scholarly journals Picrotoxin blocks arousal-associated suppression caused by basal forebrain stimulation in cerebral motor cortical neurons of the rat

1998 ◽  
Vol 76 ◽  
pp. 90
Author(s):  
Miyuki Yokoyama ◽  
Keiko Arai ◽  
Tomokazu Oshima
Keyword(s):  
Basal Forebrain ◽  
Cortical Neurons ◽  
Motor Cortical

Dopaminergic modulation of transcallosal activity of cat motor cortical neurons

1999 ◽  
Vol 33 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Kadrul Huda ◽  
Thucidydes L. Salunga ◽  
Syed A. Chowdhury ◽  
Takashi Kawashima ◽  
Ken’ichi Matsunami
Keyword(s):  
Cortical Neurons ◽  
Dopaminergic Modulation ◽  
Motor Cortical

Effect of Nicorandil on the Spatial Arrangement of Primary Motor Cortical Neurons in the Sub-Acute Phase of Stroke in a Rat Model

2021 ◽  
pp. 102000
Author(s):  
Maryam Owjfard ◽  
Zohreh Taghadosi ◽  
Mohammad Reza Bigdeli ◽  
Anahid Safari ◽  
Asadollah Zarifkar ◽  
...  
Keyword(s):  
Acute Phase ◽  
Rat Model ◽  
Cortical Neurons ◽  
Spatial Arrangement ◽  
Motor Cortical

Computer Simulation of Post-Spike Facilitation in Spike-Triggered Averages of Rectified EMG

1998 ◽  
Vol 80 (3) ◽  
pp. 1391-1406 ◽  
Author(s):  
S. N. Baker ◽  
R. N. Lemon
Keyword(s):  
Computer Simulation ◽  
Action Potential ◽  
Motor Unit ◽  
Cortical Neurons ◽  
Emg Activity ◽  
Motor Unit Action Potential ◽  
Cortical Cells ◽  
Motor Unit Action ◽  
Motor Cortical ◽  
Unit Action

Baker, S. N. and R. N. Lemon. Computer simulation of post-spike facilitation in spike-triggered averages of rectified EMG. J. Neurophysiol. 80: 1391–1406, 1998. When the spikes of a motor cortical cell are used to compile a spike-triggered average (STA) of rectified electromyographic (EMG) activity, a post-spike facilitation (PSF) is sometimes seen. This is generally thought to be indicative of direct corticomotoneuronal (CM) connections. However, it has been claimed that a PSF could be caused by synchronization between CM and non-CM cells. This study investigates the generation of PSF using a computer model. A population of cortical cells was simulated, some of which made CM connections to a pool of 103 motoneurons. Motoneurons were simulated using a biophysically realistic model. A subpopulation of the cortical cells was synchronized together. After a motoneuron discharge, a motor unit action potential was generated; these were summed to produce an EMG output. Realistic values were used for the corticospinal and peripheral nerve conduction velocity distribution, for slowing of impulse conduction in CM terminal axons, and for the amount of cortical synchrony. STA of the rectified EMG from all cortical neurons showed PSF; however, these were qualitatively different for CM versus non-CM cells. Using an epoch analysis to determine reliability in a quantitative manner, it was shown that the onset latency of PSF did not distinguish the two classes of cells after 10,000 spikes because of high noise in the averages. The time of the PSF peak and the peak width at half-maximum (PWHM) could separate CM from synchrony effects. However, only PWHM was robust against changes in motor unit action-potential shape and duration and against changes in the width of cortical synchrony. The amplitude of PSF from a CM cell could be doubled by the presence of synchrony. It is proposed that, if a PSF has PWHM <7 ms, this reliably indicates that the trigger is a CM cell projecting to the muscle whose EMG is averaged. In an analysis of experimental data where macaque motor cortical cells facilitated hand and forearm muscle EMG, 74% of PSFs fulfilled this criterion. The PWHM criterion could be applied to other STA studies in which it is important to exclude the effects of synchrony.

Reach task-associated excitatory overdrive of motor cortical neurons following infusion with ALS-CSF

2013 ◽  
Vol 121 (1) ◽  
pp. 49-58 ◽  
Author(s):  
R. Sankaranarayani ◽  
Mohan Raghavan ◽  
A. Nalini ◽  
T. R. Laxmi ◽  
T. R. Raju
Keyword(s):  
Cortical Neurons ◽  
Motor Cortical

Primary motor cortical neurons encode functional muscle synergies

2002 ◽  
Vol 146 (2) ◽  
pp. 233-243 ◽  
Author(s):  
R. N. Holdefer ◽  
L. E. Miller
Keyword(s):  
Cortical Neurons ◽  
Muscle Synergies ◽  
Motor Cortical

Neurotransmitters in the cerebral cortex

1986 ◽  
Vol 65 (2) ◽  
pp. 135-153 ◽  
Author(s):  
Edward G. Jones
Keyword(s):  
Cerebral Cortex ◽  
Basal Forebrain ◽  
Cortical Neurons ◽  
Pyramidal Cells ◽  
Gamma Aminobutyric Acid ◽  
Content Type ◽  
Disease States ◽  
Afferent Fibers ◽  
Cortical Interneurons ◽  
Fine Print

✓ This article surveys the conventional neurotransmitters and modulatory neuropeptides that are found in the cerebral cortex and attempts to place them into the perspective of both intracortical circuitry and cortical disease. The distribution of these substances is related, where possible, to particular types of cortical neuron or to afferent or efferent fibers. Their physiological actions, where known, on cortical neurons are surveyed, and their potential roles in disease states such as the dementias, epilepsy, and stroke are assessed. Conventional transmitters that occur in afferent fibers to the cortex from brain-stem and basal forebrain sites are: serotonin, noradrenaline, dopamine, and acetylcholine. All of these except dopamine are distributed to all cortical areas: dopamine is distributed to frontal and cingulate areas only. The transmitter in thalamic afferent systems is unknown. Gamma aminobutyric acid (GABA) is the transmitter used by the majority of cortical interneurons and has a profound effect upon the shaping of receptive field properties. The vast majority of the known cortical peptides are found in GABAergic neurons, and the possibility exists that they may act as trophic substances for other neurons. Levels of certain neuropeptides decline in cases of dementia of cortical origin. Acetylcholine is the only other known transmitter of cortical neurons. It, too, is contained in neurons that also contain a neuropeptide. The transmitter(s) used by excitatory cortical interneurons and by the efferent pyramidal cells is unknown, but it may be glutamate or aspartate. It is possible that excitotoxins released in anoxic disease of the cortex may produce damage by acting on receptors for these or related transmitter agents.

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