Early pre- and postsynaptic decrease in glutamatergic and cholinergic signaling after spinalization is not modified when stimulating proprioceptive input to the ankle extensor α-motoneurons: Anatomical and neurochemical study

Stem cells have extensive proliferative potential and the ability to differentiate into one or more mature cell types. The mechanisms by which stem cells accomplish self-renewal provide fundamental insight into the origin and design of multicellular organisms. These pathways allow the repair of damage and extend organismal life beyond that of component cells, and they probably preceded the evolution of complex metazoans. Understanding the true nature of stem cells can only come from discovering how they are regulated. The concept that stem cells are controlled by particular microenvironments, also known as niches, has been widely accepted. Technical advances now allow characterization of the zones that maintain and control stem cell activity in several organs, including the brain, skin, and gut. Cholinergic neurons release acetylcholine (ACh) that mediates chemical transmission via ACh receptors such as nicotinic and muscarinic receptors. Although the cholinergic system is composed of organized nerve cells, the system is also involved in mammalian non-neuronal cells, including stem cells, embryonic stem cells, epithelial cells, and endothelial cells. Thus, cholinergic signaling plays a pivotal role in controlling their behaviors. Studies regarding this signal are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and they are expected to advance efforts to control stem cells therapeutically. The present article reviews recent findings about cholinergic signaling that is essential to control stem cell function in a cholinergic niche.

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Cholinergic Signaling, Neural Excitability, and Epilepsy

Molecules ◽

10.3390/molecules26082258 ◽

2021 ◽

Vol 26 (8) ◽

pp. 2258

Author(s):

Yu Wang ◽

Bei Tan ◽

Yi Wang ◽

Zhong Chen

Keyword(s):

Cholinergic Neurons ◽

Epileptic Seizures ◽

Brain Disorder ◽

Neural Excitability ◽

Cholinergic Signaling ◽

The Central Nervous System ◽

Muscarinic And Nicotinic Receptors ◽

Cumulative Evidence ◽

Precise Role

Epilepsy is a common brain disorder characterized by recurrent epileptic seizures with neuronal hyperexcitability. Apart from the classical imbalance between excitatory glutamatergic transmission and inhibitory γ-aminobutyric acidergic transmission, cumulative evidence suggest that cholinergic signaling is crucially involved in the modulation of neural excitability and epilepsy. In this review, we briefly describe the distribution of cholinergic neurons, muscarinic, and nicotinic receptors in the central nervous system and their relationship with neural excitability. Then, we summarize the findings from experimental and clinical research on the role of cholinergic signaling in epilepsy. Furthermore, we provide some perspectives on future investigation to reveal the precise role of the cholinergic system in epilepsy.

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Contribution of the basal forebrain to corticocortical network interactions

Brain Structure and Function ◽

10.1007/s00429-021-02290-z ◽

2021 ◽

Author(s):

Peter Gombkoto ◽

Matthew Gielow ◽

Peter Varsanyi ◽

Candice Chavez ◽

Laszlo Zaborszky

Keyword(s):

Sensory Processing ◽

Basal Forebrain ◽

Field Potential ◽

Cholinergic Neurons ◽

Attention And Memory ◽

Cortical Circuits ◽

Cholinergic Signaling ◽

Spatial Changes ◽

Gamma Power ◽

Gamma Coherence

AbstractBasal forebrain (BF) cholinergic neurons provide the cerebral cortex with acetylcholine. Despite the long-established involvement of these cells in sensory processing, attention, and memory, the mechanisms by which cholinergic signaling regulates cognitive processes remain elusive. In this study, we recorded spiking and local field potential data simultaneously from several locations in the BF, and sites in the orbitofrontal and visual cortex in transgenic ChAT-Cre rats performing a visual discrimination task. We observed distinct differences in the fine spatial distributions of gamma coherence values between specific basalo-cortical and cortico-cortical sites that shifted across task phases. Additionally, cholinergic firing induced spatial changes in cortical gamma power, and optogenetic activation of BF increased coherence between specific cortico-cortical sites, suggesting that the cholinergic system contributes to selective modulation of cortico-cortical circuits. Furthermore, the results suggest that cells in specific BF locations are dynamically recruited across behavioral epochs to coordinate interregional cortical processes underlying cognition.

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Quantification of Cardiomyocyte Beating Frequency Using Fourier Transform Analysis

Photonics ◽

10.3390/photonics5040039 ◽

2018 ◽

Vol 5 (4) ◽

pp. 39 ◽

Cited By ~ 3

Author(s):

Allison Reno ◽

Andrew Hunter ◽

Yang Li ◽

Tong Ye ◽

Ann Foley

Keyword(s):

Fourier Transform ◽

Fast Fourier Transform ◽

Sinoatrial Node ◽

Frequency Data ◽

True Rate ◽

Video Clips ◽

Organoid Culture ◽

Cholinergic Signaling ◽

Beating Frequency

Pacemaker cardiomyocytes of the sinoatrial node (SAN) beat more rapidly than cells of the working myocardium. Beating in SAN cells responds to β-adrenergic and cholinergic signaling by speeding up or slowing, respectively. Beat rate has traditionally been assessed using voltage or calcium sensitive dyes, however these may not reflect the true rate of beating because they sequester calcium. Finally, in vitro differentiated cardiomyocytes sometimes briefly pause during imaging giving inaccurate beat rates. We have developed a MATLAB automation to calculate cardiac beat rates directly from video clips based on changes in pixel density at the edges of beating areas. These data are normalized to minimize the effects of secondary movement and are converted to frequency data using a fast Fourier transform (FFT). We find that this gives accurate beat rates even when there are brief pauses in beating. This technique can be used to rapidly assess beating of cardiomyocytes in organoid culture. This technique could also be combined with field scanning techniques to automatically and accurately assess beating within a complex cardiac organoid.

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Cholinergic Signaling Exerts Protective Effects in Models of Sympathetic Hyperactivity-Induced Cardiac Dysfunction

PLoS ONE ◽

10.1371/journal.pone.0100179 ◽

2014 ◽

Vol 9 (7) ◽

pp. e100179 ◽

Cited By ~ 28

Author(s):

Mariana Gavioli ◽

Aline Lara ◽

Pedro W. M. Almeida ◽

Augusto Martins Lima ◽

Denis D. Damasceno ◽

...

Keyword(s):

Cardiac Dysfunction ◽

Protective Effects ◽

Sympathetic Hyperactivity ◽

Cholinergic Signaling

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Heterogeneity of Phasic Cholinergic Signaling in Neocortical Neurons

Journal of Neurophysiology ◽

10.1152/jn.00493.2006 ◽

2007 ◽

Vol 97 (3) ◽

pp. 2215-2229 ◽

Cited By ~ 118

Author(s):

Allan T. Gulledge ◽

Susanna B. Park ◽

Yasuo Kawaguchi ◽

Greg J. Stuart

Keyword(s):

Visual Cortex ◽

Calcium Release ◽

Pyramidal Neurons ◽

Potassium Conductance ◽

Projection Neurons ◽

Sk Channels ◽

Cortical Areas ◽

Neocortical Neurons ◽

Cholinergic Signaling ◽

Nonpyramidal Neurons

Acetylcholine (ACh) is a neurotransmitter critical for normal cognition. Here we demonstrate heterogeneity of cholinergic signaling in neocortical neurons in the rat prefrontal, somatosensory, and visual cortex. Focal ACh application (100 μM) inhibited layer 5 pyramidal neurons in all cortical areas via activation of an apamin-sensitive SK-type calcium-activated potassium conductance. Cholinergic inhibition was most robust in prefrontal layer 5 neurons, where it relies on the same signal transduction mechanism (M1-like receptors, IP3-dependent calcium release, and SK-channels) as exists in somatosensory pyramidal neurons. Pyramidal neurons in layer 2/3 were less responsive to ACh, but substantial apamin-sensitive inhibitory responses occurred in deep layer 3 neurons of the visual cortex. ACh was only inhibitory when presented near the somata of layer 5 pyramidal neurons, where repetitive ACh applications generated discrete inhibitory events at frequencies of up to ∼0.5 Hz. Fast-spiking (FS) nonpyramidal neurons in all cortical areas were unresponsive to ACh. When applied to non-FS interneurons in layers 2/3 and 5, ACh generated mecamylamine-sensitive nicotinic responses (38% of cells), apamin-insensitive hyperpolarizing responses, with or without initial nicotinic depolarization (7% of neurons), or no response at all (55% of cells). Responses in interneurons were similar across cortical layers and regions but were correlated with cellular physiology and the expression of biochemical markers associated with different classes of nonpyramidal neurons. Finally, ACh generated nicotinic responses in all layer 1 neurons tested. These data demonstrate that phasic cholinergic input can directly inhibit projection neurons throughout the cortex while sculpting intracortical processing, especially in superficial layers.

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