Frontiers in Neuroanatomy最新文献

The microbiota-gut-brain axis (MGBA) plays a significant role in the maintenance of brain structure and function. The MGBA serves as a conduit between the CNS and the ENS, facilitating communication between the emotional and cognitive centers of the brain via diverse pathways. In the initial stages of this review, we will examine the way how MGBA affects neurogenesis, neuronal dendritic morphology, axonal myelination, microglia structure, brain blood barrier (BBB) structure and permeability, and synaptic structure. Furthermore, we will review the potential mechanistic pathways of neuroplasticity through MGBA influence. The short-chain fatty acids (SCFAs) play a pivotal role in the MGBA, where they can modify the BBB. We will therefore discuss how SCFAs can influence microglia, neuronal, and astrocyte function, as well as their role in brain disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD). Subsequently, we will examine the technical strategies employed to study MGBA interactions, including using germ-free (GF) animals, probiotics, fecal microbiota transplantation (FMT), and antibiotics-induced dysbiosis. Finally, we will examine how particular bacterial strains can affect brain structure and function. By gaining a deeper understanding of the MGBA, it may be possible to facilitate research into microbial-based pharmacological interventions and therapeutic strategies for neurological diseases.

Previous studies on changes in the distribution of GABAergic interneurons and excitation/inhibition (E/I) balance in Alzheimer's disease (AD) and aging were mainly conducted in the neocortex and hippocampus. However, the limbic system is the primary and crucial location for AD progression. Therefore, in this study, we utilized AD and aging mouse models to investigate the E/I balance and the distribution of parvalbumin (PV)- and somatostatin (SST)-expressing cells in S1BF (barrel field of primary somatosensory cortex, barrel cortex), CA1 hippocampal area and brain regions beyond the neocortex and hippocampus, including retrosplenial cortex (RSC, which is composed of RSG and RSA), piriform cortex (Pir), amygdala (BMA), and hypothalamus (DM). We discovered that amyloidosis may disrupt the alignment of excitatory pre- and postsynaptic quantities. Amyloidosis reduces the quantity of synapses and SST cells, but does not impact the counts of PV cells. By contrast, aging is linked to a decline in synapses, I/E ratios, SST and PV cells. Amyloidosis affects the S1BF and BMA, while aging may harm all studied regions, including the S1BF, RSC, hippocampus, Pir, BMA, and DM. Aging mostly affects synapses and I/E ratios in Pir, BMA, and DM, and PV and SST interneurons in the hippocampus.

Introduction: Most of what is known about thalamic development comes from rodent studies, however, the increased proportion of human association cortex has co-evolved with increased thalamocortical connectivity. Higher order thalamic nuclei, relaying information between cortical regions and important in higher cognitive function, are greatly expanded.

Methods: This study mapped the emergence of thalamic nuclei in human fetal development (8-16 post conceptional weeks; PCW) by revealing gene expression patterns using in situ hybridization and immunohistochemistry for previously established thalamic development markers.

Results: In the proliferative thalamic ventricular zone, OLIG3 and NR2F1 immunoreactivity marked the extent of the thalamus, whereas PAX6 and NR2F2 were expressed in gradients, suggesting an early protomap. This was also the case for post-mitotic transcription factors ZIC4, GBX2, FOXP2 and OTX2 which marked thalamic boundaries but also exhibited opposing gradients with ZIC4 expression higher anterior/lateral, and GBX2, FOXP2 and OTX2 higher in posterior/medial. Expression patterns became increasingly compartmentalized as development progressed and by 14 PCW recognizable thalamic nuclei were observed with, for instance, the centromedian nucleus being characterized by high FOXP2 and absent GBX2 expression. SP8-like immunoreactivity was expressed in distinct thalamic locations other than the reticular formation which has not been previously reported. Markers for GABAergic neurons and their precursors revealed the location of the prethalamus and its development into the reticular formation and zona incerta. No GAD67+ neurons were observed in the thalamus at 10 PCW, but by 14 PCW the medial posterior quadrant of the thalamus at various levels was infiltrated by GAD67+/ SOX14+ cells of presumed pretectal/midbrain origin. We compared expression of the neurodevelopmental disease susceptibility gene CNTNAP2 to these patterns. It was highly expressed by glutamatergic neurons in many thalamic regions by 14 PCW, sometimes but not always in conjunction with its upstream expression regulator FOXP2.

Conclusion: In human discrete thalamic nuclei exhibiting discrete gene expression patterns emerge relatively early from a protomap of gene expression. The migration of GABAergic neurons into the thalamus occurs over a protracted period, first from the midbrain. Disruption of CNTNAP2 activity and function could be hypothezised to have a variety of effects upon thalamic development.

Individuals misusing opioids often report heightened feelings of loneliness and decreased ability to maintain social connections. This disruption in social functioning further promotes addiction, creating a cycle in which increasing isolation drives drug use. Social factors also appear to impact susceptibility and progression of opioid dependence. In particular, increasing evidence suggests that poor early social bond formation and social environments may increase the risk of opioid abuse later in life. The brain opioid theory of social attachment suggests that endogenous opioids are key to forming and sustaining social bonds. Growing literature describes the opioid system as a powerful modulator of social separation distress and attachment formation in rodents and primates. In this framework, disruptions in opioidergic signaling due to opioid abuse may mediate social reward processing and behavior. While changes in endogenous opioid peptides and receptors have been reported in these early-life adversity models, the underlying mechanisms remain poorly understood. This review addresses the apparent bidirectional causal relationship between social deprivation and opioid addiction susceptibility, investigating the role of opioid transmission in attachment bond formation and prosocial behavior. We propose that early social deprivation disrupts the neurobiological substrates associated with opioid transmission, leading to deficits in social attachment and reinforcing addictive behaviors. By examining the literature, we discuss potential overlapping neural pathways between social isolation and opioid addiction, focusing on major reward-aversion substrates known to respond to opioids.

Background and aim: Endoscopic Third Ventriculostomy (ETV) is used to treat hydrocephalus, an abnormal cerebrospinal fluid accumulation in brain ventricles. By defining a new trajectory and entry point interval, we aim to establish a standardized approach for FreeHand ETV, a vital technique when specialized tools are unavailable, or during emergencies.

Methods: 187 MRIs were analyzed, with 30 having hydrocephalus. A pathway crossing the cranial bone, interventricular foramen (of Monro) and tuber cinereum was outlined. Measurements involved distances to cranial sutures, pathway angles and depths, and distances to important anatomical landmarks. Comparisons between hydrocephalic and non-hydrocephalic patients were made while assessing variations linked to age, sex and Evan's index.

Results: Significant differences were found, notably for depth (93.520 ± 7.228 mm), coronal plane angulation (10.982° ± 6.119°), distance to the sagittal suture (18.957 ± 8.608 mm), and distance to the superior frontal sulcus (7.00 mm). Other variables did not differ significantly between groups, including for the sagittal plane angulation (2.549° ± 3.576°) and the distances to the precentral sulcus (19.93 ± 7.955 mm), and to the coronal suture (10.55 mm).

Conclusion: The new approach, situated close to cranial sutures and distant to the precentral and superior frontal sulcus, shows promise in enhancing surgical precision and outcomes for hydrocephalus management.

Denervation of neurons is a network consequence of brain injury. The effects of denervation on neurons can be readily studied in vitro using organotypic slice cultures of entorhinal cortex and hippocampus. Following transection of the entorhino-dentate projection, granule cells (GCs) are denervated and show on average a transient loss of spines on their denervated distal dendrites but not on their non-denervated proximal dendrites. In the present study, we addressed the question how single GCs and their denervated and non-denervated segments react to entorhinal denervation. Local adeno-associated virus (AAV)-injections were employed to transduce dentate GCs with tdTomato and entorhinal projection neurons with EGFP. This made it possible to visualize both innervating entorhinal fibers and their target neurons and to identify dendritic segments located in the "entorhinal" and the "hippocampal" zone of the dentate gyrus. Confocal time-lapse imaging was used to image distal and proximal segments of single GCs after entorhinal denervation. Time-matched non-denervated cultures served as controls. In line with previous reports, average dendritic spine loss was ~30% (2-4 days post-lesion) in the denervated zone. However, individual GCs showed considerable variability in their response to denervation in both layers, and both decreases as well as increases in spine density were observed at the single cell level. Based on the standard deviations and the effect sizes observed in this study, a computer simulation yielded recommendations for the minimum number of neurons that should be analyzed in future studies using the entorhinal in vitro denervation model.

Animal personalities are stable, context-dependent behavioral differences. Associations between the personality of birds and polymorphisms in the dopamine receptor D4 (DRD4) gene have been repeatedly observed. In mammals, our understanding of the role of the dopamine (DA) system in higher cognitive functions and psychiatric disorders is improving, and we are beginning to understand the relationship between the neural circuits modulating the DA system and personality traits. However, to understand the phylogenetic continuity of the neural basis of personality, it is necessary to clarify the neural circuits that process personality in other animals and compare them with those in mammals. In birds, the DA system is anatomically and molecularly similar to that in mammals; however, the function of DRD4 remains largely unknown. In this study, we used chicks as model birds to reveal the expression regions of the DA neuron-related markers tyrosine hydroxylase (TH), dopa decarboxylase (DDC), dopamine β-hydroxylase (DBH), and DRD4, as well as other DRDs throughout the forebrain. We found that DRD4 was selectively expressed in the mitral cells of the olfactory bulb (OB). Furthermore, a detailed comparison of the expression regions of DA neurons and DRD4 in the OB revealed a cellular composition similar to that of mammals. Our findings suggest that the animal personality gene DRD4 is important for olfactory information processing in birds, providing a new basis for comparing candidate neural circuits for personality traits between birds and mammals.

Hodological patterning refers to developmental mechanisms that link the location of neurons in the brain or spinal cord to specific axonal trajectories that direct connectivity to synaptic targets either within the central nervous system or in the periphery. In vertebrate motor circuits, hodological patterning has been demonstrated at different levels, from the final motor output of somatic and preganglionic autonomic neurons targeting peripheral motoneurons and ganglion cells, to premotor inputs from spinal and brainstem neuron populations targeting the somatic motoneurons and preganglionic autonomic neurons, to cortical neurons that delegate movement commands to the brainstem and spinal neurons. In many cases molecular profiling reveals potential underlying mechanisms whereby selective gene expression creates the link between location and axon trajectory. At the cortical level, somatotopic organization suggests a potential underlying hodological patterning, but this has not been proven. This review describes examples of hodological patterning in motor circuits and covers current knowledge about how this patterning arises.

Neuropathic pain is a pervasive health concern worldwide, posing significant challenges to both clinicians and neuroscientists. While acute pain serves as a warning signal for potential tissue damage, neuropathic pain represents a chronic pathological condition resulting from injury or disease affecting sensory pathways of the nervous system. Neuropathic pain is characterized by long-lasting ipsilateral hyperalgesia (increased sensitivity to pain), allodynia (pain sensation in response to stimuli that are not normally painful), and spontaneous unprovoked pain. Current treatments for neuropathic pain are generally inadequate, and prevention remains elusive. In this review, we provide an overview of current treatments, their limitations, and a discussion on the potential of capsaicin and its analog, resiniferatoxin (RTX), for complete alleviation of nerve injury-induced neuropathic pain. In an animal model of neuropathic pain where the fifth lumbar (L5) spinal nerve is unilaterally ligated and cut, resulting in ipsilateral hyperalgesia, allodynia, and spontaneous pain akin to human neuropathic pain. The application of capsaicin or RTX to the adjacent uninjured L3 and L4 nerves completely alleviated and prevented mechanical and thermal hyperalgesia following the L5 nerve injury. The effects of this treatment were specific to unmyelinated fibers (responsible for pain sensation), while thick myelinated nerve fibers (responsible for touch and mechanoreceptor sensations) remained intact. Here, we propose to translate these promising preclinical results into effective therapeutic interventions in humans by direct application of capsaicin or RTX to adjacent uninjured nerves in patients who suffer from neuropathic pain due to peripheral nerve injury, following surgical interventions, diabetic neuropathy, trauma, vertebral disc herniation, nerve entrapment, ischemia, postherpetic lesion, and spinal cord injury.

The inferior colliculus (IC) is an important midbrain station of the auditory pathway, as well as an important hub of multisensory integration. The adult mammalian IC can be subdivided into three nuclei, with distinct cyto- and myeloarchitectonical profiles and distinct calcium binding proteins expression patterns. Despite several studies about its structural and functional development, the knowledge about the human fetal IC is rather limited. In this paper we first systematically describe the histological development of the human fetal IC and its subparts in five stages of the second trimester of pregnancy: 15 gestation weeks (GW), 18 GW, 21 GW, 24 GW, and 27 GW. We 3D reconstruct and calculate the volumetric growth of IC from one stage to another, which increases from 12.85 mm³ at 15 GW to 34.27 mm³ at 27 GW in the left hemisphere. The volumetric changes in the IC were further evaluated at the cellular level using serial Nissl-stained sections, as well as glial fibrillary acidic proteins (GFAP) and calretinin immunohistochemistry. We identify stellate-like and round neurons in the central nucleus of the IC (CNIC) at 24 GW and 27 GW, comparable to the adult human IC. Novel in this study, we investigate the differential calretinin expression patterns in the IC subparts, from 15 GW to 27 GW. CR labeling is identified mainly in the cortical IC rather than in the central nucleus. Furthermore, using GFAP, we describe the radial glial fibers patterns in IC, which are dominant at 18 GW and gradually taper off at later developmental stages. Finally, we describe the development of astroglia in each of the five developmental stages. All these results indicate that the human fetal IC development and cellular maturation occur in two major stages during the second trimester.