Chapter 7 on acetylcholine provides a comprehensive overview of the role and mechanisms of this essential neurotransmitter. It discusses the synthesis of acetylcholine (ACh) by the enzyme choline acetyltransferase from choline and acetyl coenzyme A and how its production is influenced by precursor ...
TEST BANK For Psychopharmacology: Drugs, the Brain, and Behavior, 4th Edition By Meyer Nursing, Verified Chapters 1 - 20, Complete Newest Version
TEST BANK FOR PSYCHOPHARMACOLOGY: DRUGS, THE BRAIN AND BEHAVIOR 4TH EDITION BY MEYER,100% CORRECT ANSWERS, GRADED A+
PSYCHOPHARMACOLOGY DRUG THE BRAIN AND BEHAVIOR 4TH EDITION MEYER NURSING TEST BANK/LATEST UPDATE/COMPLETE GUIDE 2024
All for this textbook (27)
Written for
Athabasca University (AU
)
Psychology
PSYC450 (PSYC450)
All documents for this subject (4)
Seller
Follow
rowanballanger
Content preview
Page 1 of 7
Acetylcholine
Acetylcholine Synthesis, Release, and Inactivation
- Acetylcholine (ACh) is a crucial neurotransmitter in the peripheral nervous system (PNS),
operating at neuromuscular junctions and autonomic nervous system synapses.
- While ACh is synthesized by a limited number of neurons in the brain, these neurons are
pivotal for various behavioral functions.
- Understanding the production, release, and inactivation of ACh is vital due to the risks
associated with both excessive and insu cient levels of this neurotransmitter.
- Various agents modulate ACh levels in the body, either increasing or limiting its availability to
regulate physiological and behavioral processes.
Acetylcholine synthesis is catalyzed by the enzyme choline acetyltransferase
- Acetylcholine (ACh) is synthesized in a single step from choline and acetyl coenzyme A
(acetyl CoA).
- Choline is sourced from dietary fat or produced in the liver, while acetyl CoA is generated
within cells through sugar and fat metabolism.
- Choline acetyltransferase (ChAT) catalyzes the synthesis of ACh by transferring the acetyl
group from acetyl CoA to choline.
- ChAT is speci c to neurons that utilize ACh as a neurotransmitter, allowing for their
identi cation through ChAT staining.
- The rate of ACh synthesis is in uenced by the availability of precursors and neuronal ring
rate.
- Despite understanding regulatory mechanisms, pharmacological agents targeting ACh
synthesis have been challenging to develop.
- Boosting brain ACh levels with choline was explored for Alzheimer’s disease but proved
ine ective and caused undesirable side e ects like a shy odor due to peripheral metabolism
of choline.
Many di erent drugs and toxins can alter acetylcholine storage and release
- Cholinergic neurons store acetylcholine (ACh) in synaptic vesicles within axon terminals for
release during neuronal activity.
- Vesicular ACh transporter (VAChT) is responsible for loading ACh into synaptic vesicles, and
its inhibition by vesamicol decreases ACh storage in vesicles.
- Vesamicol treatment increases cytoplasmic ACh levels as ACh molecules that would have
been transported into vesicles remain in the cytoplasm.
- Reduced ACh release occurs in the presence of vesamicol since synaptic vesicles, the
primary source of ACh release during neuronal ring, have lower ACh content.
- Despite vesamicol treatment, empty synaptic vesicles continue to undergo exocytosis and
recycling when cholinergic neurons are activated, indicating a lack of feedback mechanisms to
prevent release of vesicles with low or no neurotransmitter content.
- Black widow spider venom induces massive ACh release at synapses in the peripheral
nervous system, leading to symptoms like muscle pain, tremors, nausea, salivation, and
sweating.
- Botulism toxins inhibit ACh release, causing muscular paralysis, which can be fatal. However,
carefully administered localized botulinum toxin injections have medical and cosmetic
applications.
ff fi ff fi fl ffiff fi fi fi
, Page 2 of 7
Acetylcholinesterase is responsible for acetylcholine breakdown
- Acetylcholine (ACh) levels are regulated by acetylcholinesterase (AChE), which breaks down
ACh into choline and acetic acid.
- AChE exists as a tetramer formed by four subunits, with the majority tethered to the cell
membrane for rapid ACh breakdown.
- A unique form of AChE, A12, is found at neuromuscular junctions, ensuring precise
transmission and rapid muscle relaxation.
- Recycled choline plays a critical role in sustaining ACh synthesis, as shown by knockout
studies of the choline transporter in mice.
- Drugs that block AChE increase postsynaptic e ects of ACh, with reversible inhibitors used to
treat age-related dementia, such as donepezil, rivastigmine, and galantamine.
- Natural reversible AChE inhibitors like physostigmine have medical applications but can be
highly toxic, with symptoms of poisoning including mental confusion and convulsions.
- Irreversible AChE inhibitors, like organophosphorus compounds, cause nearly irreversible
inhibition of AChE activity and are used as insecticides or, in more toxic forms, as nerve gases.
- Nerve gases like sarin and soman rapidly accumulate ACh, leading to symptoms such as
profuse sweating, convulsions, and eventually death due to muscle paralysis.
- During con icts, reversible AChE inhibitors like pyridostigmine are used prophylactically to
protect against nerve gas poisoning, but excessive exposure may contribute to long-term
health issues like Gulf War illness, a complex neuroimmune disorder a icting some veterans.
Several neuromuscular disorders are associated with abnormal cholinergic
functioning at the neuromuscular junction
- Myasthenia gravis is an autoimmune disorder where antibodies attack skeletal muscle
cholinergic receptors, leading to muscle weakness and fatigue.
- Loss of receptor function reduces muscle sensitivity to ACh, causing symptoms like
weakness, fatigue, speech di culties, labored breathing, and drooping eyelids.
- Diagnosis of myasthenia gravis can be challenging due to shared symptoms with other
neuromuscular disorders, but treatment involves administering AChE inhibitors like
pyridostigmine or neostigmine to enhance the e ectiveness of remaining cholinergic receptors.
- Congenital neuromuscular disorders, termed myasthenic syndromes, can result from
mutations in genes encoding ChAT or AChE, leading to insu cient ACh release or persistent
ACh activity at neuromuscular junctions.
- Symptoms of myasthenic syndromes, which appear in infancy, include muscle weakness,
respiratory distress, episodes of apnea, and drooping eyelids.
- Treatment for myasthenic syndromes caused by de cient ChAT activity involves AChE
inhibitors like pyridostigmine, but there are currently no e ective remedies for syndromes
caused by AChE gene mutations.
Organization and Function of the Cholinergic System
- Acetylcholine (ACh) serves as a neurotransmitter at the neuromuscular junction and within the
autonomic nervous system, where it was initially identi ed as a neurotransmitter in the
peripheral nervous system (PNS).
- Cholinergic cell bodies and synapses are located in both the PNS and CNS.
- The receptor subtypes for ACh will be described, along with some of the primary behavioral
and physiological functions of this neurotransmitter in the subsequent sections.
Cholinergic neurons play a key role in the functioning of both the peripheral and
central nervous systems
fl ffi ffff fi fi ff ffi ffl
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller rowanballanger. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $6.03. You're not tied to anything after your purchase.
