Neuropharmacology (MODULE 3) Flashcards
Ax/o
Axis or angle
Gangli/o
Ganglion/o
Ganglion (cluster of nerve cell bodies outside of the CNS)
Dur/o
Dura mater (hard)
Myel/o
Spinal cord
Mening/o
Meninges
Polar/o
End of axis/extreme
Esthesi/o
Sensation, sensitivity, feeling
Poli/o
Gray matter
Gen/o
Beginning/origin
Leps/o
Seizure
-on
Specific unit or particle
-ite
Related to
-ictal
Seizure/attack
-apse
Join
-ous
Pertaining to
-ization
The process of becoming
Ataxia
Condition of no coordination
Syncope
Faint
Myasthenia Gravis
Serious muscle weakness
Agonist
Something that promotes or activates a response
Antagonist
Something that acts against or opposes an action
Acetylcholine
A neurotransmitter composed of an acetylcholine group and choline, playing a crucial role in nerve signal transmission
Epinephrine
Means “above the kidney” referring to its production in the adrenal glands, which sit on top of the kidneys. It is also known as adrenaline a hormone and neurotransmitter involved in the “fight or flight response”
Norepinephrine
Means “a modified form of epinephrine”, referring to a neurotransmitter and hormone that plays a key role in the body’s stress response, alertness, and BP regulation.
Describe the four attributes contributing to resting potential.
- Capacitance - the membrane must be able to store charge. Ion interaction with one another.
- Potassium leak channels - potassium ions can diffuse out of the cell through potassium leak channels; balancing the concentration gradient. Sodium ions diffusion - sodium ions can diffuse into the cell through sodium leak channels.
- Sodium Potassium Pump - this keeps the inside more negatively charged than the outside. -70mV
- Negatively charged phosphorylation proteins - these proteins cannot leave the cell. Therefore they case interaction between the positively charged potassium and sodium ions.
Look at AP graph on slide 8 and describe each letter in correlation with the stage.
A = at rest -70mV
B = channels open and sodium comes running into cell (depolarization)
+33 inside
C = potassium gated channels opened (depolarization)
More negative
D = beyond -70mV (hyper-polarization) requires sodium potassium pump to re stabilize
refer to slide 9 for the following…
Describe the excitability and stability of the graph.
Between 1 and 2 is reaching the threshold of excitation involves INCREASING excitability.
Between 2 and 3 involves the absolute refractory period = at this point we cannot generate another AP because one is already being generated. *This is a stable period
Between 3 and 4 the excitability is increasing (not to the extent it was at rest) to restabilize the membrane potential and this leads from repolarization to hyperpolarization. *Now the membrane is more stable again
4 to 5 back to normal excitability
Summary of Excitability versus Stability
*Attribute Excitability Stability
-Rest
-Subthreshold depolarization
-Spike potential/ Absolute Refractory Period
-Repolarization
-Hyperpolarization
Attribute Excitability Stability
Rest - Normal - Normal
Subthreshold depolarization - increasing - decreasing
Spike potential/ Absolute Refractory Period - least excitable - most stable
Repolarization - increasing - decreasing
Hyper-polarization - decreasing - increasing
Subthreshold potentials result from what receptors?
Ligand binding receptors
_________ _________ are those changes resulting in depolarizing changes, inhibitory potentials are those that result in increases in the membrane potentials beyond rest.
Excitatory potentials
Ligand - Dependent Receptors involves what?
And will always result in what?
Channel closed until neurotransmitter binds to it. Open channel permits diffusion of specific ions. Fast Subthreshold potential changes, as soon as the receptor is bound, a change to the ion channel occurs, either allowing it increased or decreased conductance of ions.
Will ALWAYS result in excitatory depolarizing potentials.
Explain Excitability.
Explain Stability.
Not to the very detail but understand the concept.
Excitability:
This is the ability of a neuron to respond to a stimulus and generate an action potential.
Resting Membrane Potential: Neurons maintain a resting membrane potential of around -70 mV, primarily due to the differential distribution of ions (like Na+, K+, Cl-) across the membrane, maintained by the sodium-potassium pump. The neuron is excitable but not active.
Threshold: When a stimulus depolarizes the membrane potential to a critical threshold (typically around -55 mV), voltage-gated sodium channels open, leading to a rapid influx of Na+ ions. This depolarization triggers an action potential.
Depolarization: This is the rising phase of the action potential, where the inside of the neuron becomes more positive as sodium ions flood in.
Repolarization: After reaching the peak of depolarization, sodium channels close, and voltage-gated potassium channels open. Potassium ions (K+) exit the cell, restoring the negative internal charge (repolarizing the membrane).
Hyperpolarization: Sometimes the neuron becomes slightly more negative than its resting potential due to the continued efflux of K+, which is eventually corrected by the sodium-potassium pump.
Refractory Period: After an action potential, the neuron enters a brief period where it is less excitable (absolute refractory period) and then a slightly longer period where it requires a stronger stimulus to fire (relative refractory period).
2. Stability:
This refers to the neuron’s ability to return to and maintain its resting state after excitation.
Restoration of Resting Potential: Once the neuron has fired an action potential, the sodium-potassium pump actively transports Na+ out and K+ in to restore the resting membrane potential.
Ion Gradient Maintenance: Stability is largely dependent on the continued function of the sodium-potassium pump, which ensures the proper ionic gradient is maintained for future excitability.
Inhibition: Various mechanisms (like the action of neurotransmitters) can stabilize a neuron by preventing excessive excitability, ensuring that the neuron does not continuously fire.
EPSP stand for what?
Is it specific or non-specific?
Excitatory Postsynaptic Potential
Non-specific because it allows both sodium and potassium to move
IPSP stand for what?
Is it specific or non-specific?
Specific
Because it only allows either Potassium or Chloride ions
T or F
IPSP makes the synaptic potential more negative
T
As more chloride ion comes into the cell it makes the inside more negative
Non- specific channels (EPSP) increase ?
Excitability
Specific channels (IPSP) increase what?
Stability
T or F
fEPSPs bring the membrane potential closer and closer to threshold
T
Why is the AP important/the reason it occurs.
Is conducts to the terminal where it creates the voltage change necessary to cause the release of neurotransmitters
What is the purpose of fIPSP.
(Fast inhibitory postsynaptic potential)
Make is harder for themembrane to generate AP by increasing the difference in charge between the inside and outside of the membrane. *marketing the membrane more stable
What is the purpose of fEPSP?
Bring the membrane potential closer and closer to threshold, where voltage-gated sodium channels will open and initiate AP.
In the receptor NMDA allows what types of oils to flow through its channel?
The concentrations of both Na and Ca are much higher outside the cell than inside and so they flow in, and K. Which will occur. EPSP or IPSP?
Na+, K+, Ca++
EPSP, because the receptors are coupled to the channel directly
*this channel is most sensitive to glutamate
Once the neurotransmitter has been released from the presynaptic terminal, diffuses across the cleft and binds its receptor, in what two ways does it stop?
Chemical inactivation - breaking down the molecule
Reuptake - receptor on presynaptic cell that causes molecules to be taken back up
Endogenous
Born within
Substance make by and secreted from within a cell
Exogenous
Born outside
Substance made outside the body
T or F
Almost all antagonists are exogenous
T
Potentiators
Act to enhance the activity or effect of the agonist, without binding to the receptor of the agonist
Explain reuptake inhibitors as potentiators
By blocking the reuptake of neurotransmitters, these drugs increase the synaptic concentration of the neurotransmitter, which amplifies or potentiates its effects. This can lead to:
- enhanced neurotransmission
- increased signaling strength
Inhibitors act to?
Lessen the activity or effect of agonist, without binding to the receptor of the agonist
AChE is an…. Inhibitor or Activator?
Inhibitor
Cannabinoids is looked at as a treatment for Alzheimer’s disease. Why is that?
Inhibition of AChE (acetylcholinesterase) activity = improvement of dementia
Nervous system ligands binding non-specific receptors coupled directly to ion channels result in:
A. Inhibitory slow potentials
B. fEPSP
C. fIPSP
D. Excitatory slow potentials
B
Resting membrane potential generation and maintenance requires THREE of the following attributes:
- a sodium / potassium pump
- thin membranes exhibiting capacitance
- passive leak channels for K+ and Na+
- specific extracellular protein receptors
- second messenger systems
A sodium/ potassium pump
Thin membranes exhibiting capacitace
Passive lead channels for K+ and Na+
Affecting change of the resting membrane potential leading to action potential always requires:
A. enzymes necessary to create fIPSP
B. increasing the stability of the membrane
C. ligand receptors for acetylcholine
D. voltage dependent sodium channels
D
Conductance of which ion is most important in generating resting potential?
A. calcium
B. sodium
C. potassium
D. chloride
C
Which one of these molecules is most responsible for the net negative charge difference between the inside and outside of the membrane at rest?
A. sodium chloride
B. phosphorylated membrane proteins
C. calcium carbonate
B
As the membrane potential moves closer to threshold, it becomes more excitable.
True
False
T
During absolute refractory period, which TWO of these are true?
- the membrane is most stable
- the membrane is in hyperpolarization
- voltage dependent sodium channels are fully open
- the membrane is most excitable
The membrane is most stable
Voltage dependent sodium channels are fully open
During the membrane potential change from 0mv to -70mV, the membrane is:
A. hyperpolarizing
B. experiencing fIPSP
C. undergoing repolarization
C
Whenever the membrane potential moves away from threshold, the cell is becoming:
A. more stable, less excitable
B. hyperexcitable
C. less stable, more excitable
D. more permeable to sodium
A
Fast subthreshold potentials are created by:
A. ligands binding receptors coupled to ion channels
B.opening voltage-dependent channels
C. opening specific channels, only
D. opening non-specific channels, only
A
fEPSPs are created by:
A. opening ion channels that increase conductance to only potassium
B. increasing the number of potassium leak channels in the membrane
C. closing ion channels conducting sodium
D. opening ion channels that allow increased conductance to both sodium and potassium
D
Choose TWO methods of neurotransmitter inactivation:
- add exogenous antagonists
- add exogenous inhibitors
- endogenous reuptake mechanisms
- chemical substances that breakdown the neurotransmitter
- increase endogenous agonists
Endogenous reuptake mechansims
Chemical substances that breakdown the neurotransmitter
Define endogenous agonist.
A. substance made and secreted by the neuron that binds and activates the receptor
B. substance synthesized outside the body, and, when injected binds and activates the receptor
C. substance made and secreted by the neuron that blocks the receptor
D. substance that is made by the neuron that increases the release of a neurotransmitter
A
Given an example of an acetylcholine potentiator.
A. acetylcholinesterase inhibitors
B. botulinum toxin
C. acetylcholinesterase
D. selective serotonin reuptake inhibitors
A
Given an example of an exogenous antagonist
A. substance injected into the body that causes damage or death to the host
B. substance from outside the body that inhibits the release of the agonist
C. substance injected into the body that enhances the action of the agonist
D. substance injected into the body that binds and blocks the receptor site of the agonist
D
Name the enzyme that transforms choline into acetylcholine?
Choline Acetyltransferase (ChAT)
What is the enzyme used by a the neuron to synthesize ACh?
A. ACh Receptor
B. Acetyltreansferase
C. Choline Acetyl Transferase
C
Choline is conserved by a reuptake mechanism.. after the chemical inactivation by AChE, choline is taken back up into the terminal where it is coupled to acetate ions from Acetylene Co-A from the mitochondria by ChAT.
*The fact that choline is taken up and conserved and the at the transmitter is reformed in the terminal explains why muscle fatigue and tremor do not result from insufficient NT.
Acetylcholinesterase (AChE) is the chemical of inactivation for ____
ACh = acetylcholine
Name the two agonists of acetylcholine.
Nicotinic - causes muscle contraction and affects mRNAs post-transitionally to cause the outcomes associated with addiction…. And by similar methods, enhance learning and memory in people suffering from dementia and short-term memory loss.
Muscarinic - not on slide
The __________ of AP, and the number of of AP reaching the skeletal muscle cells will ultimately affect the __________ of ___________.
Frequency
Strength of contraction
The GSE and its ability to conduct the AP is known as the ?
“Final Common Pathway”
If the GSE is damaged, muscle cells cannot contract. This is indicative of ?
PNS lesion
______________ is realeased from GSE axons that synapse on skeletal muscle.
Acetylcholine (ACh)
Most antagonists are _________
Exogenous
Curare is considered an:
A. Agonist
B. ACh
C. fEPSP
D. Antagonist
Why is this?
D
It binds and blacks the site, causes no action to occur
Bupropion: Nicotinic Cholinergic Antagonsits has been found to:
A. Increase fIPSI reaction
B. Inhibit nAch
C. Antagonize Nicotinic cholenergic receptors in the brain
D. Enhance cognition within the brain
C
Potentiation are known to do what?
Act to enhance the action of agonist, without binding the receptor
Inhibitors are known for what?
Descreasing the action of the agonist without binding the receptor
EX: Botulinum Toxis (Botox)
Glycine does what to the GSE?
Inhibits the GSE
What is tetanus toxin relationship to ACh?
It is a potentiator of acetylcholine release.
It stops the renchaw cell and if the renchaw cell cannot release glycine, then there is no self control and the SCE will have higher level of excitations.
Briefly explain the relationship of GSE and renshaw cell.
Activation of the GSE causes ACh to depolarize the Renshaw cell…. The Renshaw cell releases the amino acid NTx glycine which is inhibitory to the GSE.
Tetanus toxin blocks release of glycine… the result being that the GSE fires more…. causing more muscle contraction. Tetanus would be an agonist
How can an inhibitor be a potentiator?
Myasthenia gravis: Immune system makes antibodies against N/C receptors. This causes the receptors to clump together and be destroyed by immune mechanisms.
autoimmune, antibodies against nAChR; antcholinesterase are part of a treatment plan
Sarin is an ___________ AChE inhibitor.
IRREVERSIBLE
By binding the esteric site, it is not able to be quickly cleared from the molecule before the patient has suffered irreparable harm.
Regarding muscarinic acetylcholine receptors: M2 would be inhibitory or stimulatory?
Inhibitory, muscle heart contraction
What is atropine?
Classical antagonist for muscarinic receptors.
Acts as M2 receptors in the heart, blocks the action of parasympathetic acetylcholine whose function at the M2 receptor is to decrease heart rate and conduction, and when this occurs pathologically atropine can be given to block activity, thus restoring the heart rate.
Explain the steps of slow postsynaptic potentials.
- There is a first messenger, and it does binds to a receptor
- That receptor is not coupled to an ion channel, but instead, to a G-protein
- The G-protien activates an intrmembrane enzyme system; in this example it is adrenal cyclase.
- Adeline
*Finish if needed
What’s the mechanism of action for the slow M2 receptors?
For slow potentials, the receptor site is NOT on the channel… there is a second messenger system that must be activated in order to cause the action of a channel. This takes longer to accomplish that the direction binding and activation, they also last a lot longer.
In this case of the M2 receptor the G-protien IS the second messenger… when ACh hinds the G-protein affects the OPENING of a K+ channel. Allowing potassium to leave the cell, causing sIPSP. This is one way the parasympathetic system inhibitors the heart at the SA node.
Besides channel opening or closing… second messenger systems can cause other intracellular repossess. This includes:
Post-traslational changes in the activity of mRNA… production of hormones or release of them… release of calcium from mitochondria.
Describe the two muscarinic second messenger actions.
First = simplest type of M2 receptor found on the SA node of the heart, the G-protien is the second messenger that is coupled to the K channel. When bound, the G-protein causes the channel to open, and sIPSP occurs.
Second = also functions at M2 receptors primarily at the heart, activation inhibits adrenal cyclase, decreasing cAMP activity, and repulsing in dephophorylation of cellular processes, effectively resulting in decreased heart rate and cardiac output.
The peripheral nervous system has two motor systems. These are
Somatic system and autonomic system
PNS motor system uses tow neurons from the CNS to the effector. Theses are?
Preganglionic and postganglionic neurons. Both are called GVE
The preganglionic neuron always releases _____ at Nicotinic cholinergic receptors on the postganglionic cell.
ACh
Autonomic ACh Scheme overview.
Summarize the pharmacology of the acetylcholine system within the autonomic system.
Watch lecture video or draw diagram at minute 42 of unit 3 video. Slide #57
T or F
The parasympathetic system has post ganglionic neurons and the sympathetic system has post ganglion neurons.
T
Nervous system endogenous ligands binding nicotinic cholinergic receptors include:
A. atropine
B. nicotine
C. acetylcholine
D. muscarine
C
Which TWO of these are true of nicotinic cholinergic receptors?
- they use botulinum toxin as the specific antagonist
- when activated result in fEPSP
- they are found on smooth muscle cell membranes
- when bound they result in fIPSP
- can be found at all pre- to postganglionic autonomic synapses
When activated result in fEPSP
Can be found at all pre- to Postganglionic autonomic synapses
The synthesis of acetylcholine requires which TWO of these:
- acetylcholinesterase
- dietary choline
- choline acetyltransferase
Dietary choline
Choline acetyltransferase
Increased conductance of which ion/s occurs when nicotinic cholinergic receptors are bound?
A.sodium, only
B. sodium and potassium
C. chloride, only
D. potassium, only
B
Which one of these is responsible for the fEPSPs at pre- to postganglionic synapses in the parasympathetic system?
A. nicotinic cholinergic receptors
B. M+ muscarinic cholinergic receptors
C. M2 muscarinic cholinergic receptors
D. M- muscarinic cholinergic receptors
A
Which one of these is an exogenous agonist at acetylcholine receptors?
A. atropine
B. Bo-Tox
C. curare
D. muscarine
D
Which two of these act as potentiators at nicotinic cholinergic receptors?
A. curare
B. muscarine
C. Black Widow spider venom
D. AChE inhibitors
C and D
Muscarinic cholinergic receptors all act via:
A. hyperpolarizing slow potentials
B. fIPSP
C. second messenger systems
C
Neurotransmitters using second messenger systems result in slow excitatory or inhibitory effects because:
A. they do not exhibit sites for exogenous antagonists
B. they all result in hyperpolarizing currents
C. they require more receptors to be bound before an action occurs
D. they require first messengers and second messengers
D
What is the mechanism of action for M2 receptors?
A. fEPSP using non-specific ion channel activation
B. sIPSP using the G-protein as the second messenger
C. fIPSP using specific potassium ion channel activation
D. sEPSP using the second messenger cAMP to cause the release of intracellular calcium
B
Sympathetic postganglionic endogenous ligands binding adrenergic receptors include (one is correct):
A. acetylcholine
B. atropine
C. muscarine
D. norepinephrine
D
Which TWO of these are true of adrenergic receptors?
A. they are found on skeletal muscle cell membranes
B. can be found at postganglionic sympathetic / effector synapses
C. they use botulinum toxin as the specific antagonist
D. when bound they result in fIPSP
E. when activated result in slow excitatory or inhibitory activities
B and E
The synthesis of norepinephrine requires which TWO of these:
A. dopamine
B. tyrosine
C. tryptophan
A and B
Which of these describes the root structure of both norepinephrine and epinephrine?
A. catechol ring
B. muscarine
C. acetyl Co-A
A
Beta-1 receptors cause _______ mainly at the ______ of the heart.
A. decreased intracellular Ca++ release; SA node
B. increased intracellular Ca++ release; AV node
C. increased K+ conductance at the SA node
D. increased sodium conductance; AV node
B
Which one of these is an exogenous agonist at beta-2 receptors on bronchial smooth muscle and glands?
A. Ventolin™
B. Wellbutrin™
C. Prozac™
A
Which two of these act as potentiators at adrenergic receptors?
A. Norepinephrine reuptake blockers
B. Morphine
C. Botulinum toxin
D. MAO inhibitors
A and D
______ receptors are responsible for vasoconstriction in most vessels of the body.
A. Alpha-1 adrenergic
B. Nicotinic-cholinergic
C. Muscarinic-cholinergic
A
The neurotransmitter _____ at _______ receptors is responsible for inhibition of the SA node of the heart :
A. acetylcholine; M+
B. norepinephrine; beta-2
C. acetylcholine; M2
C
Beta-1 receptors on the AV node of the heart bind _____ released from _______ axon terminals?
A. norepinephrine; postganglionic sympathetic
B. acetylcholine; postganglionic parasympathetic
C. epinephrine; postganglionic sympathetic
A
The neurotransmitter _________ binds ________ receptors at all pre- to postganglionic GVE synapses in the body:
A. acetylcholine; nicotinic-cholinergic
B. norepinephrine; nicotinic-cholinergic
C. norepinephrine; alpha-1
A
Which TWO of these axon classes innervate bronchial smooth muscle?
A. GVE preganglionic sympathetic
they use botulinum toxin as the specific antagonist
B. GSE
C. GVE postganglionic sympathetic
D. GVE postganglionic parasympathetic
C and D
Which two drug treatments would be reasonable to treat asthma presenting with excess mucous and wheezing?
A. beta-2 adrenergic agonists
B. nicotinic agonists
C. muscarinic antagonists
A and C
T or F
Acetylcholine is used as the neurotransmitter at all parasympathetic post ganglionic neurons sites
T
____________ is made from the essential amino acid phenylalanine. Therefore, availability of phenylalanine is a rate limiting step in this process.
Tyrosine
50% of the phenylalanine in our bodies issues for making tyrosine.
T or F
Norepinephrine and epinephrine binds the same receptors, but bind them a little differentially.
T
T or F
Dopamine binds receptors with tyrosine
F
Dopamine binds its own receptors
What monoamine oxidase worlds inside the terminal to the neuron to break down no nephrite and serotonin?
Monoamine oxidase A
Explain the process of monoamine oxidase (MAO) in a neuron.
- Norepinephrine (NE) is released and binds, it is taken back up and (norepinephrine inhibitor like disipemine (antidepressants) can be used to inhibit that reuptake mechanism)) monoamine oxidase breaks that norepinephrine down if that’s necessary to keep the level of norepinephrine level. Same happens with serotonin.
- Slides Explanation: MAO-A works inside the terminal to breaks down NE and serotonin. When NE is taken back into the cell, MAO-A breaks it down into metabolites in order to help keep the levels of NE appropriate to the conditions. Carecholamines also employ reuptake mechanism for inactivation. When the levels of these transmitters are low, due to genetic/synthesis defects, or other causes, a treatment strategy is to inhibit reuptake… this is where SSRIs and tricycle antidepressants come into play.
Chat GPT Explaination -
Name the sympathetic neurotransmitters for epinephrine and norepinephrine.
Adrenergic Receptors
What are the two main types of adrenergic receptors?
What are they linked to?
Alpha and beta, both linked to G-proteins and each with subtypes
T or F
Noradrenaline has a greater affinity for (a) receptors, adrenaline for (B) receptors
T
Alpha - 1 and Beta 1 and 2 are all ____-_________
Alpha - 2 receptors may be ____________ and ___-___________
Post-synaptic
Presynaptic and post-synaptic
Adrenergic Receptors:
NOTE: NE or EPI will bind, though alpha-1 has more affinity for NE, beta-1 more for EPI.
What affects does Alpha-1 have within neurological response?
Alpha-1 + (excitatory)
Vasoconstriction, pupillary dilation, GI sphincter if contraction, gluconeogenesis, erection
What affects do Beta-1 have neurologically?
Beta-1 + (excitatory)
Importantly on the AV and SA nodes of Purkinje cells of the heart
What affects does Beta-2 have neurologically?
Beta-2 - (Inhibitory)
Broncholdiation, inhibition of glandular secretion in the lungs and GI, vasodilation in some areas
Explain the effects of Alpha 1 Adrenergic Receptors.
Act by binding NE, EPI, and by using second messengers, cause the intracelllular increase of Ca++ causing contraction of smooth muscle. At the radial smooth muscle of the iris, contraction causes pupillary dilation.
At circular smooth muscle of vascular components, contraction causes vasoconstriction. At circular smooth muscle of the GI and urinary system sphincters, binding also causes contraction.
*SMOOTH MUSCLE CONTRACTION is the result of
T or F
Alpha-2 receptors have net inhibitory activity… mainly in a presynaptic position
T
Beta-1 are _____ ______
Beta-2 are _____ ______
Beta-1 are slow excitatory receptors (binding norepinephrine and increases cardiac output)
Beta-2 are slow inhibitory (smooth muscle relaxation)
T or F
Beta - 1 receptors are secondary messengers
T
Beta-1 receptors are second messenger driven receptors that, va calcium induction at the AV node and Purkinje fibers of the heart, cause increased contraction strength, conduction, and rate of contraction of the heart, all leading to increased cardiac output. What is the clinical significance of this process?
Beta-blockers, used to calm the heart after heart attach, decrease rate of contraction in arrhythmia, or decrease angina or hypertension: atenolol, propranolol and lopressor are examples of these blockers
Beta-2 receptors are inhibitory, resulting in…
Smooth muscle relaxation
Beta-2 receptors are found on many organs, notably…
The brachial smooth muscle and glands, where decreasing smooth muscle contraction will relax in dilation o the branching and decreased mucous secretion.
*you can probably guess that drugs to treat asthma would be examples of beta-2 agonists, and you would be right. (EX: albuterol (ventolin)
T or F
Beta-1 are slow excitatory receptors.
T
Beta-1 receptors bind ____________ and this increases _____ _____.
Norepinephrine and increasing cardiac output
T or F
Epinephrine will bind the beta-1 adrenergic receptor better than norepinephrine
T
Epinephrine is mainly coming from the _____ ______, and so is acting like a hormone. Whereas noephinephrine comes from _______ ________ where it acts as a neurotransmitter.
Adrenal medulla
Postganglionic sympathetic where it acts as a neurotransmitter
Describe the process of innervation of the heart (parasympathetic)
- The PE input arises from the nucleus ambiguous in the medulla of the brainstem. This is one of the nuclei contributing axons to cranial nerve C (the vagus nerve). From the medulla, CN-X preganglionic GVE axons project to the cardiopulmonary ganglion where they use ACh at Nicotinic sites to create fEPSP and cause the postganglionic PE GVE neuron to fire.
- The postganglionic projects to the SA node, mainly. It releases ACh that binds M2 receptors causing slow mediated inhibition by opening K+ channels. Thus, decreasing rate, strength, and conduction between the SA and AV nodes of the heart.
- The over-all affect is to decrease cardiac output.
Describe the process of innervation of the heart (sympathetic)
- The sympathetic input to the heart begins with the preganglionic E GVE neurons that arise in the spinal cord gray matter in a nucleus called the IML (intermediolateral nucleus) in segments T1-t4,5. The IML extends farther in the cord, but these are the segments involved in innervation of the heart. From here, the preggl axon makes its way to the sympathetic chain, where it synapses on postggl E GVE using ACh at nicotinic receptors causing fEPSP that excite the postggl.
- The postgglE GVE passes through the cardiopulmonary gal on its way to the AV node and purkinje fibers of the heart. Here it releases NE at B1 receptors causing slow excitatory activity resulting in increased strength of contraction, rate of contraction, and increased conduction to the ventricles via the purkinje fibers.
- Overall, this results in increased cardiac output.
M2 is what and does what?
M2 (muscarinic receptors) are G-protein-coupled, and mediate parasympathetic effects on the heart. Leading to slowing of the HR, conduction velocity, and contraction.
Describe the innervation of the bronchi (sympathetic)
- The sympathetic input to the bronchi begins with the preganglionic E GVE neurons that arise in the spinal cord gray matter in a nucleus called the IML (intermediolateral nucleus) in segments T1-t4,5. The IML extends farther in the cord, but these are the segments involved in innervation of the bronchi (yes, the same levels that innervate the heart). From here, the preggi E GVE axon makes its way to the sympathetic chain, where it synapses on postggl using ACh at nicotinic receptors causing fEPSP that excite the postggl.
- The postggl E GVE passes through the cardiopulmonary gal (same as with the heart) on its way to the smooth muscle and glands of the bronchi. Here it releases NE at B2 receptors causing slow inhibitory activity resulting in dilation of the bronchi and decreased mucous secretion.
- Overall, this results in increased area for O2 to pass into the lungs without being impeded by narrow bronchi and excessive mucous.
Describe the innervation of the bronchi (parasympathetic)
- Proper functioning of the bronchi requires input from both sympathetic and parasympathetic system axons. The PE input arises from the dorsal motor nucleus in the medulla of the brainstem. This is another one of the nuclei contributing axons to cranial nerve X (the vagus nerve). From the medulla, CN-X preganglionic PE GVE axons project to the cardiopulmonary ganglion where they use ACh at nicotinic sites to create fEPSP and cause the postganglionic PE GVE neuron to fire. - The postggl projects to bronchial smooth muscle and mucous glands. It releases ACh that binds M+ receptors causing slow mediated excitation, resulting in bronchial constriction and increased mucous secretion.
- Thus, protecting the lungs from excessively cold air, particulates in the air, or dry air.
T or F
Norepinephrine and epinephrine are adrenergic receptors that are subdivided into alpha 1, 2 and beta 1, 2
T
Beta-1 adrenergic receptors invoke what?
Stimulates: Increased HR, contraction, BP, and BV.
Heart, Juxtaglomerular cells (kidneys). Importantly on the AV and SA nodes and pukinje cells of the heart.
Beta-2 adrenergic receptors invoke what?
Inhibits: All Smooth muscle, glands, organs, bronchodilation, inhibition of glandular secretion in the lungs and GI, vasodilation in some areas. (vasodialates)
Alpha-1 adrenergic receptors invoke what?
Stimulate: all smooth muscle, glands, organs, pupillary dilation, GI sphincter if contraction, gluconeogensis, erection. (Vasoconstrict peripheral vessels)
Name two cholinergic receptors. These receptors are what?
Nicotinic and muscarinic
Parasympathetic receptors
Name two adrenergic receptors. These receptors are what?
Norepinephrine and Epinephrine (or adrenaline)
Sympathetic
