UNASSIGNED: Infarction of the artery of Percheron (AOP) is a rare vascular condition where a single arterial branch supplies blood to the thalamic and midbrain regions, leading to neurological deficits. The challenge lies in its often-delayed diagnosis due to its rarity and diverse clinical presentations, necessitating heightened awareness among clinicians for expedited diagnosis and appropriate therapeutic interventions.
UNASSIGNED: All relevant studies involving patients diagnosed with infarction of AOP were retrieved from PubMed, Google Scholar, Web of Science, and Scopus. Only human studies that were published in full English-language reports were included. Included in the search were the terms \"Artery of Percheron,\" \"infarction,\" \"stroke,\" and \"demarcation\". Age, gender, presenting symptoms, treatment, recovery time, and outcome of patients with AOP infarction were all recorded.
UNASSIGNED: A systematic review was conducted on a total of 530 articles, out of which 130 articles met the specified requirements. The average age is 59, with men comprising 57.7% of the population. The symptoms reported were visual disturbance in 43.9% of cases and changed mental state in 77.2% of cases. Treatment options include conservative management (85.4%), thrombolysis (11.3%), and other approaches. The optimal age range for recovery is between 41 and 50 years old.
UNASSIGNED: Our study on acute AOP infarction highlights male predominance, common comorbidities like hypertension and diabetes, and prevalent symptoms including visual disturbance and altered mental state. Early recognition is crucial, with thrombolytic therapy within the critical time window showing promising outcomes. These findings offer insights for enhanced clinical management of AOP infarction.

Recent work across species has shown that midbrain dopamine neurons signal not only errors in the prediction of reward value but also in the prediction of value-neutral sensory features. To support learning of associative structures in downstream areas, identity prediction errors (iPEs) should signal specific information about the mis-predicted outcome. Here, we used pattern-based analysis of functional magnetic resonance imaging (fMRI) data acquired during reversal learning to characterize the information content of iPE responses in the human midbrain. We find that fMRI responses to value-neutral identity errors contain information about the identity of the unexpectedly received reward (positive iPE+) but not about the identity of the omitted reward (negative iPE-). Exploratory analyses revealed representations of iPE- in the dorsomedial prefrontal cortex. These results demonstrate that ensemble midbrain responses to value-neutral identity errors convey information about the identity of unexpectedly received outcomes, which could shape the formation of novel stimulus-outcome associations that constitute cognitive maps.

Chronic unpredictable and unavoidable stress is associated with mental health problems such as depression and anxiety, whereas cycles of stress and stress relief strengthen resilience. It has been suggested that increased breakdown of brain endocannabinoids (eCB) promotes a feeling of adversity. To assess the impact of stress on bioactive lipid homeostasis, we analyzed eCB, sphingolipids, and ceramides in seven brain regions and plasma in a mouse model of chronic unpredictable mild stress. Chronic unpredictable mild stress (CUMS) was associated with low levels of anandamide in hippocampus and prefrontal cortex in association with indicators of anxiety (elevated plus maze). Oppositely, CUMS caused elevated levels of sphingosine-1-phosphate (S1P d18:1) and sphinganine-1-phosphate (S1P d18:0) in the midbrain and thalamus, which was associated with readouts of increased stress resilience, i.e., marble burying and struggling in the tail suspension tests. In the periphery, elevated plasma levels of ceramides revealed similarities with human major depression and suggested unfavorable effects of stress on metabolism, but plasma lipids were not associated with body weight, sucrose consumption, or behavioral features of depression or anxiety. The observed brain site-specific lipid changes suggest that the forebrain succumbs to adverse stress effects while the midbrain takes up defensive adjustments.

Increased activation of inflammatory macrophages and altered expression of dopamine markers are found in the midbrains of people with schizophrenia (SZ). The relationship of midbrain macrophages to dopamine neurons has not been explored, nor is it known if changes in midbrain macrophages are also present in bipolar disorder (BD) or major depressive disorder (MDD). Herein, we determined whether there were differences in CD163+ cell density in the Substantia Nigra (SN), and cerebral peduncles (CP) of SZ, BD, and MDD compared to controls (CTRL). We also analyzed whether CD163 protein and dopamine-synthesizing enzyme tyrosine hydroxylase (TH) mRNA levels differed among diagnostic groups and if they correlated with the density of macrophages. Overall, perivascular CD163+ cell density was higher in the gray matter (SN) than in the white matter (CP). Compared to CTRL, we found increased density of parenchymal CD163+ cells in the SN of the three psychiatric groups and increased CD163 protein levels in SZ. CD163 protein was positively correlated with density of perivascular CD163+ cells. TH mRNA was reduced in SZ and BD and negatively correlated with parenchymal CD163+ cell density. We provide the first quantitative and molecular evidence of an increase in the density of parenchymal macrophages in the midbrain of major mental illnesses and show that the presence of these macrophages may negatively impact dopaminergic neurons.

Sinusoidal amplitude modulation (SAM) is a key feature of complex sounds. While psychophysical studies have characterized SAM perception, and neurophysiological studies in anesthetized animals report a transformation from the cochlear nucleus\' (CN; brainstem) temporal code to the inferior colliculus\' (IC; midbrain\'s) rate code, none have used awake animals or nonhuman primates to compare CN and IC\'s coding strategies to modulation-frequency perception. To address this, we recorded single-unit responses and compared derived neurometric measures in the CN and IC to psychometric measures of modulation frequency (MF) discrimination in macaques. IC and CN neurons often exhibited tuned responses to SAM in rate and spike-timing measures of modulation coding. Neurometric thresholds spanned a large range (2-200 Hz DMF). The lowest 40% of IC thresholds were less than or equal to psychometric thresholds, regardless of which code was used, while CN thresholds were greater than psychometric thresholds. Discrimination at 10-20 Hz could be explained by indiscriminately pooling 30 units in either structure, while discrimination at higher MFs was best explained by more selective pooling. This suggests that pooled CN activity was sufficient for AM discrimination. Psychometric and neurometric thresholds decreased as stimulus duration increased, but IC and CN thresholds were higher and more variable than behavior at short durations. This slower subcortical temporal integration compared to behavior was consistent with a drift diffusion model which reproduced individual differences in performance and can constrain future neurophysiological studies of temporal integration. These measures provide an account of AM perception at the neurophysiological, computational, and behavioral levels.

BACKGROUND: Understanding the intricate relationship between consciousness and the midbrain\'s structures remains a significant challenge in neuroscience. Transient lesions are perfect examples of the physiological functioning mechanism of these structures.
METHODS: The authors present the case of a 49-year-old female who experienced a transient disorder of consciousness due to a midbrain hematoma following surgical interventions to remove a cavernous malformation in the midbrain. This case explores the interplay between the ascending reticular activating system (ARAS) and the thalamic centers, highlighting the role of structural disruptions in influencing consciousness levels. Notably, the patient\'s recovery correlated with the resolution of midbrain edema, reinstating normal ARAS function and consciousness.
CONCLUSIONS: In patients affected by midbrain lesions, edema can lead to a fluctuating neurological status, which can be difficult to diagnose. This case highlights the midbrain\'s crucial role in the consciousness network and the need to comprehend the intricate connections between subcortical and cortical structures for a comprehensive understanding of human consciousness. https://thejns.org/doi/10.3171/CASE2411.

The Ca2+-dependent activator protein for secretion (CAPS/CADPS) family protein facilitates catecholamine release through the dense-core vesicle exocytosis in model neuroendocrine cell lines. However, it remains unclear if it induces dopamine release in the central neurons. This study aimed to examine the expression and function of CADPS2, one of the two CADPS paralogs, in dopamine neurons of the mouse midbrain. This study shows that CADPS2 was expressed in tyrosine hydroxylase and the vesicular monoamine transporter 2 (VMAT2)-positive dopaminergic neurons of the midbrain samples and primary mesencephalic cell cultures. Subcellular fractions rich in dopamine were collected using immunoaffinity for CADPS2 from midbrain protein extracts. Cell imaging using fluorescent false neurotransmitter FFN511 as a substrate for VMAT2 showed decreased activity-dependent dopamine release in Cadps2-deficient cultures, compared to that in wild-type cultures. These results suggest that CADPS2 is involved in dopamine release from the central neurons, indicating its involvement in the central dopamine pathway.

The cerebellum is heavily connected with other brain regions, sub-serving not only motor but also non-motor functions. Genetic mutations leading to cerebellar dysfunction are associated with mental diseases, but cerebellar outputs have not been systematically studied in this context. Here, we present three dimensional distributions of 50,168 target neurons of cerebellar nuclei (CN) from wild-type mice and Nlgn3R451C mutant mice, a mouse model for autism. Our results derived from 36 target nuclei show that the projections from CN to thalamus, midbrain and brainstem are differentially affected by Nlgn3R451C mutation. Importantly, Nlgn3R451C mutation altered the innervation power of CN→zona incerta (ZI) pathway, and chemogenetic inhibition of a neuronal subpopulation in the ZI that receives inputs from the CN rescues social defects in Nlgn3R451C mice. Our study highlights potential role of cerebellar outputs in the pathogenesis of autism and provides potential new therapeutic strategy for this disease.

Major depressive disorder (MDD) is prevalent with a high subjective and socio-economic burden. Despite the effectiveness of classical treatment methods, 20-30% of patients stay treatment-resistant. Deep Brain Stimulation of the superolateral branch of the medial forebrain bundle is emerging as a clinical treatment. The stimulation region (ventral tegmental area, VTA), supported by experimental data, points to the role of dopaminergic (DA) transmission in disease pathology. This work sets out to develop a workflow that will allow the performance of analyses on midbrain DA-ergic neurons and projections in subjects who have committed suicide. Human midbrains were retrieved during autopsy, formalin-fixed, and scanned in a Bruker MRI scanner (7T). Sections were sliced, stained for tyrosine hydroxylase (TH), digitized, and integrated into the Montreal Neurological Institute (MNI) brain space together with a high-resolution fiber tract atlas. Subnuclei of the VTA region were identified. TH-positive neurons and fibers were semi-quantitatively evaluated. The study established a rigorous protocol allowing for parallel histological assessments and fiber tractographic analysis in a common space. Semi-quantitative readings are feasible and allow the detection of cell loss in VTA subnuclei. This work describes the intricate workflow and first results of an investigation of DA anatomy in VTA subnuclei in a growing naturalistic database.

Social play is pervasive in juvenile mammals, yet it is poorly understood in terms of its underlying brain mechanisms. Specifically, we do not know why young animals are most playful and why most adults cease to social play. Here, we analyze the synaptic mechanisms underlying social play. We found that blocking the rat periaqueductal gray (PAG) interfered with social play. Furthermore, an age-related decrease of neural firing in the PAG is associated with a decrease in synaptic release of glycine. Most importantly, modulation of glycine concentration-apparently acting on the glycinergic binding site of the N-methyl-D-aspartate (NMDA) receptor-not only strongly modulates social play but can also reverse the age-related decline in social play. In conclusion, we demonstrate that social play critically depends on the neurotransmitter glycine within the PAG.