scholarly journals Gated feedforward inhibition in the frontal cortex releases goal-directed action

2020 ◽  
Author(s):  
Jae-Hyun Kim ◽  
Dong-Hyun Ma ◽  
Eunji Jung ◽  
Ilsong Choi ◽  
Seung-Hee Lee
Keyword(s):  
Frontal Cortex ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Anterior Cingulate ◽  
Network Activity ◽  
Striatal Neurons ◽  
Strong Suppression ◽  
Directed Action ◽  
Feedforward Inhibition ◽  
Motor Signals

Cortical circuits process sensory information and generate motor signals in animals performing perceptual tasks. However, it is still unclear how sensory inputs generate motor signals in the cortex to initiate goal-directed action. Here, we identified a visual-to-motor inhibitory circuit in the anterior cingulate cortex (ACC) that induced action initiation in mice performing visual Go/No-go tasks. Interestingly, higher activity in sensory neurons and faster suppression in motor neurons of the ACC predicted faster reaction times. Notably, optogenetic activation of visual inputs in the ACC evoked strong suppression of neighboring motor neurons by activating fast-spiking sensory neurons and drove task-relevant actions in mice via activating striatal neurons. Finally, the ACC network activity maintained low during spontaneous and perceptual actions and increased during action cancellation in response to the stop signals. Collectively, our data demonstrate that visual salience in the frontal cortex exerts gated feedforward inhibition to release goal-directed actions.

scholarly journals Gated feedforward inhibition in the frontal cortex releases goal-directed action

2021 ◽  
Author(s):  
Jae-Hyun Kim ◽  
Dong-Hyun Ma ◽  
Eunji Jung ◽  
Ilsong Choi ◽  
Seung-Hee Lee
Keyword(s):  
Frontal Cortex ◽  
Directed Action ◽  
Feedforward Inhibition

scholarly journals Correlation between Traits of Emotion-Based Impulsivity and Intrinsic Default-Mode Network Activity

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Jizheng Zhao ◽  
Dardo Tomasi ◽  
Corinde E. Wiers ◽  
Ehsan Shokri-Kojori ◽  
Şükrü B. Demiral ◽  
...  
Keyword(s):  
Brain Activity ◽  
Low Frequency ◽  
Cingulate Cortex ◽  
Posterior Cingulate Cortex ◽  
Anterior Cingulate ◽  
Network Activity ◽  
High Risk Behaviors ◽  
Posterior Cingulate ◽  
Healthy Humans ◽  
Dorsolateral Prefrontal

Negative urgency (NU) and positive urgency (PU) are implicated in several high-risk behaviors, such as eating disorders, substance use disorders, and nonsuicidal self-injury behavior. The current study aimed to explore the possible link between trait of urgency and brain activity at rest. We assessed the amplitude of low-frequency fluctuations (ALFF) of the resting-state functional magnetic resonance imaging (fMRI) signal in 85 healthy volunteers. Trait urgency measures were related to ALFF in the lateral orbitofrontal cortex, dorsolateral prefrontal cortex, ventral and dorsal medial frontal cortex, anterior cingulate, and posterior cingulate cortex/precuneus. In addition, trait urgency measures showed significant correlations with the functional connectivity of the posterior cingulate cortex/precuneus seed with the thalamus and midbrain region. These findings suggest an association between intrinsic brain activity and impulsive behaviors in healthy humans.

Connections between thoraco-coxal proprioceptive afferents and motor neurons in the locust

2000 ◽  
Vol 203 (3) ◽  
pp. 435-445
Author(s):  
M. Wildman
Keyword(s):  
Electrical Stimulation ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Chordotonal Organ ◽  
Synaptic Connections ◽  
Afferent Neurons ◽  
Postsynaptic Potentials ◽  
The Common ◽  
Proprioceptive Afferents ◽  
Stimulation Of

The position of the coxal segment of the locust hind leg relative to the thorax is monitored by a variety of proprioceptors, including three chordotonal organs and a myochordotonal organ. The sensory neurons of two of these proprioceptors, the posterior joint chordotonal organ (pjCO) and the myochordotonal organ (MCO), have axons in the purely sensory metathoracic nerve 2C (N2C). The connections made by these afferents with metathoracic motor neurons innervating thoraco-coxal and wing muscles were investigated by electrical stimulation of N2C and by matching postsynaptic potentials in motor neurons with afferent spikes in N2C. Stretch applied to the anterior rotator muscle of the coxa (M121), with which the MCO is associated, evoked sensory spikes in N2C. Some of the MCO afferent neurons make direct excitatory chemical synaptic connections with motor neurons innervating the thoraco-coxal muscles M121, M126 and M125. Parallel polysynaptic pathways via unidentified interneurons also exist between MCO afferents and these motor neurons. Connections with the common inhibitor 1 neuron and motor neurons innervating the thoraco-coxal muscles M123/4 and wing muscles M113 and M127 are polysynaptic. Afferents of the pjCO also make polysynaptic connections with motor neurons innervating thoraco-coxal and wing muscles, but no evidence for monosynaptic pathways was found.

The role of interneurons in controlling the tail-withdrawal reflex in Aplysia: a network model

1993 ◽  
Vol 70 (5) ◽  
pp. 1777-1786 ◽  
Author(s):  
J. A. White ◽  
I. Ziv ◽  
L. J. Cleary ◽  
D. A. Baxter ◽  
J. H. Byrne
Keyword(s):  
Synaptic Plasticity ◽  
Sensory Neurons ◽  
Network Model ◽  
Motor Neurons ◽  
Excitatory Postsynaptic Potential ◽  
Layer Model ◽  
Neural Network Models ◽  
Plastic Properties ◽  
Withdrawal Reflex ◽  
Long Duration

1. The contributions of monosynaptic and polysynaptic circuitry to the tail-withdrawal reflex in the marine mollusk Aplysia californica were assessed by the use of physiologically based neural network models. Effects of monosynaptic circuitry were examined by the use of a two-layer network model with four sensory neurons in the input layer and one motor neuron in the output layer. Results of these simulations indicated that the monosynaptic circuit could not account fully for long-duration responses of tail motor neurons elicited by tail stimulation. 2. A three-layer network model was constructed by interposing a layer of two excitatory interneurons between the input and output layers of the two-layer network model. These interneurons had properties mimicking those of the recently described interneuron LP117, receiving excitatory input from pleural sensory neurons and evoking a biphasic excitatory postsynaptic potential (EPSP) in pedal motor neurons (Cleary and Byrne 1993). The three-layer model could account for long-duration responses in motor neurons. 3. Sensory neurons are a known site of plasticity in Aplysia. Synaptic plasticity was incorporated into the three-layer model by altering the magnitudes of conductance changes evoked in motor neurons and interneurons by presynaptic sensory neurons. In these simulations the excitatory interneurons converted an amplitude-coded input into an amplitude- and duration-coded output, allowing the three-layer network to support a large range of output amplitudes and durations. 4. Synaptic plasticity at more than one locus modified dramatically the input-output relationship of the three-layer network model. This feature gave the model redundancy in its plastic properties and points to the possibility of distributed memory in the circuitry mediating withdrawal reflexes in Aplysia. Multiple sites of control over the response of the network would likely allow a more diverse repertoire of responses.

Sensitization of the gill and siphon withdrawal reflex of Aplysia: multiple sites of change in the neuronal network

1993 ◽  
Vol 70 (3) ◽  
pp. 1210-1220 ◽  
Author(s):  
L. E. Trudeau ◽  
V. F. Castellucci
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Neuronal Network ◽  
Feedback Inhibition ◽  
Excitatory Input ◽  
Major Mechanism ◽  
Withdrawal Reflex ◽  
The Difference ◽  
Central Synapses

1. Recent studies have emphasized the major contribution of interneuronal transmission to the mediation and learning-associated modulation of the gill and siphon withdrawal (GSW) reflex of Aplysia. We wish to provide more direct support for the hypothesis that inhibitory junctions are crucial sites of plasticity. 2. In parallel experiments we investigated modulation at five major sites of synaptic transmission in the GSW network: 1) from sensory neurons to motor neurons, 2) from sensory neurons to excitatory interneurons (INTs+) 3) from INTs+ to motor neurons (MNs), 4) from inhibitory interneurons (INTs-) to INTs+, and 5) from INTs+ to INTs-. 3. While recording simultaneously from a single sensory neuron of the LE cluster, an INT+, and a MN, we found that both LE-MN and LE-INTs+ synapses were facilitated by the activation of modulator neurons by stimulation of the left pleuroabdominal connective (185 and 93%, respectively) as well as by serotonin (5-HT) (191 and 84%). Junctions of the second type were therefore less facilitated. The difference in the magnitude of facilitation at these two sites is an indication of a branch-specific, differential efficacy in the modulation of different central synapses made by a single neuron. 4. Although INT(+)-MN junctions have the capacity to display marked posttetanic potentiation, they are not significantly potentiated after connective stimulation. Sensitization of the GSW reflex is therefore not necessarily accompanied by a modification of transmission at these synapses. 5. Inhibitory transmission to INTs+ is significantly reduced by connective stimulation (36%) and by 5-HT (71%). This supports the hypothesis that a reduction of feedback inhibition into INTs+ is a major mechanism of reflex sensitization and may account for the increased evoked firing of INTs+ that is observed after connective stimulation. 6. The excitatory input to INTs- is selectively decreased by 5-HT (50%) and by the molluscan neuropeptide small cardioactive peptide B (38%). This latter effect, which could produce disinhibition of INTs+, may explain the previous observation that this peptide is able to potentiate the evoked input to MNs of the reflex at a concentration (1 microM) that fails to modify monosynaptic sensory-motor transmission. 7. These results indicate that transmission through a small neuronal network that mediates a withdrawal reflex in Aplysia may be modulated at multiple sites and by different mechanisms. These mechanisms include: 1) branch-specific facilitation of sensory neuron outputs and 2) inhibition of INT(-)-INT+ inhibitory postsynaptic potentials by endogenous modulatory neurons and by 5-HT.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Adenosine Kinase Expression in the Frontal Cortex in Schizophrenia

2019 ◽  
Vol 46 (3) ◽  
pp. 690-698
Author(s):  
Cassidy L Moody ◽  
Adam J Funk ◽  
Emily Devine ◽  
Ryan C Devore Homan ◽  
Detlev Boison ◽  
...  
Keyword(s):  
Protein Expression ◽  
Frontal Cortex ◽  
Splice Variant ◽  
Adenosine Kinase ◽  
Anterior Cingulate ◽  
Gene And Protein Expression ◽  
Significant Difference ◽  
Dorsolateral Prefrontal ◽  
Kinase Expression ◽  
Short Splice Variant

Abstract The adenosine hypothesis of schizophrenia posits that reduced availability of the neuromodulator adenosine contributes to dysregulation of dopamine and glutamate transmission and the symptoms associated with schizophrenia. It has been proposed that increased expression of the enzyme adenosine kinase (ADK) may drive hypofunction of the adenosine system. While animal models of ADK overexpression support such a role for altered ADK, the expression of ADK in schizophrenia has yet to be examined. In this study, we assayed ADK gene and protein expression in frontocortical tissue from schizophrenia subjects. In the dorsolateral prefrontal cortex (DLPFC), ADK-long and -short splice variant expression was not significantly altered in schizophrenia compared to controls. There was also no significant difference in ADK splice variant expression in the frontal cortex of rats treated chronically with haloperidol-decanoate, in a study to identify the effect of antipsychotics on ADK gene expression. ADK protein expression was not significantly altered in the DLPFC or anterior cingulate cortex (ACC). There was no significant effect of antipsychotic medication on ADK protein expression in the DLPFC or ACC. Overall, our results suggest that increased ADK expression does not contribute to hypofunction of the adenosine system in schizophrenia and that alternative mechanisms are involved in dysregulation of this system in schizophrenia.

scholarly journals Depression Is Associated With Preserved Cortical Thickness Relative to Apathy in Frontotemporal Dementia

2020 ◽  
pp. 089198872096425
Author(s):  
Rakshathi Basavaraju ◽  
Xinyang Feng ◽  
Jeanelle France ◽  
Edward D. Huey ◽  
Frank A. Provenzano
Keyword(s):  
Neurodegenerative Disease ◽  
Frontal Cortex ◽  
Frontotemporal Dementia ◽  
Cortical Thickness ◽  
Gray Matter ◽  
Anterior Cingulate ◽  
Parietal Lobes ◽  
Neuroimaging Data ◽  
Rostral Anterior Cingulate Cortex ◽  
The Right

Objectives: To understand the differential neuroanatomical substrates underlying apathy and depression in Frontotemporal dementia (FTD). Methods: T1-MRIs and clinical data of patients with behavioral and aphasic variants of FTD were obtained from an open database. Cortical thickness was derived, its association with apathy severity and difference between the depressed and not depressed were examined with appropriate covariates. Results: Apathy severity was significantly associated with cortical thinning of the lateral parts of the right sided frontal, temporal and parietal lobes. The right sided orbitofrontal, parsorbitalis and rostral anterior cingulate cortex were thicker in depressed compared to patients not depressed. Conclusions: Greater thickness of right sided ventromedial and inferior frontal cortex in depression compared to patients without depression suggests a possible requisite of gray matter in this particular area for the manifestation of depression in FTD. This study demonstrates a method for deriving neuroanatomical patterns across non-harmonized neuroimaging data in a neurodegenerative disease.

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