Few investigations have analyzed the neuroanatomical substrate of empathic capacities in healthy subjects, and most of them have neglected the potential involvement of cerebellar structures. The main ...aim of the present study was to investigate the associations between bilateral cerebellar macro- and micro-structural measures and levels of cognitive and affective trait empathy (measured by Interpersonal Reactivity Index, IRI) in a sample of 70 healthy subjects of both sexes. We also estimated morphometric variations of cerebral Gray Matter structures, to ascertain whether the potential empathy-related peculiarities in cerebellar areas were accompanied by structural differences in other cerebral regions. At macro-structural level, the volumetric differences were analyzed by Voxel-Based Morphometry (VBM)- and Region of Interest (ROI)-based approaches, and at a micro-structural level, we analyzed Diffusion Tensor Imaging (DTI) data, focusing in particular on Mean Diffusivity and Fractional Anisotropy. Fantasy IRI-subscale was found to be positively associated with volumes in right cerebellar Crus 2 and pars triangularis of inferior frontal gyrus. The here described morphological variations of cerebellar Crus 2 and pars triangularis allow to extend the traditional cortico-centric view of cognitive empathy to the cerebellar regions and indicate that in empathizing with fictional characters the cerebellar and frontal areas are co-recruited.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Trauma-related disorders are debilitating psychiatric conditions that influence people who have directly or indirectly witnessed adversities. Dramatic brain/body transformations and altered person's ...relationship with self, others, and the world occur when experiencing multiple types of traumas. In turn, these unfortunate modifications may contribute to predisposition to trauma-related vulnerability conditions, such as externalizing (aggression, delinquency, and conduct disorders) problems. This mini-review analyzes the relations between traumatic experiences (encoded as implicit and embodied procedural memories) and bodily self, sense of safety for the own body, and relationship with others, also in the presence of externalizing conducts. Furthermore, an emerging research area is also considered, highlighting principles and techniques of body-oriented and sensorimotor therapies designed to remodel bodily self-aspects in the presence of trauma, discussing their potential application with individuals showing externalizing problems.
The superordinate division of emotions is distributed along a bipolar dimension of affective valence, from approaching rewarding situations to avoiding punitive situations. Avoiding and approaching ...behaviors determine the disposition to the primary emotions of fear and attachment and the behavioral responses to the environmental stimuli of danger, novelty and reward. Approach or avoidance behaviors are associated with the brain pathways controlling cognitive and attentional function, reward sensitivity and emotional expression, involving prefrontal cortex, amygdala, striatum and cerebellum. Individual differences in approach and avoidance behavior might be modulated by normal variance in the level of functioning of different neurotransmitter systems, such as dopaminergic, serotoninergic, noradrenergic and endocannabinoid systems as well as many peptides such as corticotropin releasing hormone. These substances act at various central target areas to increase intensity of appetitive or defensive motivation. Physiologically, personality temperaments of approach and avoidance are viewed as instigators of propensity. They produce immediate affective, cognitive and behavioral inclinations in response to stimuli and orient individuals across domains and situations in a consistent fashion. Although the action undoubtedly emerges directly from these temperamental proclivities, ultimate behavioral outcomes are often a function of the integration among goal pursuit, self-regulation, and temperament trait. Defective coping strategies to aversive or rewarding stimuli characterize the patho-physiology of anxiety- and stress-related disorders or compulsive and addiction behaviors, respectively. Individuals with neuropsychiatric symptoms such as depression, suicidal behavior, bipolar mania, schizophrenia, substance use disorders, pathological gambling and anxiety disorders have scores which fall at the extreme tails of the normal distribution for a specific temperamental trait. The present Research Topic on the individual differences in emotional and motivational processing emphasizes the link between neuronal pattern and behavioral expression. The Topic includes experimental and clinical researches addressing the individual differences related to approach and avoidance and their behavioral characterization, structural and neurochemical profiles, synaptic connections, and receptor expressions. Studies are organized in a framework that puts in evidence the phenotypic expression and neurobiological patterns characterizing the individual differences and their biological variance.
Schizophrenia is a complex and severe mental disorder that affects approximately 1% of the global population. It is characterized by a wide range of symptoms, including delusions, hallucinations, ...disorganized speech and behavior, and cognitive impairment. Recent research has suggested that the immune system dysregulation may play a significant role in the pathogenesis of schizophrenia, and glial cells, such as astroglia and microglia known to be involved in neuroinflammation and immune regulation, have emerged as potential players in this process. The aim of this systematic review is to summarize the glial hallmarks of schizophrenia, choosing as cellular candidate the astroglia and microglia, and focusing also on disease-associated psychological (cognitive and emotional) changes. We conducted a systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched PubMed, Scopus, and Web of Science for articles that investigated the differences in astroglia and microglia in patients with schizophrenia, published in the last 5 years. The present systematic review indicates that changes in the density, morphology, and functioning of astroglia and microglia may be involved in the development of schizophrenia. The glial alterations may contribute to the pathogenesis of schizophrenia by dysregulating neurotransmission and immune responses, worsening cognitive capabilities. The complex interplay of astroglial and microglial activation, genetic/epigenetic variations, and cognitive assessments underscores the intricate relationship between biological mechanisms, symptomatology, and cognitive functioning in schizophrenia.
To promote efficient explorative behaviors, subjects adaptively select spatial navigational strategies based on landmarks or a cognitive map. The hippocampus works alone or in conjunction with the ...dorsal striatum, both representing the neuronal underpinnings of the navigational strategies organized on the basis of different systems of spatial coordinate integration. The high expression of cannabinoid type 1 (CB1) receptors in structures related to spatial learning—such as the hippocampus, dorsal striatum and amygdala—renders the endocannabinoid system a critical target to study the balance between landmark- and cognitive map-based navigational strategies. In the present study, mice treated with the CB1-inverse agonist/antagonist AM251 or vehicle were trained on a Circular Hole Board, a task that could be solved through either navigational strategy. At the end of the behavioral testing, c-Fos immunoreactivity was evaluated in specific nuclei of the hippocampus, dorsal striatum and amygdala. AM251 treatment impaired spatial learning and modified the pattern of the performed navigational strategies as well as the c-Fos immunoreactivity in the hippocampus, dorsal striatum and amygdala. The present findings shed light on the involvement of CB1 receptors as part of the selection system of the navigational strategies implemented to efficiently solve the spatial problem.
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Systemic inflammation might cause neuronal damage and sustain neurodegenerative diseases and behavior impairment, with the participation of pro-inflammatory cytokines, like tumor necrosis factor ...(TNF)-α and interleukin (IL)-18. However, the potential contribution of these cytokines to behavioral impairment in the long-term period has not been fully investigated.
Wistar rats were treated with a single intraperitoneal injection of LPS (5 mg/kg) or vehicle. After 7 days and 10 months, the animal behavior was evaluated by testing specific cognitive functions, as mnesic, discriminative, and attentional functions, as well as anxiety levels. Contextually, TNF-α and IL-18 protein levels were measured by ELISA in defined brain regions (that is, frontal cortex, hippocampus, striatum, cerebellum, and hypothalamus).
Behavioral testing demonstrated a specific and persistent cognitive impairment characterized by marked deficits in reacting to environment modifications, possibly linked to reduced motivational or attentional deficits. Concomitantly, LPS induced a TNF-α increase in the hippocampus and frontal cortex (from 7 days onward) and cerebellum (only at 10 months). Interestingly, LPS treatment enhanced IL-18 expression in these same areas only at 10 months after injection.
Overall, these results indicate that the chronic neuroinflammatory network elicited by systemic inflammation involves a persistent participation of TNF-α accompanied by a differently regulated contribution of IL-18. This leads to speculation that, though with still unclear mechanisms, both cytokines might take part in long-lasting modifications of brain functions, including behavioral alteration.
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Fear-related disorders arise from inefficient fear extinction and have immeasurable social and economic costs. Here, we characterize mouse phenotypes that spontaneously show fear-independent ...behavioral traits predicting adaptive or maladaptive fear extinction. We find that, already before fear conditioning, specific morphological, electrophysiological, and transcriptomic patterns of cortical and amygdala pyramidal neurons predispose to fear-related disorders. Finally, by using an optogenetic approach, we show the possibility to rescue inefficient fear extinction by activating infralimbic pyramidal neurons and to impair fear extinction by activating prelimbic pyramidal neurons.
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•Fear footprints precede the exposure to fear conditioning in susceptible individuals•Altered transcriptome and synaptic plasticity precede inefficient fear extinction•IL optogenetic manipulations in impaired-extinction mice rescue extinction deficits•PrL optogenetic manipulations in fear-conditioned mice induce fear-extinction deficits
Laricchiuta et al. report the functional and molecular alterations in cortical and amygdala pyramidal neurons of mice with spontaneous fear-extinction deficits, pre and post fear exposure. The authors use electrophysiological and morphological measures coupled with RNA-sequencing analysis to identify these alterations, correcting them by using brain stimulation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Food restriction is a robust nongenic, nonsurgical and nonpharmacologic intervention known to improve health and extend lifespan in various species. Food is considered the most essential and ...frequently consumed natural reward, and current observations have demonstrated homeostatic responses and neuroadaptations to sustained intermittent or chronic deprivation. Results obtained to date indicate that food deprivation affects glutamatergic synapses, favoring the insertion of GluA2-lacking α-Ammino-3-idrossi-5-Metil-4-idrossazol-Propionic Acid receptors (AMPARs) in postsynaptic membranes. Despite an increasing number of studies pointing towards specific changes in response to dietary restrictions in brain regions, such as the nucleus accumbens and hippocampus, none have investigated the long-term effects of such practice in the dorsal striatum. This basal ganglia nucleus is involved in habit formation and in eating behavior, especially that based on dopaminergic control of motivation for food in both humans and animals. Here, we explored whether we could retrieve long-term signs of changes in AMPARs subunit composition in dorsal striatal neurons of mice acutely deprived for 12 hours/day for two consecutive days by analyzing glutamatergic neurotransmission and the principal forms of dopamine and glutamate-dependent synaptic plasticity. Overall, our data show that a moderate food deprivation in experimental animals is a salient event mirrored by a series of neuroadaptations and suggest that dietary restriction may be determinant in shaping striatal synaptic plasticity in the physiological state.
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The adolescent brain is an open window on the environment, which is vulnerable to perturbations and the traumatic experiences occurring before or during this period have an increased saliency in ...affecting cognitive, emotional, and social levels. During adolescence, trauma-related effects causing significant impairment or suffering could be manifest in internalizing and externalizing behaviors. The present mini review aimed to clarify trauma effects on adolescence by examining the neurobiological correlates associated with an increased risk of externalizing/internalizing conducts, as well as the transformative effects of multiple and multimodal therapeutic interventions.
Firing activity of external globus pallidus (GPe) is crucial for motor control and is severely perturbed in dystonia, a movement disorder characterized by involuntary, repetitive muscle contractions. ...Here, we show that GPe projection neurons exhibit a reduction of firing frequency and an irregular pattern in a DYT1 dystonia model. Optogenetic activation of the striatopallidal pathway fails to reset pacemaking activity of GPe neurons in mutant mice. Abnormal firing is paralleled by alterations in motor learning. We find that loss of dopamine D2 receptor-dependent inhibition causes increased GABA input at striatopallidal synapses, with subsequent downregulation of hyperpolarization-activated, cyclic nucleotide-gated cation (HCN) channels. Accordingly, enhancing in vivo HCN channel activity or blocking GABA release restores both the ability of striatopallidal inputs to pause ongoing GPe activity and motor coordination deficits. Our findings demonstrate an impaired striatopallidal connectivity, supporting the central role of GPe in motor control and, more importantly, identifying potential pharmacological targets for dystonia.
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•Dystonia mouse model shows altered firing rate and pattern in globus pallidus•Altered D2 receptor-dependent control disinhibits striatopallidal synapses•Pallidal neurons show downregulation of HCN channels•Enhancing HCN potassium channel function restores normal globus pallidus activity
Sciamanna et al. show overt alterations in neuronal excitability of the globus pallidus in a dystonia mouse model. Pallidal neurons show impairments in firing rate and pattern, caused by altered dopamine D2 receptor control over GABAergic striatopallidal synapses with subsequent downregulation of HCN channels.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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