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This article provides a review of the increasingly detailed imaging literature on the neurodevelopment of joint attention. Many findings from this literature support and inform the hypothesis that the neurodevelopment of joint attention contributes to the functional development of neural systems for human social cognition. Joint attention begins to develop by 5 months of age and is tantamount to the ability to adopt a common perspective with another person. It involves a whole-brain system with nodes in the: (a) dorsal and medial frontal cortex, (b) orbital frontal/insula cortex, (c) anterior/posterior cingulate cortex, (d) superior temporal cortex, (e) precuneus/parietal cortex, and (f) amygdala and striatum. This system integrates triadic information processing about (a) self-attention/action, (b) information about others' attention/action during social interactions that involve, (c) coordinated attention as well as processing a common referent in space. The results of this new imaging literature have the potential to advance current models of social cognition and the social brain, which rarely consider the contribution of the cognitive neurodevelopment of joint attention. The new neuroscience of joint attention is also extremely valuable for clinical research on social-cognitive neurodevelopmental disorders. This is most clearly the case for autism spectrum disorder (ASD) because it is consistent with the hypothesis of substantial functional neurodevelopmental continuity between the preschool impairments of joint attention, and childhood theory of mind ability that characterizes the development of ASD.

Activation of the maternal immune system (MIA) during gestation is linked to neuropsychiatric diseases like schizophrenia. While many studies address behavioural aspects, less is known about underlying cellular mechanisms. In the following study, BALB/c mice received intraperitoneal injections of polyinosinic‐polycytidylic acid (Poly I:C) (20 µg/ml) or saline (0.9%) at gestation day (GD) 9.5 before hippocampal neurons were isolated and cultured from embryonic mice for further analysis. Interestingly, strongest effects were observed when the perineuronal net (PNN) wearing subpopulation of neurons was analysed. Here, a significant reduction of aggrecan staining intensity, area and soma size could be detected. Alterations of PNNs are often linked to neuropsychiatric diseases, changes in synaptic plasticity and in electrophysiology. Utilizing multielectrode array analysis (MEA), we observed a remarkable increase of the spontaneous network activity in neuronal networks after 21 days in vitro (DIV) when mother mice suffered a prenatal immune challenge. As PNNs are associated with GABAergic interneurons, our data indicate that this neuronal subtype might be stronger affected by a prenatal MIA. Degradation or damage of this subtype might cause the hyperexcitability observed in the whole network. In addition, embryonic neurons of the Poly I:C condition developed significantly shorter axons after five days in culture, while dendritic parameters and apoptosis rate remained unchanged. Structural analysis of synapse numbers revealed an increase of postsynaptic density 95 (PSD‐95) puncta after 14 DIV and an increase of presynaptic vesicular glutamate transporter (vGlut) puncta after 21 DIV, while inhibitory synaptic proteins were not altered. [ABSTRACT FROM AUTHOR]

The common view that stopping action plans by the basal ganglia is achieved mainly by the subthalamic nucleus alone due to its direct excitatory projection onto the output nuclei of the basal ganglia has been challenged by recent findings. The proposed "pause‐then‐cancel" model suggests that the subthalamic nucleus provides a rapid stimulus‐unspecific "pause" signal, followed by a stop‐cue‐specific "cancel" signal from striatum‐projecting arkypallidal neurons. To determine more precisely the relative contribution of the different basal ganglia nuclei in stopping, we simulated a stop‐signal task with a spiking neuron model of the basal ganglia, considering recently discovered connections from the arkypallidal neurons, and cortex‐projecting GPe neurons. For the arkypallidal and prototypical GPe neurons, we obtained neuron model parameters by fitting their neuronal responses to published experimental data. Our model replicates findings of stop‐signal tasks at neuronal and behavioral levels. We provide evidence for the existence of a stop‐related cortical input to the arkypallidal and cortex‐projecting GPe neurons such that the stop responses of the subthalamic nucleus, the arkypallidal neurons, and the cortex‐projecting GPe neurons complement each other to achieve functional stopping behavior. Particularly, the cortex‐projecting GPe neurons may complement the stopping within the basal ganglia caused by the arkypallidal and STN neurons by diminishing cortical go‐related processes. Furthermore, we predict effects of lesions on stopping performance and propose that arkypallidal neurons mainly participate in stopping by inhibiting striatal neurons of the indirect rather than the direct pathway. [ABSTRACT FROM AUTHOR]

Pathological synchronization in large-scale motor networks constitutes a pathophysiological hallmark of Parkinson's disease (PD). Corticomuscular synchronization in PD is pronounced in lower frequency bands (< 10 Hz), whereas efficient cortical motor integration in healthy persons is driven in the beta frequency range. Electroencephalogram and electromyogram recordings at rest and during an isometric precision grip task were performed in four perioperative sessions in 10 patients with PD undergoing subthalamic nucleus deep-brain stimulation: (i) 1 day before (D0); (ii) 1 day after (D1); (iii) 8 days after implantation of macroelectrodes with stimulation off (D8StimOff); and (iv) on (D8StimOn). Analyses of coherence and phase delays were performed in order to challenge the effects of microlesion and stimulation on corticomuscular coherence (CMC). Additionally, local field potentials recorded from the subthalamic nucleus on D1 allowed comprehensive mapping of motor-related synchronization in subthalamocortical and cerebromuscular networks. Motor performance improved at D8StimOn compared with D0 and D8StimOff paralleled by a reduction of muscular activity and CMC in the theta band (3.9-7.8 Hz) and by an increase of CMC in the low-beta band (13.7-19.5 Hz). Efferent motor cortical drives to muscle presented mainly below 10 Hz on D8StimOff that were suppressed on D8StimOn and occurred on higher frequencies from 13 to 45 Hz. On D1, coherence of the high-beta band (20.5-30.2 Hz) increased during movement compared with rest in subthalamomuscular and corticomuscular projections, whereas it was attenuated in subcorticocortical projections. The present findings lend further support to the concept of pathological network synchronization in PD that is beneficially modulated by stimulation. [ABSTRACT FROM AUTHOR]

Abstract The substantia nigra pars compacta and the ventral tegmental area are part of a complex network in the basal ganglia involved in behaviours as diverse as motor planning, generation of pleasure and drug addiction. Here we report that in the dopaminergic neurons of the rat ventral midbrain a brief coactivation of group I metabotropic and NMDA glutamate receptors may transform a temporally dispersed synaptic GABAergic input into a rhythmic pattern (range 4.5–22.5 Hz), probably through a mechanism involving electrotonic couplings. The plastic and long-lasting modification in the temporal code of the inhibitory synaptic activity induced by glutamate may be a key element in determining the function of midbrain dopaminergic neurons in both normal and pathological behaviour. [ABSTRACT FROM AUTHOR]