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Related Concept Videos

Cholinergic Neurons: Neurotransmission01:23

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Cholinergic neurotransmission involves the synthesis and the release of acetylcholine (ACh) in order to transmit nerve impulses across the synapse. The process begins with the synthesis of acetyl CoA, a precursor for ACh, from ATP, acetate, and coenzyme A in the mitochondria. Choline, another vital precursor, is transported inside the neuron through choline transporters, including high-affinity choline transporter CHT1, low-affinity choline transporter CTL1, and lower-affinity choline...
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The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
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Parasympathetic Signaling01:30

Parasympathetic Signaling

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Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
The effects of...
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Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
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Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

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Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
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Cholinergic Receptors: Nicotinic01:15

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Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
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Biphasic Cholinergic Modulation of Reverberatory Activity in Neuronal Networks.

Xiao-Wei Li1, Yi Ren1, Dong-Qing Shi1

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Area of Science:

  • Neuroscience
  • Computational Neuroscience
  • Cellular Neuroscience

Background:

  • Acetylcholine (ACh) is a key neuromodulator influencing cognitive functions.
  • The precise mechanisms by which ACh alters neural circuit dynamics and cellular properties remain incompletely understood.

Purpose of the Study:

  • To investigate the influence of acetylcholine (ACh) on reverberatory activity in cultured neuronal networks.
  • To elucidate the dose-dependent effects of ACh on neuronal excitability and synaptic transmission.

Main Methods:

  • Utilized cultured neuronal networks and whole-cell electrophysiology to record neuronal activity.
  • Employed dose-response experiments with varying concentrations of ACh.
  • Used muscarinic and nicotinic receptor antagonists to identify signaling pathways.
  • Developed computational models to simulate cellular and network changes.

Main Results:

  • ACh exhibited biphasic effects on evoked reverberation, suppressing it at low/moderate doses and less so at high doses.
  • High ACh doses increased reverberation duration and spontaneous neuronal activity.
  • ACh inhibited excitatory postsynaptic currents (EPSCs) and increased neuronal firing in a dose-dependent manner.
  • Effects were mediated by muscarinic, not nicotinic, receptors.

Conclusions:

  • ACh modulates neural network dynamics in a biphasic manner.
  • This modulation is likely achieved by inhibiting excitatory synaptic transmission and enhancing neuronal excitability via muscarinic pathways.
  • Findings provide insights into ACh's role in cognitive processes through network-level effects.