scholarly journals IDENTIFICATION OF A NOVEL BDNF-SPECIFIC CORTICOSTRIATAL CIRCUITRY

2021 ◽  
Author(s):  
Yann Ehinger ◽  
Drishti Soneja ◽  
Khanhky Phamluong ◽  
Dorit Ron
Keyword(s):  
Motor Cortex ◽  
Orbitofrontal Cortex ◽  
Neural Circuit ◽  
Dorsal Striatum ◽  
Medial Part ◽  
Striatal Neurons ◽  
Bdnf Expression ◽  
Axon Terminals ◽  
Bdnf Signaling

BDNF is released from axon terminals originating in the cerebral cortex onto striatal neurons. Here, we characterized BDNF in the corticostriatal circuitry. First, we utilized Bdnf-Cre and Ribotag transgenic mouse lines to label BDNF-positive cells in the cortex, and detected BDNF expression in the motor cortex, medial prefrontal cortex (mPFC) and the orbitofrontal cortex (OFC). Next, we used a retrograde viral tracing strategy, in combination with Bdnf-Cre knockin mice, to map the cortical outputs of BDNF neurons in the dorsal striatum. We found that the BDNF-positive prefrontal regions differentially project to the dorsal striatum. Specifically, BDNF-expressing neurons located in the mPFC project to both dorsolateral striatum (DLS) and dorsomedial striatum (DMS), and those located in the motor cortex project to the DLS. Surprisingly however, the BDNF-expressing OFC neurons differentially target the dorsal striatum depending on their mediolateral location. Specifically, the DMS is mainly innervated by the medial part of the OFC (mOFC) whereas, the DLS receives projections specifically from the ventrolateral region of the OFC (vlOFC). Next, using an anterograde viral tracing strategy, we confirmed the presence of a BDNF-specific vlOFC-DLS circuit. Finally, we show that overexpression of BDNF in the vlOFC activates TrkB signaling specifically in the DLS but not in the DMS demonstrating the functionality of this circuit. Our study uncovers a previously unknown neural circuit composed of BDNF-positive vlOFC neurons projecting to the DLS. These findings could have important implications for the role of BDNF signaling in the OFC as well as in other corticostriatal circuitries.

The Neural Substrates of In-Group Bias

2008 ◽  
Vol 19 (11) ◽  
pp. 1131-1139 ◽  
Author(s):  
Jay J. Van Bavel ◽  
Dominic J. Packer ◽  
William A. Cunningham
Keyword(s):  
Orbitofrontal Cortex ◽  
Dorsal Striatum ◽  
Mixed Race ◽  
Neural Substrates ◽  
Brain Regions ◽  
Functional Magnetic Resonance ◽  
Intergroup Perception ◽  
Amygdala Activity ◽  
Group Members

Classic minimal-group studies found that people arbitrarily assigned to a novel group quickly display a range of perceptual, affective, and behavioral in-group biases. We randomly assigned participants to a mixed-race team and used functional magnetic resonance imaging to identify brain regions involved in processing novel in-group and out-group members independently of preexisting attitudes, stereotypes, or familiarity. Whereas previous research on intergroup perception found amygdala activity—typically interpreted as negativity—in response to stigmatized social groups, we found greater activity in the amygdala, fusiform gyri, orbitofrontal cortex, and dorsal striatum when participants viewed novel in-group faces than when they viewed novel out-group faces. Moreover, activity in orbitofrontal cortex mediated the in-group bias in self-reported liking for the faces. These in-group biases in neural activity were not moderated by race or by whether participants explicitly attended to team membership or race, a finding suggesting that they may occur automatically. This study helps clarify the role of neural substrates involved in perceptual and affective in-group biases.

scholarly journals Role of the orbitofrontal cortex and dorsal striatum in regulating the dose-related effects of self-administered cocaine

2009 ◽  
Vol 201 (1) ◽  
pp. 128-136 ◽  
Author(s):  
Kathleen M. Kantak ◽  
Yasmin Mashhoon ◽  
David N. Silverman ◽  
Amy C. Janes ◽  
Claudia M. Goodrich
Keyword(s):  
Orbitofrontal Cortex ◽  
Dorsal Striatum

scholarly journals Cortical and thalamic influences on striatal involvement in instructed, serial reversal learning; implications for the organisation of flexible behaviour.

2021 ◽  
Author(s):  
Brendan Williams ◽  
Anastasia Christakou
Keyword(s):  
Functional Connectivity ◽  
Cognitive Flexibility ◽  
Reversal Learning ◽  
Orbitofrontal Cortex ◽  
Dorsal Striatum ◽  
Response Strategy ◽  
Flexible Control ◽  
The Right ◽  
Serial Reversal

Cognitive flexibility is essential for enabling an individual to respond adaptively to changes in their environment. Evidence from human and animal research suggests that the control of cognitive flexibility is dependent on an array of neural architecture. Cortico-basal ganglia circuits have long been implicated in cognitive flexibility. In particular, the role of the striatum is pivotal, acting as an integrative hub for inputs from the prefrontal cortex and thalamus, and modulation by dopamine and acetylcholine. Striatal cholinergic modulation has been implicated in the flexible control of behaviour, driven by input from the centromedian-parafascicular nuclei of the thalamus. However, the role of this system in humans is not clearly defined as much of the current literature is based on animal work. Here, we aim to investigate the roles corticostriatal and thalamostriatal connectivity in serial reversal learning. Functional connectivity between the left centromedian-parafascicular nuclei and the associative dorsal striatum was significantly increased for negative feedback compared to positive feedback. Similar differences in functional connectivity were observed for the right lateral orbitofrontal cortex, but these were localised to when participants switched to using an alternate response strategy following reversal. These findings suggest that connectivity between the centromedian-parafascicular nuclei and the striatum may be used to generally identify potential changes in context based on negative outcomes, and the effect of this signal on striatal output may be influenced by connectivity between the lateral orbitofrontal cortex and the striatum.

scholarly journals Role of Individual Basal Ganglia Nuclei in Force Amplitude Generation

2007 ◽  
Vol 98 (2) ◽  
pp. 821-834 ◽  
Author(s):  
Matthew B. Spraker ◽  
Hong Yu ◽  
Daniel M. Corcos ◽  
David E. Vaillancourt
Keyword(s):  
Basal Ganglia ◽  
Motor Cortex ◽  
Globus Pallidus ◽  
Neural Circuit ◽  
Activation Volume ◽  
Force Amplitude ◽  
Percent Signal Change ◽  
Signal Change ◽  
Increased Activity

The basal ganglia-thalamo-cortical loop is an important neural circuit that regulates motor control. A key parameter that the nervous system regulates is the level of force to exert against an object during tasks such as grasping. Previous studies indicate that the basal ganglia do not exhibit increased activity with increasing amplitude of force, although these conclusions are based mainly on the putamen. The present study used functional magnetic resonance imaging to investigate which regions in the basal ganglia, thalamus, and motor cortex display increased activity when producing pinch-grip contractions of increasing force amplitude. We found that the internal portion of the globus pallidus (GPi) and subthalamic nucleus (STN) had a positive increase in percent signal change with increasing force, whereas the external portion of the globus pallidus, anterior putamen, posterior putamen, and caudate did not. In the thalamus we found that the ventral thalamic regions increase in percent signal change and activation volume with increasing force amplitude. The contralateral and ipsilateral primary motor/somatosensory (M1/S1) cortices had a positive increase in percent signal change and activation volume with increasing force amplitude, and the contralateral M1/S1 had a greater increase in percent signal change and activation volume than the ipsilateral side. We also found that deactivation did not change across force in the motor cortex and basal ganglia, but that the ipsilateral M1/S1 had greater deactivation than the contralateral M1/S1. Our findings provide direct evidence that GPi and STN regulate the amplitude of force output. These findings emphasize the heterogeneous role of individual nuclei of the basal ganglia in regulating specific parameters of motor output.

Role of the orbitofrontal cortex and the dorsal striatum in incentive motivation for cocaine

2019 ◽  
Vol 372 ◽  
pp. 112026 ◽  
Author(s):  
Ellie-Anna Minogianis ◽  
Alice Servonnet ◽  
Marie-Pier Filion ◽  
Anne-Noël Samaha
Keyword(s):  
Orbitofrontal Cortex ◽  
Dorsal Striatum ◽  
Incentive Motivation

scholarly journals GABAA presynaptic inhibition regulates the gain and kinetics of retinal output neurons

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Jenna Nagy ◽  
Briana Ebbinghaus ◽  
Mrinalini Hoon ◽  
Raunak Sinha
Keyword(s):  
Presynaptic Inhibition ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Ganglion Cells ◽  
Gain Control ◽  
Light Response ◽  
Mouse Retina ◽  
Axon Terminals ◽  
Kinetics Of

Output signals of neural circuits, including the retina, are shaped by a combination of excitatory and inhibitory signals. Inhibitory signals can act presynaptically on axon terminals to control neurotransmitter release and regulate circuit function. However, it has been difficult to study the role of presynaptic inhibition in most neural circuits due to lack of cell-type specific and receptor-type specific perturbations. In this study, we used a transgenic approach to selectively eliminate GABAA inhibitory receptors from select types of second order neurons - bipolar cells - in mouse retina and examined how this affects the light response properties of the well-characterized ON alpha ganglion cell retinal circuit. Selective loss of GABAA receptor-mediated presynaptic inhibition causes an enhanced sensitivity and slower kinetics of light-evoked responses from ON alpha ganglion cells thus highlighting the role of presynaptic inhibition in gain control and temporal filtering of sensory signals in a key neural circuit in the mammalian retina.

Pax3 induces neural circuit repair through a developmental program of directed axon outgrowth

2021 ◽  
Author(s):  
JS Jara ◽  
HX Avci ◽  
I Kouremenou ◽  
M Doulazmi ◽  
J Bakouche ◽  
...  
Keyword(s):  
Neural Circuit ◽  
Polysialic Acid ◽  
Treatment Strategies ◽  
Axon Outgrowth ◽  
Bdnf Expression ◽  
Axon Terminals ◽  
Developmental Program ◽  
Neural Cell Adhesion ◽  
Neuronal Connections ◽  
Underlying Mechanisms

ABSTRACTAlthough neurotrophins can reorganise surviving neuronal connections after a lesion, clinical improvement is minimal and underlying mechanisms ill-defined, which impedes the development of effective treatment strategies. Here we show that the neurotrophin brain derived neurotrophic factor (BDNF) upregulates the transcription factor Pax3, which in turn induces axon outgrowth and synaptogenesis to repair a neural circuit. This repair depends on Pax3 increasing polysialic acid-neural cell adhesion molecule (PSA-NCAM), which is both essential for, and mediates the amount of, reinnervation. Pax3 acts pre-synaptically: its expression in reinnervating neurons induces significant axonal growth, and Pax3 knockdown abolishes reinnervation induced by BDNF, either endogenous BDNF expression during spontaneous developmental repair, or exogenous BDNF treatment in the mature nervous system. This is a novel role for Pax3. We propose that neuronal Pax3 induces PSA-NCAM expression on axon terminals to increase their motility and outgrowth, thereby promoting neural circuit reorganisation and repair.

scholarly journals Role of the Medial Orbitofrontal Cortex and Ventral Tegmental Area in Effort-Related Responding

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Alexandra Münster ◽  
Angeline Votteler ◽  
Susanne Sommer ◽  
Wolfgang Hauber
Keyword(s):  
Ventral Tegmental Area ◽  
Orbitofrontal Cortex ◽  
Neural Circuit ◽  
Progressive Ratio ◽  
Dopamine Neurons ◽  
Gamma Aminobutyric Acid ◽  
Related Function ◽  
Pharmacological Inhibition ◽  
Ventral Tegmental

Abstract The posterior subdivision of the medial orbitofrontal cortex (mOFC-p) mediates the willingness to expend effort to reach a selected goal. However, the neural circuitry through which the mOFC-p modulates effort-related function is as yet unknown. The mOFC-p projects prominently to the posterior ventral tegmental area (pVTA). Therefore, we analyzed the role of the mOFC-p and interactions with the pVTA in effort-related responding using a combination of behavioral, pharmacological, and neural circuit analysis methods in rats. Pharmacological inhibition of the mOFC-p was found to increase lever pressing for food under a progressive ratio (PR) schedule of reinforcement. These findings provide further support for a modulation of effort-related function by the mOFC-p. Then, we investigated effects of disconnecting the mOFC-p and pVTA on PR responding using unilateral pharmacological inhibition of both areas. This asymmetric intervention was also found to increase PR responding suggesting that the mOFC-p controls effort-related function through interactions with the pVTA. Possibly, a reduced excitatory mOFC-p drive on pVTA gamma-aminobutyric acid (GABA)ergic relays disinhibits VTA dopamine neurons which are known to support PR responding. Collectively, our findings suggest that the mOFC-p and pVTA are key components of a neural circuit mediating the willingness to expend effort to reach a goal.

scholarly journals Stable representation of sounds in the posterior striatum during flexible auditory decisions

2017 ◽  
Author(s):  
Lan Guo ◽  
William I. Walker ◽  
Nicholas D. Ponvert ◽  
Phoebe L. Penix ◽  
Santiago Jaramillo
Keyword(s):  
Discrimination Task ◽  
Sensory Information ◽  
Dorsal Striatum ◽  
Striatal Neurons ◽  
Anterior Dorsal ◽  
Stable Representation ◽  
Direct Input ◽  
Sound Discrimination ◽  
Stimulus Features

AbstractThe neuronal pathways that link sounds to rewarded actions remain elusive. It is unclear whether neurons in the posterior tail of the dorsal striatum (which receive direct input from the auditory system) mediate action selection, as other striatal circuits do. Here, we examined the role of posterior striatal neurons in auditory decisions in mice. We found that, in contrast to the anterior dorsal striatum, activation of the posterior striatum did not elicit systematic movement. However, activation of posterior striatal neurons during sound presentation in an auditory discrimination task biased the animals’ choices, and transient inactivation of these neurons largely impaired sound discrimination. Moreover, the activity of these neurons reliably encoded stimulus features, but was only minimally influenced by the animals’ choices. Our results suggest that posterior striatal neurons play an essential role in auditory decisions, yet these neurons provide sensory information downstream rather than motor commands during well-learned sound-driven tasks.

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