Exam 2 review Flashcards
2 Main nervous system categories:
Central and Peripheral nervous system
Afferent division
Go toward CNS (sensory info)
Efferent division
Go away from CNS (motor system)
2 divisions of peripheral nervous system:
Somatic (conscious control) and Autonomic (unaware)
2 branches of Autonomic nervous system:
Sympathetic and Parasympathetic
Where are the cell bodies of a neuron located in the somatic nervous system?
In the brain
How many neurons create a chain in the autonomic nervous system?
2
Sympathetic response:
Fight or flight increase HR increase BP dilate bronchioles shunt blood to muscles restrict blood flow to GI
Parasympathetic response:
rest and digest
conserve energy
shunts blood to GI, endocrine, urogenital
What branch of the autonomic nervous system is dominate most of the time?
parasympathetic
Origin of fibers of parasympathetic:
craniosacral
Origin of fibers of sympathetic:
thoracolumbar
Length of fibers for Parasympathetic:
Long pre-ganglion and short post-ganglion
Length of fibers for sympathetic:
Short pre-ganglion and long post-ganglion
Primary neurotransmitter for parasympathetic nervous system:
ACH
Parasympathetic works through: blood stream or direct innervation?
direct innervation
Sympathetic work through: blood stream or direct innervation?
Both
Pre-ganglionic fibers in the autonomic system release what neurotransmitter?
ACH
Post-ganglionic fibers in the autonomic system release what neurotransmitter?
Norepi or ACH
Can be inhibitory or excitatory based on the receptor they bind to (not the neurotransmitter)
Sympathomimetics:
Drugs that mimic the effect of sympathetic nervous system activation.
Direct acting Sympathomimetics:
Bind to same places as Norepi (adrenergic receptor).
Epi, isoproterenol, albuterol
Indirect acting Sympathomimetics:
Don’t bind to the same receptor Norepi does, they prolong the effect of norepi.
Ephedrine and amphetamine
Inotropic
increase force
Chronotropic
increase rate
Sympatholytics
Stop the effects of the sympathetic nervous system (primarily given to decrease BP)
Receptor selective
Cholinergic receptors:
Will bind ACH
Muscarinic
Nicotinic
Adrenergic Receptors:
Will bind Norepi
Alpha, beta, dopamine
All are G-protein coupled receptors
Muscarinic M1:
Will inhibit sympathetic response. (activates downstream signaling; excitatory)
In CNS, sympathetic post-ganglionic neurone, some pre-synaptic sites.
Muscarinic M2:
In myocardium, smooth muscle, some pre-synaptic sites, CNS (Think of slowing down heart) (inhibitory)
Muscarinic M3:
Exocrine glands, vessels (smooth muscle and endothelium), CNS (excitatory)
Nicotinic-n (neuronal)
Post-ganglionic neurons, some pre-synaptic cholinergic terminals
Nicotinic-m (muscular)
Skeletal muscle neuromuscular end plates
Alpha-1
Primarily responsible for constriction of smooth muscle.
Usually found on peripheral vascular.
Postsynaptic effector cells (especially smooth muscle)
Alpha-2
Shutting down response of Alpha1 (if we stimulate A2=relax smooth muscle).
Presynaptic adrenergic nerve terminals, platelets, lipocytes, smooth muscle
Beta-1
Primarily heart.
Increases force and rate of contractions.
Juxtaglomerular apparatus of renal tubules
Beta-2
Relaxes smooth muscle in lungs.
Dopamine receptors:
D1 (AD1) & D5
Brain, effector tissue (especially smooth muscle of renal vascular bed)
Autoreceptor
A receptor that is on a neuron that binds to the same neurotransmitter being released by that neuron.
Inhibitory= negative feedback
Excitatory= positive feedback
Alpha-1 activates:
Phospholipase C which releases IP3 and DAG
Alpha-2 inhibits:
Adenylate cyclase which decreases cAMP
All Betas activate:
Adenylate cyclase which produces cAMP
Nicotinic receptors are..
ion channels
fast
located in NMJ
M1, M3, M5 activate:
Phospholipase C
M2, M4 inhibit:
Adenylate cyclase
Heteroreceptors
Receptors on a neuron that bind to a different neurotransmitter than the one the neuron is releasing.
Another term for “parasympathomimetics”
Cholinomimetics
Another term for “parasympatholytics”
Antimuscarinics
Example of sympatholytic drug classes:
Alphs-blockers, Beta-blockers
Example of sympathomimetics:
Epi/norepi and dopamine
2 types of synapses:
Chemical and electrical
Chemical synapses:
Release neurotransmitters
Electrical synapses:
Are gap junctions between adjacent cells
En Passant synapses:
Bulging areas along an axon that can release neurotransmitters. (occur primarily in CNS
Telodendria
Branches off of the axon of a neuron
Synaptic terminal
The pre-synaptic end of an axon
Neurotransmitter fate:
1- diffused across synapse
2-degraded by enzymes
3-uptake into presynaptic cell
4-uptake into surrounding cells
Neurotransmitter class:
Esters
ACH
Neurotransmitter class:
Monoamines
Norepi/epi
Serotonin
Dopamine
Neurotransmitter class:
Amino acids
Glutamate (excitatory)
GABA (inhibitory)
Neurotransmitter class:
Purines
Adenosine
ATP
Neurotransmitter class:
Peptides
Substance P
Endorphins
Neurotransmitter class:
Inorganic gases
Nitric oxide (NO) Created but not stored bc it freely diffuses across membrane
ACH is released where?
Almost all preganglionic fibers
All somatic fibers (skeletal)
Postganglionic neurons in parasympathetic (& few sympathetic)
Monoamines
Amino acid derivatives (tyrosine)
Glutamate
Amino Acid
most important excitatory NT in brain.
learning and memory.
Can be over produced (parkinson’s)
Glycine
Inhibitory
Can enhance effects of glutamate
GABA
Inhibitory
ACH is synthesized in..
..the cytoplasm
Choline Acetyltransferase (ChAT)
Puts together Acetyl-CoA and Choline to make ACh
Acetylcholinesterase (AChE)
Breaks down ACh into Acetyl-CoA and Choline
Cholinetransferase (CHT)
Transports Choline and Na+ into synaptic terminal
Vesicular Ach Transporter (VAT)
Transports ACH into storage vesicle
Synaptotagmin
Ca++ sensor
Anchoring/Docking
SNARE complex which anchors vesicle near release site
SNARE complex 3 proteins:
- Syntaxin
- SNAP-25 (in presynaptic membrane)
- VAMP (on vesicle)
Priming
- ATP Dependent
- Supports rapid exocytosis
Fusion
- Ca++ induced (synaptotagmin)
- Fusion of membrane (fast)
- Fusion pore forms
Botulinum toxin
Blocks SNAP25 preventing vesicle from fusing with cell membrane
Hemicholiniums block..
..CHT
Vesamicol blocks..
..VAT
Sarin nerve gas inhibits..
..AChE
How is NE broken down?
It is transported back into the presynaptic terminal by NET and broken down by MAO
Vesicular monoamine transporter (VMAT)
transports any monoamine into storage vesicle (dopamine, dopa, epi, norepi, etc)
Metyrosine inhibits..
..the conversion of tyrosine
Reserpine inhibits..
..VMAT
Bretylium and guanethidine inhibit..
..VAMP & SNAP
Cocaine and tricyclic antidepressants inhibit..
..NET
MAOIs inhibit..
MAO which inhibits the breakdown of NE.
Cholinomimetics
Simulate activity of ACh
“parasympathetic”
Cholinomimetics Direct-acting:
Bind to and activate M or N receptors
Cholinomimetics Indirect-acting:
Inhibit action of AChE, prolonging effects of ACh released at junction
Esters of Choline:
ACh (methacholine, carbachol, bethanechol) Charged insoluble in lipids Don't cross blood brain barrier typically given inhalation or injection
Giving ACh directly into the eye can cause..
..pupillary constriction
Alkaloids:
Nicotine (absorbed well), Muscarine (not absorbed as well)
plant based
Indirect acting cholinomimetic chemical categories:
Simple alcohols (5-15min duration)
Carbonic acid esters of alcohols (0.5-8hrs)
Organophosphates(100hours)
Major therapeutic uses for cholinomimetics:
Eye diseases
GI/Urinary tract (post-op ileus)
NMJ (myasthenia gravis)
Atropine overdose
Mydriasis
dilated pupils
Miosis
pupil constriction
Signs of Muscarine toxicity and Organophosphate exposure:
SLUDGE-M Salivation Lacrimation Urination Defecation Gastrointestinal mobility Emesis Miosis
What is the treatment for muscarine toxicity and organophosphate exposure?
Atropine
Signs of atropine/belladona OD?
BRAND Blind Red Absent bowel sounds Nuts Dry
Treatment for atropine/belladona OD?
Physostigmine
Atropine applied directly to the eye causes?
Mydriasis
Tx for parkinsons:
L-DOPA
Tx for motion sickness:
Scopolamine
Ophthalmic drug given for eye exam dilation
Topical tropicamide
Direct Adrenergic agonist
Bind to same sight as NE
Indirect adrenergic agonist
Stimulate release of catecholamines or prevent re-uptake of catecholamines.
Catechol-O-Methyltransferase (COMT)
inactivates Catecholamines
why can’t you take Catecholamines orally?
because COMT is located in the gut
Non-catecholamines
not inactivated by COMT
longer half-life
increased lipid solubility
increased oral bioavailability
Epinephrine
Potent vasoconstrictor -Alpha1 Cardiac stimulant -Beta 1 -postitive Inotropic and chronotropic Beta2 dilation of skeletal muscle