Cerebral Pyramidal Neurons Research Articles

Neuroprotective effects of Apis dorsata forest honey on the neurons count in cerebrum and cerebellum of mice (Mus musculus) exposed to monosodium glutamate

Introduction: Monosodium glutamate or MSG can have an effect on increasing the production of reactive oxygen species (ROS) in the brain. Apis dorsata forest honey is known to have higher antioxidant activity than Apis mellifera and Apis cerana honey. This study aims to determine the preventive effect of Apis dorsata honey on the number of pyramidal cerebrum neurons and purkinje cerebellum neurons of mice (Mus musculus) exposed to monosodium glutamate (MSG). Material and Methods: This study used 25 mice which were divided into 5 groups. In the K- group only aquadest was given. The K+ group was given 4mg/gBB of MSG. Groups P1, P2, and P3 given Apis dorsata honey at a dose of 53.82mg/20gBW, 107.64mg/20gBW, and 161.46mg/20gBW. All treatments were carried out orally for 52 days. Results: The results showed that the average number of cerebral pyramidal neurons in the K-, K+, P1, P2, and P3 groups was 12.24±0.607; 7.24±2.875; 12.48±1.513; 15.72±0.944; and 19.28±2.827. The mean number of purkinje cerebellar neurons was 4.8±1.456; 2.08±0.807; 3.08±1.035; 3.56±0.434; and 4.68±1.390. Discussion: The average number of pyramidal neurons and purkinje neurons in the group given preventive dose of Apis dorsata honey and exposed to MSG was higher and there is a significant difference compared to the group that was only exposed to MSG. It can be concluded that the administration of Apis dorsata honey can maintain the number of pyramidal cerebrum neurons and purkinje cerebellar neurons in mice exposed to MSG.

Immune-Triggered Forms of Plasticity Across Brain Regions.

Immune cells play numerous roles in the host defense against the invasion of microorganisms and pathogens, which induces the release of inflammatory mediators (e.g., cytokines and chemokines). In the CNS, microglia is the major resident immune cell. Recent efforts have revealed the diversity of the cell types and the heterogeneity of their functions. The refinement of the synapse structure was a hallmark feature of the microglia, while they are also involved in the myelination and capillary dynamics. Another promising feature is the modulation of the synaptic transmission as synaptic plasticity and the intrinsic excitability of neurons as non-synaptic plasticity. Those modulations of physiological properties of neurons are considered induced by both transient and chronic exposures to inflammatory mediators, which cause behavioral disorders seen in mental illness. It is plausible for astrocytes and pericytes other than microglia and macrophage to induce the immune-triggered plasticity of neurons. However, current understanding has yet achieved to unveil what inflammatory mediators from what immune cells or glia induce a form of plasticity modulating pre-, post-synaptic functions and intrinsic excitability of neurons. It is still unclear what ion channels and intracellular signaling of what types of neurons in which brain regions of the CNS are involved. In this review, we introduce the ubiquitous modulation of the synaptic efficacy and the intrinsic excitability across the brain by immune cells and related inflammatory cytokines with the mechanism for induction. Specifically, we compare neuro-modulation mechanisms by microglia of the intrinsic excitability of cerebellar Purkinje neurons with cerebral pyramidal neurons, stressing the inverted directionality of the plasticity. We also discuss the suppression and augmentation of the extent of plasticity by inflammatory mediators, as the meta-plasticity by immunity. Lastly, we sum up forms of immune-triggered plasticity in the different brain regions with disease relevance. Together, brain immunity influences our cognition, sense, memory, and behavior via immune-triggered plasticity.

CRMP1 and CRMP4 are required for proper orientation of dendrites of cerebral pyramidal neurons in the developing mouse brain

Neural circuit formation is a critical process in brain development. Axon guidance molecules, their receptors, and intracellular mediators are important to establish neural circuits. Collapsin response mediator proteins (CRMPs) are known intercellular mediators of a number of repulsive guidance molecules. Studies of mutant mice suggest roles of CRMPs in dendrite development. However, molecular mechanisms of CRMP-mediated dendritic development remain to elucidate. In this study, we show abnormal orientation of basal dendrites (extension to deeper side) of layer V pyramidal neurons in the cerebral cortex of CRMP4−/− mice. Moreover, we observed severe abnormality in orientation of the basal dendrites of these neurons in double knockout of CRMP1 and 4, suggesting redundant functions of these two genes. Redundant gene functions were also observed in proximal bifurcation phenotype in apical dendrites of hippocampal CA1 pyramidal neurons. These results indicate that CRMP1 and CRMP4 regulate proper orientation of the basal dendrites of layer V neurons in the cerebral cortex.

Satb2 Is Required for Dendritic Arborization and Soma Spacing in Mouse Cerebral Cortex

Self-avoidance is a mechanism by which dendrites from the same neuron repel one another in order to establish uniform coverage of the dendritic field. The importance of self-avoidance for the development of complex arborization patterns has been highlighted by studies of Drosophila sensory and mouse retinal neurons. However, it is unclear whether branch patterning in the mammalian central nervous system is also governed by this strategy. We reduced Satb2 expression in a population of layer II/III pyramidal neurons in vivo by RNA interference and found that the somas of Satb2-deficient neurons clumped together, and their dendrites failed to expand laterally but instead formed fascicles. Furthermore, experiments showed that reducing Satb2 caused the adhesion of not only neighboring Satb2-deficient neurons but also neighboring wild-type neurons. Our results indicate a cell autonomous and non-cell autonomous role for Satb2 in regulating the adhesive and/or repulsive properties of cerebral pyramidal neurons.

Principles of Long-Term Dynamics of Dendritic Spines

Long-term potentiation of synapse strength requires enlargement of dendritic spines on cerebral pyramidal neurons. Long-term depression is linked to spine shrinkage. Indeed, spines are dynamic structures: they form, change their shapes and volumes, or can disappear in the space of hours. Do all such changes result from synaptic activity, or do some changes result from intrinsic processes? How do enlargement and shrinkage of spines relate to elimination and generation of spines, and how do these processes contribute to the stationary distribution of spine volumes? To answer these questions, we recorded the volumes of many individual spines daily for several days using two-photon imaging of CA1 pyramidal neurons in cultured slices of rat hippocampus between postnatal days 17 and 23. With normal synaptic transmission, spines often changed volume or were created or eliminated, thereby showing activity-dependent plasticity. However, we found that spines changed volume even after we blocked synaptic activity, reflecting a native instability of these small structures over the long term. Such "intrinsic fluctuations" showed unique dependence on spine volume. A mathematical model constructed from these data and the theory of random fluctuations explains population behaviors of spines, such as rates of elimination and generation, stationary distribution of volumes, and the long-term persistence of large spines. Our study finds that generation and elimination of spines are more prevalent than previously believed, and spine volume shows significant correlation with its age and life expectancy. The population dynamics of spines also predict key psychological features of memory.

Protracted juvenile neuronal ceroid lipofuscinosis—An autopsy report and immunohistochemical analysis

The juvenile form of neuronal ceroid lipofuscinosis (JNCL) is caused by mutations in the CLN3 gene, and is characterized by progressive loss of vision and development of motor deficits. A few patients exhibit a more protracted clinical course and are diagnosed with protracted JNCL (PJNCL). Here, we report the autopsy in a case of PJNCL in a 55-year-old male and immunohistochemical examination of the involvement of oxidative stress and glutamate excitotoxicity in neurodegeneration. The patient was born to consanguineous parents (I assume this means that the parents were related. If not, then the sentence will need to be changed again.) and had brothers with similar neurological disease. He showed mental retardation and visual impairment in the first decade which gradually developed along with motor dysfunction for over 40 years. At autopsy, the cerebral pyramidal neurons revealed deposition of lipopigments, which demonstrated ‘finger print’ and curvilinear profiles on electron microscopy. He also exhibited cerebellar cortical atrophy, fibrillary gliosis in the white matter, and rarefication in the globus pallidus. Immunohistochemically, the number of neurons immunoreactive for advanced glycation end product was elevated in the cerebellar cortex and midbrain. Immunoreactivity for excitatory amino acid transporter 1 was reduced in the cerebellar dentate and inferior olivary nuclei. These findings suggest that oxidative damage to proteins and disturbed glutamate transport can be involved in PJNCL.

Basal Forebrain Cholinergic Dysfunction in Alzheimer’s Disease – Interrelationship with β-amyloid, Inflammation and Neurotrophin Signaling

Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks. Deposition of extracellular neuritic, beta-amyloid peptide-containing plaques (senile plaques) in cerebral cortical regions of Alzheimer patients is accompanied by the presence of intracellular neurofibrillary tangles in cerebral pyramidal neurons. Basal forebrain cholinergic dysfunction is also a consistent feature of Alzheimer's disease, which has been suggested to cause, at least partly, the cognitive deficits observed in patients with Alzheimer's disease. Impaired cortical cholinergic neurotransmission may also contribute to beta-amyloid plaque pathology in Alzheimer's disease by affecting expression and processing of the beta-amyloid precursor protein (APP). Vice versa, low level of soluble beta-amyloid has been observed to inhibit cholinergic synaptic function. Deposition of beta-amyloid plaques in Alzheimer's disease is also accompanied by a significant plaque-associated glial up-regulation of interleukin-1, which has been attributed to affect expression and metabolism of APP and to interfere with cholinergic transmission. Understanding the molecular mechanisms underlying the interrelationship between cortical cholinergic dysfunction, beta-amyloid formation and deposition, as well as local inflammatory upregulation, would allow to derive potential treatment strategies to pharmacologically intervene in the disease-causing signaling cascade.

Restricted occurrence of an unusual ganglioside GD1 alpha in rat brain and its possible involvement in dendritic growth of cerebellar Purkinje neurons.

The spatial pattern of expression of a minor disialosyl ganglioside GD1 alpha in the rat brain was investigated immunohistochemically using a specific murine monoclonal antibody KA-17. The antibody shows noticeable immunoreactivity in the proximal dendrites and neuronal cell bodies of restricted populations of neurons including cerebral pyramidal neurons and cerebellar Purkinje neurons. Immunocytochemical analysis revealed that Purkinje neurons maintained in a dissociate culture condition also express GD1 alpha in the dendrites and cell bodies. We have examined the functional involvement of this ganglioside in the growth of brain neurons using KA-17 antibody. Addition of the antibody to cerebellar primary cultures caused perturbation of the dendritic development of Purkinje neurons in a dose-dependent manner. The length and branching of the dendrites were severely decreased by the antibody treatment. When other anti-glycoconjugate or sphingolipid monoclonal antibodies were tested, only HNK-1 monoclonal antibody that recognizes sulfoglucuronic residues in glycolipids and glycoproteins had similar but moderate inhibitory actions on the dendritic development of these neurons. In contrast to the morphological alterations observed in Purkinje cells, other cerebellar cells including granule neurons appear to be almost normal following the antibody treatment. These observations lead to the possibility that GD1 alpha ganglioside has a role in the development of Purkinje cell dendrites.