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Questions and Answers
What distinguishes neurotransmission from neuromodulation based on their signaling speed?
What distinguishes neurotransmission from neuromodulation based on their signaling speed?
Which of the following receptor types directly forms an ion channel as part of its structure?
Which of the following receptor types directly forms an ion channel as part of its structure?
What is the primary mechanism by which metabotropic receptors initiate intracellular signaling?
What is the primary mechanism by which metabotropic receptors initiate intracellular signaling?
Considering the scope of signaling, how does endocrine signaling differ from paracrine signaling as described in the content?
Considering the scope of signaling, how does endocrine signaling differ from paracrine signaling as described in the content?
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Which of the following receptor types is exemplified by the nicotinic acetylcholine receptor (nAchR)?
Which of the following receptor types is exemplified by the nicotinic acetylcholine receptor (nAchR)?
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What is the primary distinction in the mechanism of action between ionotropic and metabotropic receptors?
What is the primary distinction in the mechanism of action between ionotropic and metabotropic receptors?
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During G protein activation in metabotropic signaling, which event directly follows ligand binding to the receptor?
During G protein activation in metabotropic signaling, which event directly follows ligand binding to the receptor?
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In the cyclic AMP signaling system, what is the immediate consequence of adenylyl cyclase activation?
In the cyclic AMP signaling system, what is the immediate consequence of adenylyl cyclase activation?
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Which of the following is a second messenger produced by phospholipase C in the phosphatidylinositol signaling system?
Which of the following is a second messenger produced by phospholipase C in the phosphatidylinositol signaling system?
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Phosphorylation of target proteins by protein kinases, a downstream effect of metabotropic receptor activation, can directly modulate the function of which cellular component?
Phosphorylation of target proteins by protein kinases, a downstream effect of metabotropic receptor activation, can directly modulate the function of which cellular component?
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What is the primary effect of muscarinic acetylcholine receptors (mAchR) on cardiac muscle?
What is the primary effect of muscarinic acetylcholine receptors (mAchR) on cardiac muscle?
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Which type of receptor is directly linked to an ion channel and mediates fast synaptic transmission?
Which type of receptor is directly linked to an ion channel and mediates fast synaptic transmission?
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In cardiac muscle, activation of muscarinic acetylcholine receptors (mAchR) leads to:
In cardiac muscle, activation of muscarinic acetylcholine receptors (mAchR) leads to:
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Which of the following is a characteristic of metabotropic receptors?
Which of the following is a characteristic of metabotropic receptors?
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Curare is known to block nicotinic acetylcholine receptors (nAChR). What would be the expected physiological effect of curare?
Curare is known to block nicotinic acetylcholine receptors (nAChR). What would be the expected physiological effect of curare?
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In sympathetic ganglia, muscarinic acetylcholine receptors (mAchR) activation leads to a slow EPSP by:
In sympathetic ganglia, muscarinic acetylcholine receptors (mAchR) activation leads to a slow EPSP by:
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Atropine is an antagonist for muscarinic acetylcholine receptors (mAchR). Which of the following effects would be consistent with atropine administration?
Atropine is an antagonist for muscarinic acetylcholine receptors (mAchR). Which of the following effects would be consistent with atropine administration?
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Nicotine acts as an agonist at nicotinic acetylcholine receptors (nAChR). Where would nicotine primarily exert its agonistic effects?
Nicotine acts as an agonist at nicotinic acetylcholine receptors (nAChR). Where would nicotine primarily exert its agonistic effects?
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Which form of synaptic plasticity is characterized by changes occurring at the same synapse where the activity modification originates?
Which form of synaptic plasticity is characterized by changes occurring at the same synapse where the activity modification originates?
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According to the 'residual calcium hypothesis', what is the primary mechanism underlying homo-synaptic facilitation?
According to the 'residual calcium hypothesis', what is the primary mechanism underlying homo-synaptic facilitation?
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Long-term potentiation (LTP), a form of homo-synaptic plasticity associated with learning and memory, is prominently observed in which brain structures?
Long-term potentiation (LTP), a form of homo-synaptic plasticity associated with learning and memory, is prominently observed in which brain structures?
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Activation of NMDA glutamate receptors in the post-synaptic neuron leads to an influx of $Ca^{2+}$. What is a downstream effect of this calcium influx in the context of synaptic plasticity?
Activation of NMDA glutamate receptors in the post-synaptic neuron leads to an influx of $Ca^{2+}$. What is a downstream effect of this calcium influx in the context of synaptic plasticity?
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Hetero-synaptic plasticity is defined by synaptic changes resulting from activity at:
Hetero-synaptic plasticity is defined by synaptic changes resulting from activity at:
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In pre-synaptic facilitation, an interneuron modulates neurotransmitter release by:
In pre-synaptic facilitation, an interneuron modulates neurotransmitter release by:
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Enkephalin, released by pre-synaptic interneurons in the spinal cord, modulates pain pathways by what mechanism of hetero-synaptic plasticity?
Enkephalin, released by pre-synaptic interneurons in the spinal cord, modulates pain pathways by what mechanism of hetero-synaptic plasticity?
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Hetero-synaptic inhibition, leading to a reduction in neurotransmitter release, can be mediated by:
Hetero-synaptic inhibition, leading to a reduction in neurotransmitter release, can be mediated by:
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Study Notes
Cell Signaling and Neurotransmission
- Ionotropic receptors vs. metabotropic receptors
- G protein-coupled receptors (G proteins)
- Focus on acetylcholine (ACh) receptors in skeletal muscle, heart, and central nervous system (CNS)
Second Messenger Systems
- Cyclic AMP (cAMP) and cyclic GMP (cGMP)
- Phosphatidylinositol
- Calcium (Ca2+) and calmodulin
- Protein kinases
Synaptic Plasticity
- Homosynaptic and heterosynaptic mechanisms
- Functional significance of neuromodulation
Local Signaling in Tissues
- Direct neurochemical transmission (paracrine or autocrine)
- Neurotransmission (fast) vs. neuromodulation (slow)
Ligand-Gated Receptors
- Ionotropic receptors: Ligand-gated ion channels, fast chemical transmission
- Metabotropic receptors: G protein-coupled receptors, slow chemical transmission and modulation
Metabotropic Receptors
- G protein-coupled receptors
- Acetylcholine receptors (mAchR) are metabotropic
- Slow chemical transmission, e.g., mAchR inhibiting cardiac muscle
- Slow chemical modulation: neuro-hormonal, modulatory second messenger production; activation of protein kinases
- "2nd and 3rd messengers" are biochemical signals
Ionotropic vs Metabotropic ACh Receptor Summary
- Ionotropic (nAchR): Nicotinic, directly-gated, ion channel, fast, example: skeletal muscle.
- Metabotropic (mAchR): Muscarinic, indirectly-gated, G protein, slow, example: cardiac muscle.
ACh Receptor Pharmacology
- Ionotropic (nicotinic): Agonist (e.g., nicotine), Antagonists (e.g., curare, bungarotoxin)
- Metabotropic (muscarinic): Agonist (e.g., muscarine), antagonists (e.g., atropine, scopolamine)
- ACh affects skeletal muscle (excitatory) and cardiac muscle (inhibitory) in the CNS, both types of ACh receptors are involved
ACh Pharmacology - Specific Agonists and Antagonists
- Nicotinic: Nicotine,
- Nicotinic: Curare, bungarotoxin
- Muscarinic: Muscarine
- Muscarinic: Atropine, scopolamine
ACh Receptor Pharmacology: Heart
- Otto Loewi's "vagustuffe" experiment
- Metabotropic (muscarinic) ACh receptors
- Ach activates G protein, activates K channels
- Cardiac muscle hyperpolarizes; heartbeat slows down
ACh Receptor Pharmacology: Sympathetic Ganglion
- Ionotropic (nicotinic) receptors
- Ach activates fast EPSP
- Metabotropic (muscarinic) receptors
- G protein blocks "M" type K channel
- Slow EPSP, increases response to arriving signals
Neurotransmission vs. Neuromodulation
- Ionotropic receptors: 4 transmembrane (TM) subunits, ligand binding to receptor, altered Vm (voltage), neurotransmission.
- Metabotropic receptors: 7 TM segments, ligand binding to receptor, G protein activation, enzyme activation, second messenger production, protein kinase activation, phosphorylation of targets, ion channels, other second messengers systems, DNA binding proteins, phosphatases terminate signals - slow response, amplified response
G-protein-coupled Receptors
- Extracellular domain binds ligands
- Intracellular domain activates GTP-binding protein
- G protein trimer binds GDP (inactive)
- G protein a subunit binds GTP and dissociates (active)
- a subunit directly gates ion channel (rare), activates enzyme, e.g, adenylate or guanylate cyclases, phospholipases C or A.
Cyclic AMP Signaling System
- First messenger (ligand) binds receptor
- G protein activation
- Adenylyl cyclase activation
- cAMP (second messenger) production
- Protein kinase A activation
- Phosphorylation of enzymes, ion channels, nuclear proteins
Phosphatidyl Inositol Signaling System
- First messenger binds receptor
- G protein activation
- Phospholipase C activation
- Production of second messengers (inositol trisphosphate, diacyl glycerol)
- Increase in intracellular calcium (Ca2+)
- Activation of protein kinase C and calmodulin (other)
- Phosphorylation of enzymes, ion channels, nuclear proteins
Other Biochemical Systems
- cGMP (photoreceptors)
- Calcium/calmodulin/CamK II (learning)
- Nitric oxide (NO) and arachidonic acid
Synaptic Plasticity: Homo-Synaptic
- Homo-synaptic facilitation (during stimulation)
- Homo-synaptic potentiation (post-tetanic potentiation)
- Homo-synaptic depression
- Mechanism: levels of nerve terminal calcium, more or less neurotransmitter (NT) release, consequence of action potentials (AP) from input train, acting on Ca++ channels, residual calcium
Synaptic Plasticity: Hetero-Synaptic
- Heterosynaptic plasticity: increase or decrease in synaptic efficacy
- Pre-synaptic facilitation: interneuron increases NT release/augments pre-synaptic AP
- Pre-synaptic inhibition: interneuron inhibits NT release/inhibits pre-synaptic AP
Enkephalin in Spinal Cord Modulation
- Pain stimuli release substance P
- Presynaptic interneurons release enkephalin (inhibitory)
- Reduced substance P release; Enkephalin is 5 amino acids
How Hetero-Synaptic Plasticity Works to Alter NT Release
- Enkephalin example: inhibits
- Pre-synaptic action potential shorter
- Less Calcium influx
- Less substance P released
- Serotonin example: augments, Pre-synaptic action potential longer, Increased calcium influx, more neurotransmitter released.
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Description
Test your knowledge on cell signaling, neurotransmission, and the role of various receptors including ionotropic and metabotropic receptors. Delve into the mechanisms of synaptic plasticity and second messenger systems. This quiz covers important concepts related to acetylcholine receptors and neurochemical transmission.
