Dysfunction of Orbitofrontal GABAergic Interneurons Leads to Impaired Reversal Learning in a Mouse Model of Obsessive-Compulsive Disorder.

Cognitive inflexibility is a cardinal symptom of obsessive-compulsive disorder (OCD) and often manifests as impaired reversal learning. Abnormal recruitment of the orbitofrontal cortex (OFC)-striatal circuit is implicated in reversal learning deficits in patients with OCD. However, the precise circuitry mechanism underlying normal and impaired reversal learning remains elusive.

Lateral orbitofrontal dysfunction in the Sapap3 knockout mouse model of obsessive–compulsive disorder.

Background: Obsessive–compulsive disorder (OCD) is a common psychiatric disorder that affects about 2% of the population, but the underlying neuropathophysiology of OCD is not well understood. Although increasing lines of evidence implicate dysfunction of the orbitofrontal cortex (OFC) in OCD, a detailed understanding of the functional alterations in different neuronal types in the OFC is still elusive.

Methods: We investigated detailed activity pattern changes in putative pyramidal neurons and interneurons, as well as local field potential oscillations, in the lateral OFC underlying OCD-relevant phenotypes.

SAPAP4 Deletion Causes Synaptic Dysfunction in the nucleus accumbens.

SAP90/PSD95-associated proteins (SAPAPs) are one type of scaffold protein in the postsynaptic density (PSD). Scaffold proteins play an important role in synaptic function. Recently, many studies have shown that mutations associated with scaffold proteins cause dysfunction in neuronal circuitry and in behavior.

Neuronal activity pattern defects in the striatum in awake mouse model of Parkinson's disease.

Previous studies showed the loss of dopaminergic neurons directly leads to both changes in firing rate and neuronal synchrony in the striatum by pharmacogenetic approach, but physiological observation of striatal neurons in awake animal is rare up to now due to the limitation of recording methods. We use multichannel in vivo recording system, to record the activity pattern of both medium spiny projecting neurons (MSNs) and fast spiking interneurons (FSIs) in awake mouse model of Parkinson's disease (PD), created by injection of 6-hydroxyl-dopamine (6-OHDA) into dorsolateral striatum bilaterally and unilaterally. The abnormal discharge of neurons, including oscillations, burst activity and firing rate were systematically observed, and we used these index together to comprehensively analyse the functional change of striatal neurons in PD mouse model.

Axon guidance pathways served as common targets for human speech/language evolution and related disorders.

Human and several nonhuman species share the rare ability of modifying acoustic and/or syntactic features of sounds produced, i.e. vocal learning, which is the important neurobiological and behavioral substrate of human speech/language.

Fusion of Ssm6a with a protein scaffold retains selectivity on Na 1.7 and improves its therapeutic potential against chronic pain.

Voltage-gated sodium channel Na 1.7 serves as an attractive target for chronic pain treatment. Several venom peptides were found to selectively inhibit Na 1.

Manipulation of a central auditory representation shapes learned vocal output.

Learned vocalizations depend on the ear's ability to monitor and ultimately instruct the voice. Where is auditory feedback processed in the brain, and how does it modify motor networks for learned vocalizations? Here we addressed these questions using singing-triggered microstimulation and chronic recording methods in the singing zebra finch, a small songbird that relies on auditory feedback to learn and maintain its species-typical vocalizations. Manipulating the singing-related activity of feedback-sensitive thalamic neurons subsequently triggered vocal plasticity, constraining the central pathway and functional mechanisms through which feedback-related information shapes vocalization.

Synaptic integration of olfactory information in mouse anterior olfactory nucleus.

Individual odorants activate only a small fraction of mitral cells in the mouse main olfactory bulb (MOB). Odor mixtures are represented by a combination of activated mitral cells, forming reproducible activation maps in the olfactory bulb. However, how the activation of a cohort of narrowly tuned mitral cells by odor mixtures is read out synaptically by neurons in higher-level olfactory structures, such as the anterior olfactory nucleus (AON), is mostly unknown.