Mitral/tufted cells (M/TCs) form complex local circuits with interneurons in the olfactory bulb and are powerfully inhibited by these interneurons. The horizontal limb of the diagonal band of Broca (HDB), the only GABAergic/inhibitory source of centrifugal circuit with the olfactory bulb, is known to target olfactory bulb interneurons, and we have shown targeting also to olfactory bulb glutamatergic neurons in vitro. However, the net efficacy of these circuits under different patterns of activation in vivo and the relative balance between the various targeted intact local and centrifugal circuits was the focus of this study. Here channelrhodopsin-2 (ChR2) was expressed in HDB GABAergic neurons to investigate the short-term plasticity of HDB-activated disinhibitory rebound excitation of M/TCs. Optical activation of HDB interneurons increased spontaneous M/TC firing without odor presentation and increased odor-evoked M/TC firing. HDB activation induced disinhibitory rebound excitation (burst or cluster of spiking) in all classes of M/TCs. This excitation was frequency dependent, with short-term facilitation only at higher HDB stimulation frequency (5 Hz and above). However, frequency-dependent HDB regulation was more potent in the deeper layer M/TCs compared with more superficial layer M/TCs. In all neural circuits the balance between inhibition and excitation in local and centrifugal circuits plays a critical functional role, and this patterned input-dependent regulation of inhibitory centrifugal inputs to the olfactory bulb may help maintain the precise balance across the populations of output neurons in different environmental odors, putatively to sharpen the enhancement of tuning specificity of individual or classes of M/TCs to odors.NEW & NOTEWORTHY Neuronal local circuits in the olfactory bulb are modulated by centrifugal long circuits. In vivo study here shows that inhibitory horizontal limb of the diagonal band of Broca (HDB) modulates all five types of mitral/tufted cells (M/TCs), by direct inhibitory circuits HDB → M/TCs and indirect disinhibitory long circuits HDB → interneurons → M/TCs. The HDB net effect exerts excitation in all types of M/TCs but more powerful in deeper layer output neurons as HDB activation frequency increases, which may sharpen the tuning specificity of classes of M/TCs to odors during sensory processing.

Mouse auditory cortex is composed of six sub-fields: primary auditory field (AI), secondary auditory field (AII), anterior auditory field (AAF), insular auditory field (IAF), ultrasonic field (UF) and dorsoposterior field (DP). Previous studies have examined thalamo-cortical connections in the mice auditory system and learned that AI, AAF, and IAF receive inputs from the ventral division of the medial geniculate body (MGB). However, the functional and thalamo-cortical connections between nonprimary auditory cortex (AII, UF, and DP) is unclear. In this study, we examined the locations of neurons projecting to these three cortical sub-fields in the MGB, and addressed the question whether these cortical sub-fields receive inputs from different subsets of MGB neurons or common. To examine the distributions of projecting neurons in the MGB, retrograde tracers were injected into the AII, UF, DP, after identifying these areas by the method of Optical Imaging. Our results indicated that neuron cells which in ventral part of dorsal MGB (MGd) and that of ventral MGB (MGv) projecting to UF and AII with less overlap. And DP only received neuron projecting from MGd. Interestingly, these three cortical areas received input from distinct part of MGd and MGv in an independent manner. Based on our foundings these three auditory cortical sub-fields in mice may independently process auditory information.

Parkinson\'s disease (PD) is a progressive neurodegenerative disease with a global burden that affects more often in the elderly. The basal ganglia (BG) is believed to account for movement disorders in PD. More recently, new findings in the original regions in BG involved in motor control, as well as the new circuits or new nucleuses previously not specifically considered were explored. In the present review, we provide up-to-date information related to movement disorders and modulations in PD, especially from the perspectives of brain regions and neuronal circuits. Meanwhile, there are updates in deep brain stimulation (DBS) and other factors for the motor improvement in PD. Comprehensive understandings of brain regions and neuronal circuits involved in motor control could benefit the development of novel therapeutical strategies in PD.

The prefrontal cortex (PFC) is well known as the executive center of the brain, combining internal states and goals to execute purposeful behavior, including social actions. With the advancement of tools for monitoring and manipulating neural activity in rodents, substantial progress has been made in understanding the specific cell types and neural circuits within the PFC that are essential for processing social cues and influencing social behaviors. Furthermore, combining these tools with translationally relevant behavioral paradigms has also provided novel insights into the PFC neural mechanisms that may contribute to social deficits in various psychiatric disorders. This review highlights findings from the past decade that have shed light on the PFC cell types and neural circuits that support social information processing and distinct aspects of social behavior, including social interactions, social memory, and social dominance. We also explore how the PFC contributes to social deficits in rodents induced by social isolation, social fear conditioning, and social status loss. These studies provide evidence that the PFC uses both overlapping and unique neural mechanisms to support distinct components of social cognition. Furthermore, specific PFC neural mechanisms drive social deficits induced by different contexts.

Predictive processing is a computational framework that aims to explain how the brain processes sensory information by making predictions about the environment and minimizing prediction errors. It can also be used to explain some of the key symptoms of psychotic disorders such as schizophrenia. In recent years, substantial advances have been made in our understanding of the neuronal circuitry that underlies predictive processing in cortex. In this review, we summarize these findings and how they might relate to psychosis and to observed cell type-specific effects of antipsychotic drugs. We argue that quantifying the effects of antipsychotic drugs on specific neuronal circuit elements is a promising approach to understanding not only the mechanism of action of antipsychotic drugs but also psychosis. Finally, we outline some of the key experiments that should be done. The aims of this review are to provide an overview of the current circuit-based approaches to psychosis and to encourage further research in this direction.

The auditory midbrain, also known as the inferior colliculus (IC), serves as a crucial hub in the auditory pathway. Comprising diverse cell types, the IC plays a pivotal role in various auditory functions, including sound localization, auditory plasticity, sound detection, and sound-induced behaviors. Notably, the IC is implicated in several auditory central disorders, such as tinnitus, age-related hearing loss, autism and Fragile X syndrome. Accurate classification of IC neurons is vital for comprehending both normal and dysfunctional aspects of IC function. Various parameters, including dendritic morphology, neurotransmitter synthesis, potassium currents, biomarkers, and axonal targets, have been employed to identify distinct neuron types within the IC. However, the challenge persists in effectively classifying IC neurons into functional categories due to the limited clustering capabilities of most parameters. Recent studies utilizing advanced neuroscience technologies have begun to shed light on biomarker-based approaches in the IC, providing insights into specific cellular properties and offering a potential avenue for understanding IC functions. This review focuses on recent advancements in IC research, spanning from neurons and neural circuits to aspects related to auditory diseases.

Temperature has a significant effect on all physiological processes of animals. Suitable temperatures promote responsiveness, movement, metabolism, growth, and reproduction in animals, whereas extreme temperatures can cause injury or even death. Thus, thermosensation is important for survival in all animals. However, mechanisms regulating thermosensation remain unexplored, mostly because of the complexity of mammalian neural circuits. The fruit fly Drosophila melanogaster achieves a desirable body temperature through ambient temperature fluctuations, sunlight exposure, and behavioral strategies. The availability of extensive genetic tools and resources for studying Drosophila have enabled scientists to unravel the mechanisms underlying their temperature preference. Over the past 20 years, Drosophila has become an ideal model for studying temperature-related genes and circuits. This review provides a comprehensive overview of our current understanding of thermosensation and temperature preference in Drosophila. It encompasses various aspects, such as the mechanisms by which flies sense temperature, the effects of internal and external factors on temperature preference, and the adaptive strategies employed by flies in extreme-temperature environments. Understanding the regulating mechanisms of thermosensation and temperature preference in Drosophila can provide fundamental insights into the underlying molecular and neural mechanisms that control body temperature and temperature-related behavioral changes in other animals.

The disconnection of neuronal circuitry through synaptic loss is presumed to be a major driver of age-related cognitive decline. Age-related cognitive decline is heterogeneous, yet whether genetic mechanisms differentiate successful from unsuccessful cognitive decline through maintenance or vulnerability of synaptic connections remains unknown. Previous work using rodent and primate models leveraged various techniques to imply that age-related synaptic loss is widespread on pyramidal cells in prefrontal cortex (PFC) circuits but absent on those in area CA1 of the hippocampus. Here, we examined the effect of aging on synapses on projection neurons forming a hippocampal-cortico-thalamic circuit important for spatial working memory tasks from two genetically distinct mouse strains that exhibit susceptibility (C57BL/6J) or resistance (PWK/PhJ) to cognitive decline during aging. Across both strains, synapse density on CA1-to-PFC projection neurons appeared completely intact with age. In contrast, we found synapse loss on PFC-to-nucleus reuniens (RE) projection neurons from aged C57BL/6J but not PWK/PhJ mice. Moreover, synapses from aged PWK/PhJ mice but not from C57BL/6J exhibited altered morphologies that suggest increased efficiency to drive depolarization in the parent dendrite. Our findings suggest resistance to age-related cognitive decline results in part by age-related synaptic adaptations, and identification of these mechanisms in PWK/PhJ mice could uncover new therapeutic targets for promoting successful cognitive aging and extending human health span.

An implicit tenet of the alcohol use disorder (AUD) research field is that knowledge of how alcohol interacts with the brain is critical to the development of an understanding of vulnerability to AUD and treatment approaches. Gaining this understanding requires the mapping of brain function critical to specific components of this heterogeneous disorder. Early approaches in humans and animal models focused on the determination of specific brain regions sensitive to alcohol action and their participation in AUD-relevant behaviors. Broadly speaking, this research has focused on three domains, Binge/Intoxication, Negative Affect/Withdrawal, and Preoccupation/Anticipation, with a number of regions identified as participating in each. With the generational advances in technologies that the field of neuroscience has undergone over the last two decades, this focus has shifted to a circuit-based analysis. A wealth of new data has sharpened the field\'s focus on the specific roles of the interconnectivity of multiple brain regions in AUD and AUD-relevant behaviors, as well as demonstrating that the three major domains described above have much fuzzier edges than originally thought.In this chapter, we very briefly review brain regions previously implicated in aspects of AUD-relevant behavior from animal model research. Next, we move to a more in-depth overview of circuit-based approaches, and the utilization of these approaches in current AUD research.

The brain is a remarkably complex organ responsible for a wide range of functions, including the modulation of emotional states and movement. Neuronal circuits are believed to play a crucial role in integrating sensory, cognitive, and emotional information to ultimately guide motor behavior. Over the years, numerous studies employing diverse techniques such as electrophysiology, imaging, and optogenetics have revealed a complex network of neural circuits involved in the regulation of emotional or motor processes. Emotions can exert a substantial influence on motor performance, encompassing both everyday activities and pathological conditions. The aim of this review is to explore how emotional states can shape movements by connecting the neural circuits for emotional processing to motor neural circuits. We first provide a comprehensive overview of the impact of different emotional states on motor control in humans and rodents. In line with behavioral studies, we set out to identify emotion-related structures capable of modulating motor output, behaviorally and anatomically. Neuronal circuits involved in emotional processing are extensively connected to the motor system. These circuits can drive emotional behavior, essential for survival, but can also continuously shape ongoing movement. In summary, the investigation of the intricate relationship between emotion and movement offers valuable insights into human behavior, including opportunities to enhance performance, and holds promise for improving mental and physical health. This review integrates findings from multiple scientific approaches, including anatomical tracing, circuit-based dissection, and behavioral studies, conducted in both animal and human subjects. By incorporating these different methodologies, we aim to present a comprehensive overview of the current understanding of the emotional modulation of movement in both physiological and pathological conditions.