scholarly journals Structural and Functional Maturation of Rat Primary Motor Cortex Layer V Neurons

2020 ◽  
Vol 21 (17) ◽  
pp. 6101
Author(s):  
Bruno Benedetti ◽  
Dominik Dannehl ◽  
Jan Maximilian Janssen ◽  
Corinna Corcelli ◽  
Sébastien Couillard-Després ◽  
...  
Keyword(s):  
Cell Growth ◽  
Motor Cortex ◽  
Postnatal Development ◽  
Primary Motor Cortex ◽  
Continuous Process ◽  
Network Activity ◽  
Functional Maturation ◽  
Sensory Cortices ◽  
Layer V ◽  
Functional Output

Rodent neocortical neurons undergo prominent postnatal development and maturation. The process is associated with structural and functional maturation of the axon initial segment (AIS), the site of action potential initiation. In this regard, cell size and optimal AIS length are interconnected. In sensory cortices, developmental onset of sensory input and consequent changes in network activity cause phasic AIS plasticity that can also control functional output. In non-sensory cortices, network input driving phasic events should be less prominent. We, therefore, explored the relationship between postnatal functional maturation and AIS maturation in principal neurons of the primary motor cortex layer V (M1LV), a non-sensory area of the rat brain. We hypothesized that a rather continuous process of AIS maturation and elongation would reflect cell growth, accompanied by progressive refinement of functional output properties. We found that, in the first two postnatal weeks, cell growth prompted substantial decline of neuronal input resistance, such that older neurons needed larger input current to reach rheobase and fire action potentials. In the same period, we observed the most prominent AIS elongation and significant maturation of functional output properties. Alternating phases of AIS plasticity did not occur, and changes in functional output properties were largely justified by AIS elongation. From the third postnatal week up to five months of age, cell growth, AIS elongation, and functional output maturation were marginal. Thus, AIS maturation in M1LV is a continuous process that attunes the functional output of pyramidal neurons and associates with early postnatal development to counterbalance increasing electrical leakage due to cell growth.

scholarly journals Refinement of Active and Passive Membrane Properties of Layer V Pyramidal Neurons in Rat Primary Motor Cortex During Postnatal Development

2021 ◽  
Vol 14 ◽  
Author(s):  
Patricia Perez-García ◽  
Ricardo Pardillo-Díaz ◽  
Noelia Geribaldi-Doldán ◽  
Ricardo Gómez-Oliva ◽  
Samuel Domínguez-García ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Postnatal Development ◽  
Primary Motor Cortex ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Membrane Properties ◽  
Neuronal Membrane ◽  
Maturation Process ◽  
Postnatal Maturation ◽  
Layer V

Achieving the distinctive complex behaviors of adult mammals requires the development of a great variety of specialized neural circuits. Although the development of these circuits begins during the embryonic stage, they remain immature at birth, requiring a postnatal maturation process to achieve these complex tasks. Understanding how the neuronal membrane properties and circuits change during development is the first step to understand their transition into efficient ones. Thus, using whole cell patch clamp recordings, we have studied the changes in the electrophysiological properties of layer V pyramidal neurons of the rat primary motor cortex during postnatal development. Among all the parameters studied, only the voltage threshold was established at birth and, although some of the changes occurred mainly during the second postnatal week, other properties such as membrane potential, capacitance, duration of the post-hyperpolarization phase or the maximum firing rate were not defined until the beginning of adulthood. Those modifications lead to a decrease in neuronal excitability and to an increase in the working range in young adult neurons, allowing more sensitive and accurate responses. This maturation process, that involves an increase in neuronal size and changes in ionic conductances, seems to be influenced by the neuronal type and by the task that neurons perform as inferred from the comparison with other pyramidal and motor neuron populations.

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.

Abstract 12: Effect of Corticospinal Tract Injury on Motor Cortex Function and Connectivity After Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Steven C Cramer ◽  
Jessica M Cassidy ◽  
Morgan Ingemanson ◽  
Ramesh Srinivasan
Keyword(s):  
Motor Cortex ◽  
Frequency Band ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Premotor Cortex ◽  
Structural Mri ◽  
Network Activity ◽  
Neural Function ◽  
Lead System ◽  
Hemiparetic Stroke

Background and Purpose: Behavioral outcome after stroke is the product of both neural injury and neural function. Little is known about how injury to the corticospinal tract (CST) affects the function of motor cortex. The purpose of this study was to understand how subcortical injury to the CST affects function and connectivity of motor cortex. Methods: Patients with chronic hemiparetic stroke completed (1) a 3-minute resting-state EEG recording using a dense-array (256-lead) system, (2) a structural MRI scan, and (3) behavioral testing. Motor cortex activity was defined as EEG power within the high beta (20-30 Hz) frequency band commonly associated with motor network activity. Motor cortex connectivity was defined as coherence in the same frequency band. CST injury was defined as % lesion overlap with CST. Results: Of the 39 subjects (56 ± 14 years, 10 females, 15 ± 25 months post-stroke), none had injury to ipsilesional primary motor cortex (M1). Spearman correlation analyses revealed that increased CST injury was significantly related to reduced cortical activity in EEG leads overlying M1 (r= -0.48, p <0.002), dorsal premotor cortex (r= -0.41, p= 0.01), and supplementary motor area (r= -0.41, p= 0.01), but not in any other brain region, bilaterally. However, increased CST injury was not associated with any changes in M1 connectivity. Arm motor status (Fugl-Meyer score) tended to be associated with increased CST injury (r= -0.28, p= 0.08) but had no relationship with M1 connectivity. Conclusions: Increased CST injury after stroke is associated with decreased activity in those motor areas that issue descending fibers via this tract, a finding consistent with prior reports indicating that axonal injury modulates upstream function of surviving cortical elements. Increased CST injury was not associated with changes in M1 connectivity, suggesting a retained capacity for plasticity in support of behavioral recovery.

scholarly journals Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

2019 ◽  
Author(s):  
Atsushi Fukui ◽  
Hironobu Osaki ◽  
Yoshifumi Ueta ◽  
Yoshihiro Muragaki ◽  
Takakazu Kawamata ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Somatosensory Cortex ◽  
Acute Phase ◽  
Sensory Processing ◽  
Primary Motor Cortex ◽  
Temporal Coding ◽  
Network Activity ◽  
Primary Somatosensory Cortex ◽  
Inhibitory Input ◽  
Sensory Impairment

AbstractPrimary motor cortex (M1) infarction occasionally causes sensory impairment. Because sensory signal plays an important role in motor control, sensory impairment compromises recovery and rehabilitation from motor disability. Despite the importance of sensory-motor integration for rehabilitation after M1 infarction, the neural mechanism of the sensory impairment is poorly understood. We show that the sensory processing in the primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarction and recovered in a layer-specific manner in the subacute phase. This layer dependent recovery process and the anatomical connection pattern from M1 to S1 suggested the functional connectivity from M1 to S1 plays a key role in the impairment of sensory processing in S1. The simulation study demonstrated that the loss of inhibition from M1 to S1 in the acute phase of M1 infarction could cause the sensory processing impairment in S1, and the complementation of inhibition could recover the temporal coding. Taken together, we revealed how focal stroke of M1 alters cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.

Postnatal development of the human primary motor cortex: a quantitative cytoarchitectonic analysis

1995 ◽  
Vol 192 (6) ◽  
Author(s):  
Katrin Amunts ◽  
Vadim Istomin ◽  
Axel Schleicher ◽  
Karl Zilles
Keyword(s):  
Motor Cortex ◽  
Postnatal Development ◽  
Primary Motor Cortex

scholarly journals Spike Firing and IPSPs in Layer V Pyramidal Neurons during Beta Oscillations in Rat Primary Motor Cortex (M1) In Vitro

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85109 ◽  
Author(s):  
Michael G. Lacey ◽  
Gerard Gooding-Williams ◽  
Emma J. Prokic ◽  
Naoki Yamawaki ◽  
Stephen D. Hall ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Pyramidal Neurons ◽  
Beta Oscillations ◽  
Layer V ◽  
Spike Firing

scholarly journals Properties of primary motor cortex output to hindlimb muscles in the macaque monkey

2015 ◽  
Vol 113 (3) ◽  
pp. 937-949 ◽  
Author(s):  
Heather M. Hudson ◽  
Darcy M. Griffin ◽  
Abderraouf Belhaj-Saïf ◽  
Paul D. Cheney
Keyword(s):  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Rhesus Macaques ◽  
Macaque Monkey ◽  
The Other ◽  
Emg Activity ◽  
Cortical Control ◽  
Hindlimb Muscles ◽  
Intrinsic Foot Muscles ◽  
Layer V

The cortical control of forelimb motor function has been studied extensively, especially in the primate. In contrast, cortical control of the hindlimb has been relatively neglected. This study assessed the output properties of the primary motor cortex (M1) hindlimb representation in terms of the sign, latency, magnitude, and distribution of effects in stimulus-triggered averages (StTAs) of electromyography (EMG) activity recorded from 19 muscles, including hip, knee, ankle, digit, and intrinsic foot muscles, during a push-pull task compared with data reported previously on the forelimb. StTAs (15, 30, and 60 μA at 15 Hz) of EMG activity were computed at 317 putative layer V sites in two rhesus macaques. Poststimulus facilitation (PStF) was distributed equally between distal and proximal muscles, whereas poststimulus suppression (PStS) was more common in distal muscles than proximal muscles (51/49%, respectively, for PStF; 72/28%, respectively, for PStS) at 30 μA. Mean PStF and PStS onset latency generally increased the more distal the joint of a muscle's action. Most significantly, the average magnitude of hindlimb poststimulus effects was considerably weaker than the average magnitude of effects from forelimb M1. In addition, forelimb PStF magnitude increased consistently from proximal to distal joints, whereas hindlimb PStF magnitude was similar at all joints except the intrinsic foot muscles, which had a magnitude of approximately double that of all of the other muscles. The results suggest a greater monosynaptic input to forelimb compared with hindlimb motoneurons, as well as a more direct synaptic linkage for the intrinsic foot muscles compared with the other hindlimb muscles.

An experimental electron microscopy study of afferent connections to the primate motor and somatic sensory cortices

1979 ◽  
Vol 285 (1006) ◽  
pp. 199-226 ◽  
Keyword(s):  
Motor Cortex ◽  
Dendritic Spines ◽  
Asymmetric Membrane ◽  
Axon Terminals ◽  
Area 6 ◽  
Sensory Cortices ◽  
Dense Band ◽  
Layer V ◽  
Somatic Sensory Cortex ◽  
Cell Somata

An experimental electron microscope (e.m.) study has been made of the termination of the afferent connections to the primate sensori-motor cortex. Following large, stereotaxically placed thalamic lesions, degeneration in the motor and somatic sensory cortices was studied at survival periods of 4 and 5 days. Degenerating thalamocortical terminals had asymmetric membrane specializations. In the motor cortex 89.5% made synapses on to dendritic spines, 9% on to dendritic shafts and 1.5% on to cell somata; in the somatic sensory area 89% made synapses on to spines, 11 % on to dendritic shafts and one example contacted a cell soma and a spine. A considerable number of the spines receiving synapses from degenerating thalamo-cortical terminals were traced to their parent dendrites and these were of the pyramidal type whereas the dendritic shafts and cell somata contacted by degenerating thalamo-cortical terminals were mostly of the large stellate type. Most of the thalamo-cortical degeneration in both cortical areas occurred in a dense band in the upper two thirds of layer IV and the lower half of layer III but a number of degenerating terminals were found deep to this; in the motor cortex a second, less dense, band of degeneration was present in the lower part of layer V and top of layer VI. Degenerating thalamo-cortical terminals making synapses on to dendritic shafts and cell somata were scattered through the deep half of the cortex and not concentrated in the dense band of degeneration and so formed a greater proportion of the degeneration in the deep layers, particularly in the motor cortex. Sections cut parallel to the pial surface in layer IV of the motor cortex showed a statistically significant association between the degenerating thalamocortical axon terminals and the bundles of apical dendrites present at this level. Degeneration of commissural fibres was studied after removal of the contralateral sensori-motor cortex. Degenerating terminals had asymmetric membrane specializations. In the motor cortex 96% made synapses on to dendritic spines, 3% contacted dendritic shafts and one example made an axosomatic synapse; in area 3 97% made synapses on to dendritic spines and 3% contacted dendritic shafts. A number of the spines receiving synapses from degenerating commissural axon terminals were traced to their parent dendrites and these were of the pyramidal type. The cell soma and the majority of the dendritic shafts receiving synapses from commissural terminals were of the large stellate type although some of the dendritic shafts were probably those of small stellate cells. In the motor cortex degenerating commissural axon terminals were found in all cortical layers but were relatively more dense in layer I, the upper part of layer III, the upper part of layer V and the lowest part of layer V with layer V I; in the somatic sensory cortex most degenerating commissural terminals were found in the superficial half of the cortex. Following lesions of the primary somatic sensory cortex (SI) or of area 6 of the premotor cortex, degenerating terminals making asymmetric synapses were found in the motor cortex. Of the terminals of association fibres from SI, 82% made synapses on to dendritic spines and 18% on to dendritic shafts; of those fibres from area 6, 76% made synapses on to dendritic spines and 24% on to dendritic shafts. For both these association fibre connections, a proportion of the dendritic shafts contacted were clearly identifiable as those of large stellate cells. Terminals of both association connections occurred in all cortical layers with no obvious concentrations at any particular depth.

Effect of Forelimb Use on Postnatal Development of the Forelimb Motor Representation in Primary Motor Cortex of the Cat

2005 ◽  
Vol 93 (5) ◽  
pp. 2822-2831 ◽  
Author(s):  
John H. Martin ◽  
Daniel Engber ◽  
Zhuo Meng
Keyword(s):  
Botulinum Toxin ◽  
Motor Cortex ◽  
Postnatal Development ◽  
Primary Motor Cortex ◽  
Botulinum Toxin Injection ◽  
Intracortical Microstimulation ◽  
Behavioral Repertoire ◽  
Concomitant Increase ◽  
Motor Representation ◽  
Forelimb Movements

In the cat, the motor representation in motor cortex develops between wk 8 and wk 13. Motor map development is accompanied by a decrease in the current thresholds for evoking movements with a concomitant increase in the number of effective sites, an increase in the distal representation, and the representation of multijoint synergies. In this study we used intracortical microstimulation in anesthetized cats to examine how forelimb motor experiences influence development of map characteristics. To promote skilled movements during wks 8–13, animals were engaged in daily performance of a prehension task. Forelimb movements were prevented by intramuscular botulinum toxin injection or restraint. To determine whether experience-dependent changes were permanent, we examined the map in different animals between 1 wk and 1 yr after cessation of testing. Promoting forelimb use resulted in an increase in the number of sites from which multiple joint effects were produced by stimulation and the number of joints represented at those sites. The effect was maximal at 1 wk after cessation of testing, and became progressively less at 1 mo and at 4 mo. Preventing limb use resulted in a decreased number of effective sites, an increase in current thresholds for evoking responses, and a decreased representation of joints at multijoint sites. Our findings show that the motor map can respond to novel motor demands as it is forming during development but that it reverts back to one with the properties of a map in a control animal if those demands are not maintained in the animal's behavioral repertoire.

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