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The cranial part of the parasympathetic division plays a crucial role in regulating the visceral functions of the head and specific structures in the neck, thoracic, and abdominopelvic cavities. Preganglionic fibers of the parasympathetic division exit the brain through cranial nerves III (oculomotor), VII (facial), IX (glossopharyngeal), and X (vagus), delivering parasympathetic output to the respective visceral structures.
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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.
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Cholinergic Receptors: Muscarinic01:25

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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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Direct-Acting Cholinergic Agonists: Pharmacological Actions00:59

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Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...
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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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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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Stereological Estimation of Cholinergic Fiber Length in the Nucleus Basalis of Meynert of the Mouse Brain
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Cholinergic projections to the preBötzinger complex.

Vivian Biancardi1,2,3, Xiaqiu Yang1, Xiuqing Ding1

  • 1Department of Physiology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.

The Journal of Comparative Neurology
|May 22, 2023
PubMed
Summary

Researchers identified the source of acetylcholine input to the preBötzinger complex (preBötC), crucial for breathing rhythm. Contrary to previous hypotheses, the laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) are not the primary source, with inputs originating from nearby medullary regions.

Keywords:
breathingcholinergic projectionspreBötzinger complexviral tracing

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Area of Science:

  • Neuroscience
  • Respiratory Physiology
  • Neuroanatomy

Background:

  • The preBötzinger complex (preBötC) generates rhythmic inspiratory activity essential for breathing.
  • Cholinergic neurotransmission influences respiratory rhythm, with acetylcholine modulating inspiratory frequency in the preBötC.
  • The precise origin of cholinergic input to the preBötC remains unknown, despite its functional significance.

Purpose of the Study:

  • To identify the source of cholinergic inputs projecting to the preBötzinger complex (preBötC).
  • To investigate the role of the laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) in cholinergic modulation of the preBötC.

Main Methods:

  • Utilized retrograde and anterograde viral tracing techniques in transgenic mice.
  • Employed Cre-recombinase expression driven by the choline acetyltransferase promoter to track cholinergic neurons.

Main Results:

  • Observed minimal to no direct cholinergic projections from the laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) to the preBötC.
  • Identified glutamatergic and GABAergic/glycinergic neurons in the PPT/LDT projecting to the preBötC, potentially involved in state-dependent breathing regulation.
  • Indicated that primary cholinergic inputs to the preBötC originate from neighboring medullary regions, including the intermediate reticular formation, lateral paragigantocellularis, and nucleus of the solitary tract.

Conclusions:

  • The laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) are not the main source of cholinergic input to the preBötzinger complex (preBötC).
  • Cholinergic inputs to the preBötC arise from adjacent medullary nuclei.
  • Non-cholinergic projections from the PPT/LDT may contribute to state-dependent respiratory control.