFCN) from the early stages of AD. The results of this study imply that AIF-induced apoptosis may contribute to neuronal death within the hippocampus, amygdala, and BFCN in early of AD.
Subject(s)
Alzheimer Disease , Amygdala , Apoptosis , Apoptosis Inducing Factor , Brain , Cell Death , Cholinergic Neurons , Chromatin , DNA Fragmentation , Hippocampus , Mitochondria , Neurons , Prosencephalon , Reactive Oxygen SpeciesABSTRACT
In rodents, the circumvallate papilla (CVP), with its underlying minor salivary gland, the von Ebners' gland (VEG), is located on the dorsal surface of the posterior tongue. Detailed morphological processes to form the proper structure of CVP and VEG have not been properly elucidated. In particular, the specific localization patterns of taste buds in CVP and the branching formation of VEG have not yet been elucidated. To understand the developmental mechanisms underlying CVP and VEG formation, detailed histological observations of CVP and VEG were examined using a three-dimensional computer-aided reconstruction method with serial histological sections and pan-Cytokeratins immunostainings. In addition, to define the developmental processes in CVP and VEG formation, we examined nerve innervations and cell proliferation using microinjections of AM1-43 and immunostainings with various markers, including phosphoinositide 3-kinase, Ki-67, PGP9.5, and Ulex europaeus agglutinin 1 (UEA1). Results revealed specific morphogenesis of CVP and VEG with nerve innervations patterns, evaluated by the coincided localization patterns of AM1-43 and UEA1. Based on these morphological and immunohistochemical results, we suggest that nerve innervations and cell proliferations play important roles in the positioning of taste buds in CVP and branching morphogenesis of VEG in tongue development.