Download Unit 2 review sheets

UNIT 2- Review Sheets
Pathology Studied
Multiple sclerosis (MS)
Ptosis
Myasthenia Gravis
An immune-mediated inflammatory demyelinating disease of the central nervous system. Without
the myelination and because of the scarring where the myelin sheath was, the neuron is not as likely
to conduct the action potential.
Refers to the droopiness of the eye often seen in myasthenia gravis patients.
An autoimmune disorder where antibodies attack ACh receptors, which can cause flaccid paralysis
if left untreated. Ptosis of the eyelids is a sign of this disorder.
 Caused by denervation/neuropathy; sedentary life style; plaster cast; space flight (zero gravity)
 Muscle performance: degeneration of contractile proteins; decreased maximum force of
contraction and velocity of contraction
 Fiber loss can occur if disuse of muscle for 1-2 years; very difficult to replace lost fibers
Atrophy
This condition is opposite to hypertrophy (normal way to increase muscle mass)
 Caused by near maximal force development (e.g., weight lifting)
 Increases in actin and myosin
 Myofibrils split
FUNCTIONAL CLASSIFICATION OF NEUROTRANSMITTER RECEPTORS
TYPE
Example
Where found?
Channel within
receptor?
Second messenger?
ionotropic
nAChR
metabotropic
mAChR
Skeletal muscle
Postganglionic neuron of ANS
 Involuntary effectors of
parasympathetic nervous
system
 Some on skeletal muscle
 Found also on erector
pili, sweat glands, and
blood vessels to the skin
Yes
Yes
NO
NO
NO
Yes!
G protein activated
Effector protein:
phospholipase C
Second messengers:
DAG, IP3, Ca+
Late effector protein:
Protein kinase C
Effect: protein activity
changes: e.g., ion
channel permeability
changes
NO
Yes!
G protein activated
Effector protein:
adenylyl cyclase
Second messenger:
cAMP
Late effector protein:
Protein kinase A
Effect: protein activity
changes: e.g., ion
channel permeability
changes
α (1) and
β(1,2,3)

Involuntary effectors of
sympathetic nervous
system
Nervous System Chart
AUTONOMIC NERVOUS SYSTEM- two neuron chain to involuntary effectors
(cardiac muscle, smooth muscle, glands)
What
Location of the Preganglionic neuron
Parasympathetic Nervous System
(craniosacral)

T1-L2 in the intermediolateral
cell column (IMLCC) of the
spinal cord
Terminal ganglia- these are
found in the walls of the
involuntary effectors.


Sympathetic ganglia of the
sympathetic trunk
Collateral ganglia on the inferior
mesenteric, superior mesenteric
and the celiac trunk.

Long

Short

Short

Long

ACh

ACh



Cholinergic receptors
nACh receptors
ACh



Cholinergic receptors
nACh receptors
ACh if on the body wall with
muscarinic receptors on sweat
glands, erector pili muscle, and
blood vessels to the skin
Nepi and epi if the body
Adrenergic
ALWAYS FOUND IN THE CNS!


Brain-CN#3,7,9,10
S2-S4 in the sacral lateral gray
column (SLGC) the spinal
cord
Location of the Postganglionic neuron

ALWAYS FOUND OUTSIDE THE
CNS! That means they are found in
the PNS in autonomic ganglia.
Length of the Preganglionic Fiber
Length of the Postganglionic Fiber
Neurotransmitter used by
preganglionic cell
Receptor type on Postganglionic
neuron
Neurotransmitter used by
Postganglionic neuron
Sympathetic Nervous System
(thoracolumbar)


Receptors found on effectors

Muscarnic receptors


Preganglionic Fiber
Postganglionic Fiber


Cholinergic
Cholinergic


Adrenergic receptors (Alphas
and Betas)
sometimes: mACHr (see notes
above for muscarinic
explanation).
Cholinergic
Adrenergic/ sometimes
Cholinergic
SOMATIC MOTOR NERVOUS SYSTEM-one neuron to effector
(voluntary- skeletal muscle)
Cell body found where?
Ventral Gray horn of spinal cord or
brain nuclei for cranial nerves 3, 4, 5,
6, 7, 9, 10, 11, 12)
Neurotransmitter/ Receptor used
 ACh
 Primarily nAChR but some
mAChR are found, too
Effects
 Skeletal muscle contraction
SPECIFIC EFFECTS IN ORGANS INNERVATED BY THE AUTONOMIC NERVOUS SYSTEM
ORGAN
Sympathetic Effects
Eye: Iris smooth
muscle, ciliary muscle
Dilation of pupil
(contraction of radial
fibers of ciliary muscle)
Lacrimal Gland
Vasoconstriction
Salivary Gland
Scant secretion
Heart
Lungs-Bronchi
Increased rate and force
of contraction
Dilation of airways
Blood Vessels
Vasoconstriction
Gut
Decreased peristalsis
and secretion
Bladder
Inhibition of urine
Penis
Ejaculation
Adrenal Medulla
Secretion of epinephrine
into bloodstream
Skin-outer areas of the
body including head,
neck and extremities;
pilo erector muscles
and sweat glands
Vasoconstriction, sweat,
erection of pilo erector
muscles
Receptor
Neurotransmitter
Alpha Adrenergic-Nor
Epinephrine
Alpha Adrenergic-Nor
Epinephrine
Alpha Adrenergic-Nor
Epinephrine
Beta 1-Adernergic –Nor
epinephrine
Beta 2-Adernergic Nor
epinephrine
Alpha Adrenergic-Nor
Epinephrine
Adrenergic Nor
epinephrine
Parasympathetic
Constriction of pupil
(contraction of sphincter
like muscles)
Ciliary muscle contracts
for accommodation
Secretion
Receptor
Neurotransmitter
Muscarinic
Metabotropic- Ach
Increased gut motility
and secretion
Muscarinic
Metabotropic- Ach
Muscarinic
Metabotropic- Ach
Muscarinic
Metabotropic- Ach
Muscarinic
Metabotropic -Ach
Muscarinic
Metabotropic- Ach
Muscarinic
Metabotropic -Ach
Adrenergic Nor
epinephrine
Bladder contraction and
release
Muscarinic
Metabotropic- Ach
Adrenergic Nor
epinephrine
Modified
“postganglionic” cell
Erection
Muscarinic
Metabotropic- Ach
Copious Secretions
Slowed Rate
Vasoconstriction
Vasodilatation
None
Muscarinic
Metabotropic -ACh
ANS Stimulants
Type
Drug / Toxin
 Phenylephrine – stimulates alpha receptors (this is in Sudafed
PE)
Sympathetic nervous
 Isoproterenol – stimulates beta1 and beta2 receptors
system gains more
 Albuterol – stimulates beta2 receptors
control over the
 Ephedrine – increases release of norepinephrine
effector
 Amphetamine – increases release of norepinephrine
Parasympathomimetics  Nicotine – stimulates nACh receptors
 Muscarine – stimulates mACh receptors (causes profuse
Parasympathetic
sweating, gut motility (diarrhea), salivation, pupillary
nervous system gains
constriction)
more control over the  Pilocarpine – stimulates mACh receptors (causes profuse
effector
sweating, gut motility (diarrhea), salivation, pupillary
constriction)
Sympathomimetics
Effect
o Stimulates or mimics the effects of
adrenergic receptors; some
increase the release of these
neurotransmitters
o Sympathetic system gains more
control
o Stimulates receptors/ mimics the
binding of ACh on all kinds of
ACh receptors
o Parasympathetic system gains
more control
Blockers / Inhibitors
Type
Monoamine Oxidase
Inhibitor (MAOI)
Drug / Toxin
 Anti-depressant (no particular brands were
given)
Effect
o Inhibits MAO from degrading catecholamines in the synapse
Selective Serotonin
Reuptake Inhibitor
(SSRI)
 Prozac
 Ecstasy
o Inhibits reuptake of serotonin into the presynaptic membrane
o Leads to potentiated effects of serotonin (lasts longer)
Na+ VGC Blocker
 Lidocaine - used as anesthesia (dentist shoots
this into trigeminal nerve)
 Tetrodotoxin (TTX) – from liver of puffer fish
and newts
 Saxitoxin (STX) – dinoflagellates accumulate in
shellfish during red tides
 Clostridum botulinum
 “Botox”
 Undercooked turkey
 Dented food cans
 Atropine
o Flaccid paralysis
o Inhibits depolarization
Vesicle Blocker
mAChR Blocker
(blocks
parasympathetic
nervous system—
sympathetic nervous
system would gain
more control!)
nAChR Blocker
K+ VGC Blocker
 Curare – made from tree sap; large dose can
cause asphyxiation
 Tetraethylammonium (TEA)
AChE Blocker
(reversible)
 Neostigmine – typically given to a person with
Myasthenia Gravis
 Physostigmine – typically given to a person with
Myasthenia Gravis
AChE Blocker
(irreversible)
 Diisopropylfluorophosphates (DFP)
 Sarin
(must ventilate until reproduction of more AChE
occurs through gene expression!)
Inhibitory NT release
Blocker
 Tetanus exotoxin
 Black widow venom
Adrenergic Blocker
(sympathetic blocker)
 Phentolamine is an alpha receptor blocker
 Propranolol is a beta1 and beta2 receptor blocker
Allows
parasympathetic
nervous system to gain
more control!
o Flaccid paralysis
o Inhibits neurotransmitter release by blocking the ability for
vesicles to dock to synaptic membrane
o Flaccid paralysis
o Inhibits muscarinic receptors – a few found on voluntary
effector (skeletal muscle) but mainly found on the involuntary
effectors used by the parasympathetic nervous system: smooth
muscles (intestines/eye), heart, and glands (pancreas/ salivary
glands). Also sympathetic uses this receptor for sweat
glands/erector pili muscle and blood vessels to the skin.
o Would increase heart rate, bronchiole dilation, dry skin (why?),
dry mouth, constipation, pupillary dilation
o Flaccid paralysis
o Inhibits nicotinic receptors (mainly skeletal muscles)
o Spastic paralysis
o Inhibits repolarization
o Spastic paralysis
o Temporarily inhibits AChE from degrading ACh in the synapse;
therefore ACh effects are potentiated (that means they last
longer). Skeletal muscle contraction more likely to occur/lasts
longer.
o NOTE: these drugs also potentiate the effects of ACh used by
the ANS (postganglionics stimulated) and by effectors of the
parasympathetic system.
o Spastic paralysis
o Permanently inhibits AChE from degrading ACh in the synapse
o NOTE: this drugs also potentiates the effects of ACh used by
the ANS (postganglionics stimulated) and by effectors of the
parasympathetic system.
o Spastic paralysis
o Blocks the release of inhibitory neurotransmitters (e.g., GABA,
Gly), from the presynaptic neuron, therefore the post-synaptic
neuron is more likely to be excited from EPSPs that continue to
arrive (spatial summation) thus making the neuron closer to
threshold and more likely to fire an action potential. For a
somatic motor neuron, this means the skeletal muscle it
innervates will also be receiving more end plate potentials and
thus contracting more.
o Reduces the effectiveness of the sympathetic nervous system on
these receptors and lets parasympathetic NS gain more control
of body/effector
o Blocked alpha receptors (found on eye and blood vessels) would
lead to pupillary constriction (parasympathetic effects are still
fine) and vasodilation.
o Blocked B1 and B2 through propanolol leads to decreased heart
rate and bronchiole constriction (drug is contraindicated for
asthmatics!) because parasympathetic effects are in more
control.
Name
NEUROTRANSMITTERS
Receptors
Important notes
Acetylcholine
 nAChR (iontropic)
 mAChR (metabotropic- uses
IP3/DAG/Ca+2)
Glutamate
 GluR
GABA-major inhibitory
neurotransmitter
 GABA receptor
Glycine
 Gly R
Norepi/epi
 alpha 1 (eye and most blood
vessels)
 Beta (1 and 2; heart and lung,
respectively)
 Beta 3- found on adipose tissue
 These receptors are
metabotropic and would use
the cAMP pathway
Serotonin
 serotonin receptors
 this neurotransmitter is excitatory for nAChR
 neurotransmitter may be inhibitory for mAChR (e.g.,
parasympathetic innervation to the heart causes
hyperpolarization of specialized cells’ prepotential)
 Nearly all excitatory neurons found in CNS use it—e.g.,
it causes EPSP (increases sodium permeability) and is
used to stimulate somatic motor neurons in spinal cord.
 Antagonists to Glutamate receptor help stop neuronal death
after stroke- block receptor
 Too much glutamate leads to excitotoxicity in postsynaptic
neuron due to unregulated calcium influx
 Too little leads to psychosis
 Inhibitory neurotransmitter: would cause IPSP on
postsynaptic neuron by increasing permeability to K+ or
Cl-. For example, would cause an IPSP in a somatic
motor neuron in the spinal cord.
 Too little GABA leads to excitability of postsynaptic neuron
(seizures/convulsions)
 Anticonvulsants are drugs that are “GABA-like” (agonists)
and lead to inhibition of postsynaptic neuron (IPSP)
 Valium- increases release of GABA and leads to inhibition
of postsynaptic neuron (IPSP)
 Benzodiazepines- stimulate GABA receptor (more
inhibition of postsynaptic cell)
 Ethanol – stimulate GABA receptor (more inhibition of
postsynaptic cell)
 Inhibitory neurotransmitter: would cause IPSP on
postsynaptic neuron by increasing permeability to K+ or Cl.
 Stimulating these receptors would give more sympathetic
responses.
 Inhibiting these receptors would give more parasympathetic
responses.
 Stimulating alpha 1: vasoconstriction and pupillary dilation
 Stimulating B1: increased heart rate and force of
contraction
 Stimulating B2: increased bronchiole dilation
 Stimulating B3: increased adipose tissue mobilization.
 Norepi/Epi normally diffuse out of synaptic cleft very
readily, but MAO is also present to degrade
neurotransmitter.
 MAOI potentiates norepi effects (makes last longer).
 Selective serotonin reuptake pumps on presynaptic
membrane help remove serotonin from synaptic cleft.
 SSRI’- selective serotonin reuptake inhibitors are antidepressant drugs-potentiates the effects of serotonin
 Ecstasy drug inhibits SSR, too!