scholarly journals Excitatory synapses and gap junctions cooperate to improve Pv neuronal burst firing and cortical social cognition in Shank2-mutant mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Eunee Lee ◽  
Seungjoon Lee ◽  
Jae Jin Shin ◽  
Woochul Choi ◽  
Changuk Chung ◽  
...  
Keyword(s):  
Social Cognition ◽  
Gap Junctions ◽  
High Frequency ◽  
Autism Spectrum ◽  
Social Representation ◽  
Burst Firing ◽  
Excitatory Synapses ◽  
Nmdar Activation ◽  
Spectrum Disorders ◽  
And Behavior

AbstractNMDA receptor (NMDAR) and GABA neuronal dysfunctions are observed in animal models of autism spectrum disorders, but how these dysfunctions impair social cognition and behavior remains unclear. We report here that NMDARs in cortical parvalbumin (Pv)-positive interneurons cooperate with gap junctions to promote high-frequency (>80 Hz) Pv neuronal burst firing and social cognition. Shank2–/– mice, displaying improved sociability upon NMDAR activation, show impaired cortical social representation and inhibitory neuronal burst firing. Cortical Shank2–/– Pv neurons show decreased NMDAR activity, which suppresses the cooperation between NMDARs and gap junctions (GJs) for normal burst firing. Shank2–/– Pv neurons show compensatory increases in GJ activity that are not sufficient for social rescue. However, optogenetic boosting of Pv neuronal bursts, requiring GJs, rescues cortical social cognition in Shank2–/– mice, similar to the NMDAR-dependent social rescue. Therefore, NMDARs and gap junctions cooperate to promote cortical Pv neuronal bursts and social cognition.

Social Cognition in Children Autism Spectrum Disorders: An Eye Tracking Study

2019 ◽  
Author(s):  
J. Galli ◽  
F. Gitti ◽  
M. Lanaro ◽  
A. Rizzi ◽  
M.A. Pavlova ◽  
...  
Keyword(s):  
Autism Spectrum Disorders ◽  
Social Cognition ◽  
Eye Tracking ◽  
Autism Spectrum ◽  
Spectrum Disorders

Oxytocin and Vasopressin: Mechanisms for Potential Sex Differences Observed in Autism Spectrum Disorders

2013 ◽  
Author(s):  
C. Sue Carter ◽  
Suma Jacob
Keyword(s):  
Autism Spectrum Disorders ◽  
Arginine Vasopressin ◽  
Protective Factor ◽  
Brain Regions ◽  
Autism Spectrum ◽  
Sexually Dimorphic ◽  
Unique Role ◽  
Spectrum Disorders ◽  
Brain And Behavior ◽  
And Behavior

The effects of oxytocin and vasopressin on the brain and behavior can be sexually dimorphic, especially during the course of development (Bales, Kim, et al., 2004; Bales, Pfeifer, et al., 2004; Bales, Plotsky, et al., 2007; Bielsky et al., 2005a; Carter, 2003; Thompson et al., 2006; Yamamoto et al., 2005; Yamamoto et al., 2004). Given the sexual discrepancy observed in autism spectrum disorders (ASDs), these two neuropeptides, oxytocin (OT) and arginine vasopressin (AVP), have received attention for their potential role in ASDs (Green and Hollander, 2010; Insel et al., 1999; Leckman & Herman, 2002; Welch et al., 2005; Winslow, 2005; Young et al., 2002). Changes in either OT or AVP and their receptors could be capable of influencing symptom domains or behaviors associated with ASDs. Arginine vasopressin is androgen dependent in some brain regions (De Vries & Panzica, 2006), and males are more sensitive to AVP, especially during development. We hypothesize here that AVP, which has a unique role in males, must be present in optimal levels to be protective against ASDs. Either excess AVP or disruptions in the AVP system could play a role in development of the traits found in ASDs. In contrast, OT may possibly be secreted in response to adversity, especially in females, serving as a protective factor.

scholarly journals Is eye contact the key to the social brain?

2010 ◽  
Vol 33 (6) ◽  
pp. 458-459 ◽  
Author(s):  
Atsushi Senju ◽  
Mark H. Johnson
Keyword(s):  
Autism Spectrum Disorders ◽  
Social Cognition ◽  
Face Processing ◽  
Critical Role ◽  
Eye Contact ◽  
Autism Spectrum ◽  
Social Brain ◽  
Cortical Areas ◽  
The Social ◽  
Spectrum Disorders

AbstractEye contact plays a critical role in many aspects of face processing, including the processing of smiles. We propose that this is achieved by a subcortical route, which is activated by eye contact and modulates the cortical areas involve in social cognition, including the processing of facial expression. This mechanism could be impaired in individuals with autism spectrum disorders.

scholarly journals The Melatonin Receptor Agonist Ramelteon Effectively Treats Insomnia and Behavioral Symptoms in Autistic Disorder

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Kentaro Kawabe ◽  
Fumie Horiuchi ◽  
Yasunori Oka ◽  
Shu-ichi Ueno
Keyword(s):  
Autistic Disorder ◽  
Behavioral Problems ◽  
Receptor Agonist ◽  
Sleep Problems ◽  
Sleep Onset ◽  
Autism Spectrum ◽  
Melatonin Receptor ◽  
Spectrum Disorders ◽  
And Behavior ◽  
Clinical Global Impression Improvement

Children with autism spectrum disorders (ASD), including autistic disorder, frequently suffer from comorbid sleep problems. An altered melatonin rhythm is considered to underlie the impairment in sleep onset and maintenance in ASD. We report three cases with autistic disorder in whom nocturnal symptoms improved with ramelteon, a selective melatonin receptor agonist. Insomnia and behavior, assessed using the Clinical Global Impression-Improvement Scale, improved in two cases with 2 mg ramelteon and in the third case with 8 mg ramelteon. Our findings demonstrate that ramelteon is effective not only for insomnia, but for behavioral problems as well, in patients with autistic disorder.

scholarly journals Neural bases for impaired social cognition in schizophrenia and autism spectrum disorders

2008 ◽  
Vol 99 (1-3) ◽  
pp. 164-175 ◽  
Author(s):  
Amy E. Pinkham ◽  
Joseph B. Hopfinger ◽  
Kevin A. Pelphrey ◽  
Joseph Piven ◽  
David L. Penn
Keyword(s):  
Autism Spectrum Disorders ◽  
Social Cognition ◽  
Autism Spectrum ◽  
Spectrum Disorders ◽  
Neural Bases

Electrical Coupling Between Model Midbrain Dopamine Neurons: Effects on Firing Pattern and Synchrony

2002 ◽  
Vol 87 (3) ◽  
pp. 1526-1541 ◽  
Author(s):  
Alexander O. Komendantov ◽  
Carmen C. Canavier
Keyword(s):  
Gap Junctions ◽  
High Frequency ◽  
Firing Pattern ◽  
Electrical Coupling ◽  
Burst Firing ◽  
Induced Current ◽  
Single Spike ◽  
Midbrain Dopamine ◽  
Spike Firing

The role of gap junctions between midbrain dopamine (DA) neurons in mechanisms of firing pattern generation and synchronization has not been well characterized experimentally. We modified a multi-compartment model of DA neuron by adding a spike-generating mechanism and electrically coupling the dendrites of two such neurons through gap junctions. The burst-generating mechanism in the model neuron results from the interaction of a N-methyl-d-aspartate (NMDA)-induced current and the sodium pump. The firing patterns exhibited by the two model neurons included low frequency (2–7 Hz) spiking, high-frequency (13–20 Hz) spiking, irregular spiking, regular bursting, irregular bursting, and leader/follower bursting, depending on the parameter values used for the permeability for NMDA-induced current and the conductance for electrical coupling. All of these firing patterns have been observed in physiological neurons, but a systematic dependence of the firing pattern on the covariation of these two parameters has not been established experimentally. Our simulations indicate that electrical coupling facilitates NMDA-induced burst firing via two mechanisms. The first can be observed in a pair of identical cells. At low frequencies (low NMDA), as coupling strength was increased, only a transition from asynchronous to synchronous single-spike firing was observed. At high frequencies (high NMDA), increasing the strength of the electrical coupling in an identical pair resulted in a transition from high-frequency single-spike firing to burst firing, and further increases led to synchronous high-frequency spiking. Weak electrical coupling destabilizes the synchronous solution of the fast spiking subsystems, and in the presence of a slowly varying sodium concentration, the desynchronized spiking solution leads to bursts that are approximately in phase with spikes that are not in phase. Thus this transitional mechanism depends critically on action potential dynamics. The second mechanism for the induction of burst firing requires a heterogeneous pair that is, respectively, too depolarized and too hyperpolarized to burst. The net effect of the coupling is to bias at least one cell into an endogenously burst firing regime. In this case, action potential dynamics are not critical to the transitional mechanism. If electrical coupling is indeed more prominent in vivo due to basal level of modulation of gap junctions in vivo, these results may indicate why NMDA-induced burst firing is easier to observe in vivo as compared in vitro.

scholarly journals Relationship among Glutamine, γ-Aminobutyric Acid, and Social Cognition in Autism Spectrum Disorders

2015 ◽  
Vol 25 (4) ◽  
pp. 314-322 ◽  
Author(s):  
David M. Cochran ◽  
Elif M. Sikoglu ◽  
Steven M. Hodge ◽  
Richard A.E. Edden ◽  
Ann Foley ◽  
...  
Keyword(s):  
Autism Spectrum Disorders ◽  
Social Cognition ◽  
Autism Spectrum ◽  
Aminobutyric Acid ◽  
Spectrum Disorders
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