The study aimed to systematically analyze the empirical evidence that is available concerning batteries, tests or instruments that assess hot executive functions (EFs) in preschoolers, identifying which are the most used instruments, as well as the most evaluated hot EFs. For the review and selection of articles, the systematic review methodology PRISMA was used. The article search considered the EBSCO, Web of Science (WoS), SciELO and PubMed databases, with the keywords “Hot executive function”, “Assessment”, “test”, “evaluation”, using the Boolean operators AND and OR indistinctly, between 2000 and April 2021. Twenty-four articles were selected and analyzed. The most commonly used instruments to assess hot EFs in preschool children were the Delayed Gratification Task, the Child’s Play Task, and the Delayed Reward Task. Amongst those analyzed, 17 instruments were found to assess hot EFs in preschoolers. The accuracy and conceptual clarity between the assessment of cognitive and emotional components in EFs is still debatable. Nevertheless, the consideration of affective temperature and reward stimulus type, could be an important influence when assessing EFs in this age range. Evidence of the possible involvement of cortical and subcortical structures, as well as the limbic system, in preschool executive functioning assessment has also been incorporated.

J. Neurochem.(2011)119, 314–323. Moderate reduction in the protein content of the mother’s diet (hidden malnutrition) does not alter body and brain weights of rat pups at birth, but leads to dysfunction of neocortical noradrenaline systems together with impaired long‐term potentiation and visuo‐spatial memory performance. As β₁‐adrenoceptors and downstream protein kinase signaling are critically involved in synaptic long‐term potentiation and memory formation, we evaluated the β₁‐adrenoceptor density and the expression of cyclic‐AMP dependent protein kinase, calcium/calmodulin‐dependent protein kinase and protein kinase Fyn, in the frontal cortex of prenatally malnourished adult rats. In addition, we also studied if β₁‐adrenoceptor activation with the selective β₁agonist dobutamine could improve deficits of prefrontal cortex long‐term potentiation presenting these animals. Prenatally malnourished rats exhibited half of β₁‐adrenoceptor binding, together with a 51% and 65% reduction of cyclic AMP‐dependent protein kinase α and calcium/calmodulin‐dependent protein kinase α expression, respectively, as compared with eutrophic animals. Administration of the selective β₁agonist dobutamine prior to tetanization completely rescued the ability of the prefrontal cortex to develop and maintain long‐term potentiation in the malnourished rats. Results suggest that under‐expression of neocortical β₁‐adrenoceptors and protein kinase signaling in hidden malnourished rats functionally affects the synaptic networks subserving prefrontal cortex long‐term potentiation. β₁‐Adrenoceptor activation was sufficient to fully recover neocortical plasticity in the PKA‐ and calcium/calmodulin‐dependent protein kinase II‐deficient undernourished rats, possibly by producing extra amounts of cAMP and/or by recruiting alternative signaling cascades.

Introduction: Cytokines produced by spinal cord glia after peripheral injuries have a relevant role in the maintenance of pain states. Thus, while IL-1β is overexpressed in the spinal cords of animals submitted to experimental arthritis and other chronic pain models, intrathecal administration of IL-1β to healthy animals induces hyperalgesia and allodynia and enhances wind-up activity in dorsal horn neurons.Methods: To investigate the functional contribution of glial cells in the spinal cord nociceptive transmission, the effect of intrathecally administered IL-1β was studied in both normal and adjuvant-induced arthritic rats with or without glial inhibition. Four weeks after induction of monoarthritis, rats were treated with the glial cell inhibitor propentofylline (10 μg i.t. daily during 10 days) and submitted to a C-fiber-mediated reflex paradigm evoked by single and repetitive (wind-up) electric stimulation.Results: Both the propentofylline treatment and the monoarthritic condition modified the stimulating current required for threshold activation of C reflex responses. Intrathecal IL-1β increased spinal cord wind-up activity in normal and monoarthritic rats without propentofylline pre-treatment, but resulted in decreased wind-up activity in normal and monoarthritic propentofylline-treated animals. Intrathecal saline did not produce any effect. Thus, glial inactivation reverted into inhibition the excitatory effect of IL-1β on spinal cord wind-up, irrespective of the normal or monoarthritic condition of rats.Conclusions: The results suggest that the excitatory effect of nanomolar doses of IL-1β on spinal wind-up in healthy rats is produced by an unidentified glial mediator, while the inhibitory effects of IL-1β on wind-up activity in animals with inactivated glia resulted from a direct effect of the cytokine on dorsal horn neurons. The present study failed to demonstrate a differential sensitivity of normal and monoarthritic rats to IL-1β administration into the spinal cord and to disruption of β glial function, as both normal and monoarthritic animals changes wind-up activity in the same direction after propentofylline treatment, suggesting that after glial inhibition normal and monoarthritic animals behave similarly relative to the capability of dorsal horn neurons to generate wind-up activity when repeatedly stimulated by C-fibers.

Pannexin 1 (Panx1) is involved in the spinal central sensitization process in rats with neuropathic pain, but its interaction with well-known, pain-related, ligand-dependent receptors, such as NMDA receptors (NMDAR) and P2X7 purinoceptors (P2X7R), remains largely unexplored. Here, we studied whether NMDAR- and P2X7R-dependent nociceptive signaling in neuropathic rats require the activation of Panx1 channels to generate spinal central sensitization, as assessed by behavioral (mechanical hyperalgesia) and electrophysiological (C-reflex wind-up potentiation) indexes. Administration of either a selective NMDAR agonist i.t. (NMDA, 2 mM) or a P2X7R agonist (BzATP, 150 μM) significantly increased both the mechanical hyperalgesia and the C-reflex wind-up potentiation, effects that were rapidly reversed (minutes) by i.t. administration of a selective pannexin 1 antagonist (10panx peptide, 300 μM), with the scores even reaching values of rats without neuropathy. Accordingly, 300 μM 10panx completely prevented the effects of NMDA and BzATP administered 1 h later, on mechanical hyperalgesia and C-reflex wind-up potentiation. Confocal immunofluorescence imaging revealed coexpression of Panx1 with NeuN protein in intrinsic dorsal horn neurons of neuropathic rats. The results indicate that both NMDAR- and P2X7R-mediated increases in mechanical hyperalgesia and C-reflex wind-up potentiation require neuronal Panx1 channel activation to initiate and maintain nociceptive signaling in neuropathic rats.