scholarly journals Layer 5 Pyramidal Neurons’ Dendritic Remodeling and Increased Microglial Density in Primary Motor Cortex in a Murine Model of Facial Paralysis

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Diana Urrego ◽  
Julieta Troncoso ◽  
Alejandro Múnera
Keyword(s):  
Motor Cortex ◽  
Facial Nerve ◽  
Facial Paralysis ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Dendritic Morphology ◽  
Nerve Lesion ◽  
Facial Nerve Lesion

This work was aimed at characterizing structural changes in primary motor cortex layer 5 pyramidal neurons and their relationship with microglial density induced by facial nerve lesion using a murine facial paralysis model. Adult transgenic mice, expressing green fluorescent protein in microglia and yellow fluorescent protein in projecting neurons, were submitted to either unilateral section of the facial nerve or sham surgery. Injured animals were sacrificed either 1 or 3weeks after surgery. Two-photon excitation microscopy was then used for evaluating both layer 5 pyramidal neurons and microglia in vibrissal primary motor cortex (vM1). It was found that facial nerve lesion induced long-lasting changes in the dendritic morphology of vM1 layer 5 pyramidal neurons and in their surrounding microglia. Dendritic arborization of the pyramidal cells underwent overall shrinkage. Apical dendrites suffered transient shortening while basal dendrites displayed sustained shortening. Moreover, dendrites suffered transient spine pruning. Significantly higher microglial cell density was found surrounding vM1 layer 5 pyramidal neurons after facial nerve lesion with morphological bias towards the activated phenotype. These results suggest that facial nerve lesions elicit active dendrite remodeling due to pyramidal neuron and microglia interaction, which could be the pathophysiological underpinning of some neuropathic motor sequelae in humans.

scholarly journals ENTÉRATE DE CÓMO CAMBIA EL CEREBRO CUANDO SE LESIONA UN NERVIO

2016 ◽  
Vol 21 (1Supl) ◽  
pp. 279-285 ◽  
Author(s):  
Julieta Troncoso
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Facial Nerve ◽  
Pyramidal Neurons ◽  
Dendritic Morphology ◽  
Nerve Lesion ◽  
Nerve Injuries ◽  
Somatosensory Stimulation ◽  
Facial Nerve Lesion ◽  
The Central Nervous System

<p>Desde hace algunos años el grupo de investigación de Neurofisiología Comportamental de la Universidad Nacional de Colombia ha venido evaluando los cambios que ocurren en el sistema nervioso central luego de la lesión de un nervio periférico. Específicamente trabajamos con el modelo de lesión del nervio facial en roedores para evaluar las modificaciones funcionales y estructurales que ocurren en la corteza sensoriomotora primaria luego de la lesión. Al lesionarse el nervio facial, el cerebro entra en un programa de reorganización que incluye cambios electrofisiológicos en las neuronas de la corteza motora que comandan los movimientos faciales (M1). En este sentido, las células de la corteza motora cerebral se vuelven más excitables y modifican su respuesta ante estímulos sensoriales. La reorganización tras la lesión también incluye cambios morfológicos en M1: las células piramidales de la corteza motora retraen su árbol dendrítico y disminuye la densidad de sus espinas dendríticas. En asociación con estos cambios, las células de M1 disminuyen transitoriamente su inmunorreactividad para NeuN (marcador específico de núcleos neuronales) y aumentan la expresión de GAP43 (proteína de crecimiento axonal). Esto indica, posiblemente, un cambio metabólico celular en asociación con la búsqueda de nuevas dianas sinápticas. Finalmente, hallamos que la glía circundante en M1 (tanto astrocitos como microglía) se activa de manera muy temprana luego de lesiones del nervio facial. Esto podría indicar que el remodelamiento estructural y funcional hallado en las neuronas corticales es el resultado de la interacción entre la activación de la glía circundante y las células piramidales de M1 (aunque se necesitan muchos experimentos adicionales que así lo demuestren).</p><p> </p><p>Abstract</p><p>Our research group (Neurofisiología Comportamental, Universidad Nacional de Colombia) has evaluated changes in the central nervous system induced by peripheral nerve injuries. We have characterized facial nerve lesion-induced structural and functional changes in primary motor cortex pyramidal neurons (M1) in rodents. Following the lesion, M1 neurons modified their spontaneous basal firing frequency: they become more excitable. Moreover, we found changes in evoked-activity with somatosensory stimulation after facial nerve lesion. Morphologically, it was found that facial nerve lesion induced long-lasting changes in the dendritic morphology of M1 pyramidal neurons. Dendritic branching of the pyramidal cells underwent overall shrinkage and dendrites suffered transient spine pruning. Additionally, we evaluated the reorganization processes in the central nervous system by using both neuronal and glial markers. Decreased NeuN (neuronal nuclei antigen) immunoreactivity and increased GAP-43 (growth-associated protein 43) immunoreactivity were found M1 after facial nerve lesion. In addition, we also observed astrogliosis and microglial activation sourrounding M1 early after facial nerve injury. Taken together these findings suggest that facial nerve lesions induce widespread reorganization in M1 including neuronal shrinkage, axon sprouting as well as astrocytic and microglia activation. These results suggest that facial nerve injuries elicit active remodeling due to pyramidal neuron and glia interaction (although additional experiments that demonstrate it are needed)</p>

Optogenetic probing of nerve and muscle function after facial nerve lesion in the mouse whisker system

2018 ◽  
Author(s):  
David J. Margolis ◽  
Akhil Bandi ◽  
Aman Upadhyay ◽  
S. Olga Yiantsos ◽  
Thomas J. Vajtay ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Muscle Function ◽  
Nerve Lesion ◽  
Facial Nerve Lesion ◽  
Whisker System

scholarly journals Structural Abnormalities in Neurons Are Sufficient To Explain the Clinical Disease and Fatal Outcome of Experimental Rabies in Yellow Fluorescent Protein-Expressing Transgenic Mice

2007 ◽  
Vol 82 (1) ◽  
pp. 513-521 ◽  
Author(s):  
Courtney A. Scott ◽  
John P. Rossiter ◽  
R. David Andrew ◽  
Alan C. Jackson
Keyword(s):  
Electron Microscopy ◽  
Cerebral Cortex ◽  
Virus Infection ◽  
Hind Limb ◽  
Pyramidal Neurons ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Fatal Outcome ◽  
Histopathological Changes ◽  
Rabies Virus Infection

ABSTRACT Under natural conditions and in some experimental models, rabies virus infection of the central nervous system causes relatively mild histopathological changes, without prominent evidence of neuronal death despite its lethality. In this study, the effects of rabies virus infection on the structure of neurons were investigated with experimentally infected transgenic mice expressing yellow fluorescent protein (YFP) in neuronal subpopulations. Six-week-old mice were inoculated in the hind-limb footpad with the CVS strain of fixed virus or were mock infected with vehicle (phosphate-buffered saline). Brain regions were subsequently examined by light, epifluorescent, and electron microscopy. In moribund CVS-infected mice, histopathological changes were minimal in paraffin-embedded tissue sections, although mild inflammatory changes were present. Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling and caspase-3 immunostaining showed only a few apoptotic cells in the cerebral cortex and hippocampus. Silver staining demonstrated the preservation of cytoskeletal integrity in the cerebral cortex. However, fluorescence microscopy revealed marked beading and fragmentation of the dendrites and axons of layer V pyramidal neurons in the cerebral cortex, cerebellar mossy fibers, and axons in brainstem tracts. At an earlier time point, when mice displayed hind-limb paralysis, beading was observed in a few axons in the cerebellar commissure. Toluidine blue-stained resin-embedded sections from moribund YFP-expressing animals revealed vacuoles within the perikarya and proximal dendrites of pyramidal neurons in the cerebral cortex and hippocampus. These vacuoles corresponded with swollen mitochondria under electron microscopy. Vacuolation was also observed ultrastructurally in axons and in presynaptic nerve endings. We conclude that the observed structural changes are sufficient to explain the severe clinical disease with a fatal outcome in this experimental model of rabies.

scholarly journals Plasticity of the Cortical Motor System

2008 ◽  
Vol 20 (1) ◽  
pp. 5-22 ◽  
Author(s):  
Bogdan Sadowski
Keyword(s):  
Motor Cortex ◽  
Motor System ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Skill Learning ◽  
Dynamic Features ◽  
Cortical Motor

Plasticity of the Cortical Motor SystemThe involvement of brain plastic mechanisms in the control of motor functions under normal and pathological conditions is described. These mechanisms are based on a similar principle as the neuronal models of neuronal plasticity - long-term potentiation (LTP), and long-term depression (LTD). In the motor cortex, LTP-like phenomena play a role in strengthening synaptic connections between pyramidal neurons. LTD is important for the elimination of unnecessary inputs to the cortex. The dynamic features of the primary motor cortex activity depend on particular neuronal interconnectivity within this area. The pyramidal cells send horizontal collaterals to adjacent subregions of the primary motor cortex, and so can either excite or inhibit remote pyramidal cells. These connections can expand or shrink depending on actual physiological demands, and play a role in skill learning.

scholarly journals Dopamine D2 receptors modulate intrinsic properties and synaptic transmission of parvalbumin interneurons in the mouse primary motor cortex

2019 ◽  
Author(s):  
Jérémy Cousineau ◽  
Léa Lescouzères ◽  
Anne Taupignon ◽  
Lorena Delgado-Zabalza ◽  
Emmanuel Valjent ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Synaptic Transmission ◽  
Motor Skills ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
D2 Receptors ◽  
Receptor Subtypes ◽  
Parvalbumin Interneurons ◽  
Layer V ◽  
Gabaergic Synaptic Transmission

AbstractDopamine (DA) plays a crucial role in the control of motor and higher cognitive functions such as learning, working memory and decision making. The primary motor cortex (M1), which is essential for motor control and the acquisition of motor skills, receives dopaminergic inputs in its superficial and deep layers from the midbrain. However, the precise action of DA and DA receptor subtypes on the cortical microcircuits of M1 remains poorly understood. The aim of this work was to investigate how DA, through the activation of D2 receptors (D2R), modulates the cellular and synaptic activity of M1 parvalbumin-expressing interneurons (PVINs) which are crucial to regulate the spike output of pyramidal neurons (PNs). By combining immunofluorescence, ex vivo electrophysiology, pharmacology and optogenetics approaches, we show that D2R activation increases neuronal excitability of PVINs and GABAergic synaptic transmission between PVINs and PNs in layer V of M1. Our data reveal a mechanism through which cortical DA modulates M1 microcircuitry and might participate in the acquisition of motor skills.Significance StatementPrimary motor cortex (M1), which is a region essential for motor control and the acquisition of motor skills, receives dopaminergic inputs from the midbrain. However, precise action of dopamine and its receptor subtypes on specific cell types in M1 remained poorly understood. Here, we demonstrate in M1 that dopamine D2 receptors (D2R) are present in parvalbumin interneurons (PVINs) and their activation increases the excitability of the PVINs, which are crucial to regulate the spike output of pyramidal neurons (PNs). Moreover the activation of the D2R facilitates the GABAergic synaptic transmission of those PVINs on layer V PNs. These results highlight how cortical dopamine modulates the functioning of M1 microcircuit which activity is disturbed in hypo- and hyperdopaminergic states.

scholarly journals Bilateral Congenital Absence of the Stapes Superstructure in Two Siblings

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Jose Ignacio Undabeitia ◽  
José Undabeitia ◽  
Laura Cianci ◽  
Luis Padilla ◽  
Eduardo Petreñas ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Hearing Aid ◽  
Treatment Options ◽  
Rare Condition ◽  
Functional Results ◽  
Congenital Absence ◽  
Abnormal Development ◽  
Nerve Lesion ◽  
History Of ◽  
Facial Nerve Lesion

Middle ear ossicle malformations are an uncommon event. Among them, the congenital absence of the stapes is a very rare condition that is seldom described in the literature. We report the cases of two women, aged 19 and 22 , who presented with a long history of conductive deafness. An exploratory tympanotomy was performed and the absence of the stapes superstructure and an abnormal position of the facial nerve could be observed. A bone anchored hearing aid (BAHA) was implanted in both patients with good results. It is believed that stapes agenesis is related to an abnormal development of the facial nerve, which by the 5th to 6th week of gestation would interpose between the otic capsule and the stapes blastema, preventing these structures from contacting. A long history of nonprogressive hearing loss from birth or early childhood is the key to reach a diagnosis. Several treatment options have been described. The authors opted for a hearing aid due to the high risk of facial nerve lesion, with good functional results.

Sign in / Sign up

Export Citation Format

Share Document