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Questions and Answers
What is a potential consequence of excessive inhibitory neurotransmitter activity in the central nervous system?
What is a potential consequence of excessive inhibitory neurotransmitter activity in the central nervous system?
- Excessive dopamine production resulting in schizophrenia.
- Sedation and impaired cognitive function. (correct)
- Overexcited neurons leading to anxiety.
- Increased synaptic plasticity and enhanced learning.
How do Monoamine Oxidase Inhibitors (MAOIs) affect neurotransmitter levels in the synapse, and for what condition are they primarily used?
How do Monoamine Oxidase Inhibitors (MAOIs) affect neurotransmitter levels in the synapse, and for what condition are they primarily used?
- MAOIs prevent the breakdown of monoamines, treating depression and anxiety. (correct)
- MAOIs increase serotonin production, treating appetite disorders.
- MAOIs degrade monoamines, treating schizophrenia.
- MAOIs block the reuptake of catecholamines, treating Parkinson's disease.
Which of the following best describes the clinical application of antagonists that block acetylcholine (ACh) receptors at the neuromuscular junction?
Which of the following best describes the clinical application of antagonists that block acetylcholine (ACh) receptors at the neuromuscular junction?
- Enhancing muscle contractions to treat muscular dystrophy.
- Increasing dopamine release to alleviate Parkinson's symptoms.
- Stimulating nerve signaling to treat autism.
- Inhibiting muscle contraction, acting as a muscle relaxant. (correct)
What is the potential consequence of long-term amphetamine use, considering its effects on norepinephrine pathways and the sympathetic nervous system?
What is the potential consequence of long-term amphetamine use, considering its effects on norepinephrine pathways and the sympathetic nervous system?
What is the primary function of acetylcholine (ACh) at the neuromuscular junction (NMJ)?
What is the primary function of acetylcholine (ACh) at the neuromuscular junction (NMJ)?
How does the degradation of dopamine-producing neurons in the nigrostriatal system primarily manifest clinically, and what is a common treatment approach?
How does the degradation of dopamine-producing neurons in the nigrostriatal system primarily manifest clinically, and what is a common treatment approach?
Given the duality of dopamine's functions, what potential challenge arises when treating conditions related to dopamine imbalances?
Given the duality of dopamine's functions, what potential challenge arises when treating conditions related to dopamine imbalances?
What is the likely effect of a drug that selectively stimulates norepinephrine pathways in the central nervous system?
What is the likely effect of a drug that selectively stimulates norepinephrine pathways in the central nervous system?
Which glial cell type is primarily responsible for forming the myelin sheath around axons in the central nervous system (CNS), and what is a potential consequence if these cells are damaged?
Which glial cell type is primarily responsible for forming the myelin sheath around axons in the central nervous system (CNS), and what is a potential consequence if these cells are damaged?
How do astrocytes contribute to the function of the blood-brain barrier (BBB), and why is this significant for treating neurological disorders such as meningitis?
How do astrocytes contribute to the function of the blood-brain barrier (BBB), and why is this significant for treating neurological disorders such as meningitis?
In the context of neuronal communication, what is the primary functional difference between a sensory neuron and a motor neuron, and where are their cell bodies typically located?
In the context of neuronal communication, what is the primary functional difference between a sensory neuron and a motor neuron, and where are their cell bodies typically located?
During an action potential, how do the movements of sodium ($Na^+$) and potassium ($K^+$) ions across the neuronal membrane contribute to depolarization and repolarization, respectively?
During an action potential, how do the movements of sodium ($Na^+$) and potassium ($K^+$) ions across the neuronal membrane contribute to depolarization and repolarization, respectively?
What role do interneurons play within the central nervous system (CNS), and how does this differ from the function of sensory and motor neurons?
What role do interneurons play within the central nervous system (CNS), and how does this differ from the function of sensory and motor neurons?
How do Schwann cells facilitate rapid nerve impulse conduction in the peripheral nervous system (PNS), and what structural features are critical to this function?
How do Schwann cells facilitate rapid nerve impulse conduction in the peripheral nervous system (PNS), and what structural features are critical to this function?
What is the functional significance of the axon hillock in a neuron, and how does it contribute to the generation of action potentials?
What is the functional significance of the axon hillock in a neuron, and how does it contribute to the generation of action potentials?
During hyperpolarization, how does the change in membrane potential affect the neuron's excitability, and what ionic event is primarily responsible for this state?
During hyperpolarization, how does the change in membrane potential affect the neuron's excitability, and what ionic event is primarily responsible for this state?
During the repolarization phase of an action potential, what specific mechanism directly contributes to the membrane potential becoming more negative?
During the repolarization phase of an action potential, what specific mechanism directly contributes to the membrane potential becoming more negative?
Which of the following scenarios accurately describes the 'all or none' principle of action potentials?
Which of the following scenarios accurately describes the 'all or none' principle of action potentials?
How does myelin sheath contribute to the increased speed of action potential propagation in myelinated axons?
How does myelin sheath contribute to the increased speed of action potential propagation in myelinated axons?
What distinguishes anterograde axonal transport from retrograde axonal transport in neurons?
What distinguishes anterograde axonal transport from retrograde axonal transport in neurons?
Which structural characteristic is most closely associated with sensory neurons?
Which structural characteristic is most closely associated with sensory neurons?
Under what specific conditions is axon regeneration most likely to occur?
Under what specific conditions is axon regeneration most likely to occur?
In contrast to synapses found in the central nervous system (CNS), how do synapses in the peripheral nervous system (PNS) differ in their typical target cells?
In contrast to synapses found in the central nervous system (CNS), how do synapses in the peripheral nervous system (PNS) differ in their typical target cells?
What is the fundamental difference in the mechanism of signal transmission between electrical and chemical synapses?
What is the fundamental difference in the mechanism of signal transmission between electrical and chemical synapses?
How does the opening of voltage-gated calcium channels at the axon terminal directly facilitate neurotransmitter release?
How does the opening of voltage-gated calcium channels at the axon terminal directly facilitate neurotransmitter release?
What critically distinguishes ligand-gated ion channels from G-protein-coupled receptors in terms of their mechanism of action?
What critically distinguishes ligand-gated ion channels from G-protein-coupled receptors in terms of their mechanism of action?
How does spatial summation differ mechanistically from temporal summation in the context of postsynaptic potential integration?
How does spatial summation differ mechanistically from temporal summation in the context of postsynaptic potential integration?
How does divergent neural circuitry differ from convergent neural circuitry in terms of signal propagation?
How does divergent neural circuitry differ from convergent neural circuitry in terms of signal propagation?
What is the primary mechanism underlying long-term depression (LTD) in synaptic plasticity?
What is the primary mechanism underlying long-term depression (LTD) in synaptic plasticity?
How does synaptic inhibition prevent the postsynaptic neuron from reaching threshold and firing an action potential?
How does synaptic inhibition prevent the postsynaptic neuron from reaching threshold and firing an action potential?
How do opioids reduce pain at the synaptic level?
How do opioids reduce pain at the synaptic level?
Flashcards
Neuron
Neuron
Basic nerve cell with a cell body, axon, and dendrites; transmits electrical signals.
Cell Body (Neuron)
Cell Body (Neuron)
Main hub with nucleus and organelles for cell functions; CNS: nuclei, PNS: ganglia
Dendrites
Dendrites
Neuron branches that receive signals and contain cytoplasm and vesicles
Axon
Axon
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Sensory Neuron
Sensory Neuron
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Motor Neuron
Motor Neuron
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Interneurons
Interneurons
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Depolarization
Depolarization
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GABA Neurotransmitter
GABA Neurotransmitter
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Low GABA Effects
Low GABA Effects
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Acetylcholine (Ach)
Acetylcholine (Ach)
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Curare Action
Curare Action
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Monoamine Oxidase (MAO)
Monoamine Oxidase (MAO)
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MAO Inhibitors (MAOIs)
MAO Inhibitors (MAOIs)
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Nigrostriatal System
Nigrostriatal System
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Mesolimbic System
Mesolimbic System
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Voltage-gated Channels
Voltage-gated Channels
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All or None Law
All or None Law
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Myelin Sheaths and Conduction
Myelin Sheaths and Conduction
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Axonal Transport
Axonal Transport
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Anterograde Transport
Anterograde Transport
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Retrograde Transport
Retrograde Transport
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Unipolar Neurons
Unipolar Neurons
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Bipolar Neurons
Bipolar Neurons
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Multipolar Neurons
Multipolar Neurons
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Synapse
Synapse
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Chemical Synapse
Chemical Synapse
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Action of Chemical Synapses
Action of Chemical Synapses
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Ligand-Gated Channels
Ligand-Gated Channels
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G-Protein Coupled Channels
G-Protein Coupled Channels
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Temporal Summation
Temporal Summation
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Study Notes
- Summaries and objectives for EXS 112 Exam 2.
L6-#1 Neuron, parts, functions
- The cell body is the main hub with the nucleus and organelles and has general cell functions.
- CNS-Nuclei and PNS-Ganglia are part of the cell body.
- Dendrites receive signals and have a cytoplasm and vesicles.
- Axons generate action impulses to send out, also known as APs.
- Axons connect to dendrites.
- Collateral axons branch to other/multiple cells.
- The axon hillock is where AP generates.
- A basic neuron has a cell body, axon, and dendrite.
- A nerve is a bundle of sensory/motor axons.
L6-#2 Sensory v Motor v Interneurons
- Sensory neurons' receptors go to the CNS
- Sensory neurons are unipolar.
- Sensory Neurons are afferent.
- Sensory neurons are located in the PNS.
- Motor Neurons' effectors go from the CNS to the PNS.
- Somatic motor neurons control muscles and are voluntary.
- Autonomic motor neurons control muscles, are involuntary, and are sympathetic/parasympathetic.
- Motor neurons have ganglions.
- Interneurons integrate in the CNS and are called association neurons.
L6-#3- Neuroglial Cells
- Schwann Cells are in the PNS, and one cell forms one myelin sheath, speeding up impulse and reducing ion loss.
- Neurilemma is part of schwann cells (cytoplasm).
- Myelin Sheath (Plasma Membrane) is part of schwann cells
- Nodes of Ranvier part of Schwann Cells
- Oligodendrocytes are in the CNS, wraps around multiple axons as white matter, and makes the myelin sheath.
- Oligodendrocytes can cause MS.
- Microglia are in the CNS, remove foreign objects, and maintains healthy cells.
- Overactive microglia targets healthy cells, causing Parkinson's/Alzheimer's.
- Astrocytes maintain the extracellular environment.
- Astrocytes influence neuron to non-neuronal interactions (ex: Blood-Neuron) and drugs have difficulty treating meningitis-neural disease.
- Astrocytes are abundant.
L6-#4 Blood Brain Barrier (BBB)
- Blood capillaries are not porous.
- Normal diffusion is prevented by non-porous capillaries.
- Astrocytes regulate the barrier and release molecules for controlled diffusion.
L6-#5 Depolarization, Repolarization, Hyperpolarization
- Depolarization changes to a (+) membrane potential.
- Na (+) enters during depolarization resulting in excitatory impulses.
- Repolarization changes to a (-) membrane potential.
- K (+) exits to ECM during repolarization resulting in inhibitory impulses.
- Hyperpolarization causes a dip in (-) charge before reaching the resting membrane potential.
- Hyperpolarization is created by too much K (+) removal, resulting in a little (-) charge.
L6-#6 Na/K Movement to Action Potential
- Voltage-gated Channels are relevant.
- Stimulus brings the membrane to (-55).
- Na gates open, depolarizing (+) rapidly.
- Positive feedback loop depolarizes to (+30).
- Action potential is generated at + 30.
- K gates open, Na closes, beginning repolarization.
- K exits quickly causing repolarization.
- Hyperpolarization happens as K gates close via negative feedback loop.
- Cell polarity restores to the resting membrane potential of (-70).
L6-#7 Explain the All or None Law
- Stimulus strength depends on quantity.
- Strong stimulus does not change the speed of de/repolarization, voltage, or duration.
- Voltage and duration remain fixed, all or nothing.
- Once the process begins, the action potential is going/created.
- A strong stimulus recruits more axons, leading to more action potentials.
- All neurons require a refractory period to recharge and restore to resting membrane potential.
- Absolute refractory means there is no axon response to stimulation.
- Relative refractory occurs during hyperpolarization when a strong stimulus could generate a new AP.
L6-#8 Why do Myelin Sheaths make Conduction Quicker?
- Action potentials are generated at the nodes with Na/K channels.
- Na/K cannot diffuse through myelin.
- There is no ion loss.
- Saltatory Conduction allows action potentials to jump from node to node.
- Jumping faster than traveling down a membrane.
- Jumping reduces distance and can go further (longer distances) with a fixed AP duration.
L6- #9 Axons
- Axonal Transport moves proteins/organelles from the cell body to axon ends.
- Fast: Membrane Vesicles are transported.
- Slow: Proteins and Filaments are transported.
- Anterograde Transport goes away from the cell body.
- Retrograde Transport goes towards the cell body (viruses).
L6-#10 Neuron Structures
- Unipolar neurons are sensory and T-shaped.
- Bipolar neurons are olfactory/optical with two processes.
- Multipolar neurons are motor with several dendrites and are standard.
- Axon Regeneration sometimes occurs in the PNS.
- The cell body must be alive for axon regeneration.
- Schwann cells create a regeneration tube.
- Microglia perform phagocytosis of broken fibers.
L7-#1Defining a Synapse
- Synapse: The connection between a neuron and its target cells
- In the CNS synapses are usually neuron to neuron (pre/post synapse)
- In the PNS synapses are usually to a muscle, gland, or effector
- Synapses are either Electrical or Chemical
L7-#2 Electrical vs Chemical Synapses
- Electrical Synapses use Gap junction cells and Example: Muscle cells
- Chemical Synapses use Neutrotransmitters, found in Neurons
- Synaptic Cleft forms from pre/post synaptic cells
- Vesicles release neurotransmitters and cross the ECM
L7- #3 Release vs Action of Chemical Synapses
- When AP reaches the axon end
- Voltage-gated Ca Channels open
- Ca triggers (pre-packed) vesicles with neuros to membrane.
- Exocytosis occurs into cleft, and post receives neurotransmitters
- More AP = more Ca = more exocytosis/stimulation of post cell
- Neurotransmitter crosses the cleft and binds to a receptor protein
- The Receptor stimulates chemical regulated gates
- EPSP (excitatory): (+) membrane by entering Na/Ca/depolarization.
- IPSP (Inhibitory): (-) membrane by removing K/CI or re/hyperpolarization
L7-#4 Channels- once neurotransmitters bind to receptors (in post)
- Ligand=neurotransmitter
- “molecule-gated channel" are types of Ligand-Gated receptors
- Channel gates open when ligand binds directly to protein channel = Ligand-Gated Receptors. Example: Acetylcholine + receptor
- “GTP gated channel”
- G-Protein receptors can have multiple methodologies, A, B, C= Secondary Messenger Methodology
- Neurotransmitter binds to receptor for G-protein receptors
- Receptor activates a molecule (GTP) to go the the channel and the GTP Molecule opens channel,
- Example of G-protein receptors: dopamine->dopamine receptor, activates GTP, GTP opens channels
- G-protein channels can be opened in multiple ways
- Example1- EPSP(+): closes K channel, excites, in skeletal muscles.
- Example 2- IPSP(-): opens K channel, inhibits, in heart
L7-#5 ETC on EPSP and IPSP
- Action Potentials are triggered after the voltage reaches the threshold
- The sum of EPSPs/IPSPs will either add up to an Action Potential or not
- Spatial Summation includes Simultaneous signals from multiple inputs
- Different inputs at the same time add up to the Action Potential
- Temporal Summation includes Repeated signal inputs from the same input
- The same input sends a signal at different times close together to add up to an Action Potential
L7-#6 Neural Pathways
- Neurons with collateral axon branches form Branches to multiple cells (L6#1)
- Divergent pathways include Only 1 pre-synaptic axon
- Convergent Pathways includelots of pre-synaptic axons connecting to only 1 post-synaptic axon
L7-#7 Synaptic Plasticity
- Synaptic Plasticity: neurons adapting from the amount of stimulus to strengthen or reduce synaptic activity for that stimulus (add or reduce channels based on stimulus)
- Long-Term Potentiation (LTP) occurs to Improve synapse efficiency from repeated use of a stimulus, Ex: more Ca release
- LTP can improve the hippcampus and consequently memory
- More Channels =More efficiency
- Long-Term Depression (LTD) reduces efficiency from underused stimulus
- Example of LTD is less Ca release
- During LTD endocannabinoids are released to suppress more neurotransmitters which results in a positive feedback loop
- Less Channels result in Less Efficient Synapses
L7-#8 Synaptic Inhibition
- Synaptic Inhibition is where inhibitory neurotransmitters hyperpolarize post-synapses which...
- Ca (+) excitatory channels close
- Decreased/no excitatory neurotransmitters released
- Post-synapse has no AP
- Excitatory neurotransmitters have to work hard to depolarize- resulting in the synapse going back to default
- Clinical Application of Syanptic Inhibitors are Opioids whicheduce pain via inhibiting neurotransmitters, which inhibits the release of excitatory neurotransmitters, like Substance P, which relays pain to post-synapse
L7-#9 Neurotransmitters: Glutamate vs GABA
- Glutamate is Primarily in the CNS
- Glutamate is an Excitatory neurotransmitter, that ups synaptic plasticity
- Glutamate Releases Na+
- Overactive neurons in the CNS can cause damage leading to Alzeimer's
- Or overactive neurons can throw off the production of dopamine leading to Parkinson's
- GABA is an Inhibitory neurotransmitter
- GABA Inhibits/decreases nerve signaling
- GABA Releases Cl-
- Too little/low GABA levels can lead to overexcited neurons=anxiety, autism, schizo
- Conversely Too much/high GABA levels Need a lot of excitatory neurons to compensate= addiction to excitatory pathways
- GABA can treat anxiety, used as an anti-convulsant/sedative
L7-#10 Neurotransmitters: Acetylcholine
- Acetylcholine Located @ NMJ (neuromuscular junctions)- between muscles and neurons
- Acetycholine is Primarily used in the PNS
- Ach promotes Muscle contractions
- If Ach is Blocked by Antagonists muscle contraction will be Inhibited - Ex: Curare: Blocks Ach receptors, muscle relaxer
L7-#11 Neurotransmitters: Monoamines
- Amino acids as neurotransmitters
- Monoamines have amine groups
- Catecholamines includeDopamine, Epinephrine, and Norepinephrine
- Serotonin includesMood, Appetite, and *Behavior
- Monoamine Oxidase Inhibitors (MAO) Block/prevent monoamines from degrading in synaptic cleft
- MAOs can Treat depression/panic/anxiety
L7-#12 Neurotransmitters: Dopamine
- Primarily in the midbrain, dopamine acts as a neurotransmitter
- In the Nigrostriatal System dopamine promotes Motor movement with theClinical Application being thatDegradation of dop/receptors=Parkinson's=tremors and motor dysfunction as well as can be treated with MAOs
- In the Masolimbic System dopamine promotesEmotional rewards as well as with the Clnical Application being that Overactive dop=overstimulated responses= Schizophrenia
- There can be a Duality of Dopamine where Treating 1 may lead to other disease/symptoms
L7-#13 Nuero Transmitters:Norepinephrine
- Primarily in the PNS, Norepinephrin acts in Sympathetic neurons(autonomic) which have aBackground contraction
- Primarily in the CNS, Norepinephrin Stimulates brain neurons and Stimulates behavior
- Amphetamines Clinical Applications Stimulates norepinephrine pathways in the brain
- treat depression
- As side effects of treating with Amphetamines it Raises BP, Raises HR, Jitters b/c of stimming sympathetic PNS
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