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42 Cards in this Set
- Front
- Back
motor control can be divided into what 2 systems |
somatic (consciously controlled skeletal) and autonomic (autonomous control of glands, smooth muscle, and cardiac muscle)
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ANS can be divided into what 2 divisions |
parasympathetic (rest and digest, discrete activation (each effect can happen individually)) and sympathetic (fight or flight, diffuse activation (all its effects usually happen at the same time) ) |
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parasympathetic system: does what, controls what |
trophotropic; rest and digest so maintains essential body functions and IS essential for life; protects the eye= constriction of the pupils (miosis), near vision (accommodation), lacrimation; protects the heart (supraventricular locations only)= bradycardia; protest the resp system= broncho constriction/broncho secretion; aids in digestion= salivation, peristalsis, gastric acid secretion; aids in urination, defecation; aids in procreation (erection) |
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sympathoadrenal system: does what, controls what |
ergotropic; right or flight so used to adjust the body to stressful situations but is NOT needed for life; dilation of pupils (mydriasis); increased HR and BP; decreased blood flow to the skin and internal organs; increased blood flow to skeletal muscles, brain, and heart; dilation of bronchi, decreased nasal and pulmonary secretions; mobilize energy stores (glycogenolysis and gluconeogenesis); urination, defecation; aids in procreation (inhibits labor and delivery, aids in ejaculation) |
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the 3 autonomic neurotransmitter divisions |
cholinergic, adrenergic, and NANC |
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cholinergic autonomic neurotransmitters include |
acetylcholine
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adrenergic autonomic neurotransmitters include |
norepinephrine, epinephrine, dopamine, and acetylcholine |
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NANC autonomic neurotransmitters include |
ATP, nitric oxide, dynorphin, neuropeptide Y, substance P, vasoactive intestinal peptide |
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cholinergic terminal: what happens, what does black widow spider venom and botulinum toxin do, what are cholinomimetic drugs, AChase inhibitors, and cholinoceptor blocking agents |
Na going down the neuron stimulates release of Ca which causes vesicles filled with ACh to release into the synapse (aka junction) which then bind on receptors (either nicotinic or muscarinic); AChesterase is hanging out in synapse and immediately starts breaking it down; there are autoreceptors (activated by ACh) and heteroreceptors (activated by other things) on the nerve terminal that inhibit the release of ACh; cholinergic neurochemistry= black widow spider venom (aka alphalotrodotoxin which causes an explosive release of ACh from the nerve terminal), botulinum toxin (inhibits the release of ACh from the nerve terminal), cholinomimetic drugs (direct agonists that mimic ACh, ex. nicotine and muscarine), ACHase inhibitors (indirect agonists bc they allow ACh to stimulate the receptors for a longer period of time), cholinoceptor blocking agents (block the receptors) |
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andronergic terminal: what happens, what does reserpine and amphetamine do, what are sympathomimetic drugs and adrenoceptor blocking drugs, what does cocaine and tricyclic antidepressants do |
same release as before except NO AChase like agents here (has to slowly float away or be taken back up); there are also autoreceptors and heteroreceptors on the nerve terminal; adrenergic neurochemistry= reserpine (depletes all sympathetic nerve terminals aka causes a terminal sympathectomy throughout the body), amphetamine (gets into the nerve terminal and causes release of norepi; this is an indirect agonist), sympathomimetic drugs (direct/indirect), adrenoceptor blocking drugs, cocaine/tricyclicantidepressants (block norepi transporter back into nerve so this increases the norepi in the synapse so sympathomimetic response) |
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the biosynthetic pathway for catecholamine neurotransmitters |
there are very small differences in the chemical structure of tyrosine, dopamine, epi, and norepi but this allows for very different actions |
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termination of neurotransmission through what |
degradation (ACh through AChase), diffusion (like norepi), reuptake (like norepi) |
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autonomic receptors: 2 major types and their divisions |
cholinoceptor (acetylcholine)= nicotinic (ionotropic (n (neuron), m (muscle))), muscarinic (G protein coupled (M1-5)); adrenoceptor (epinephrine, norepinephrine, and dopamine)= alpha (alpha1 and alpha2) G protein coupled, beta (Beta1-3) G protein coupled, dopaminergic receptors (dopamine), and dopamine (D1) G protein coupled |
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nicotinic receptors |
ion channel (ionotropic) that allows sodium to go through when two ACh bind to the channel |
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muscarinic receptors |
G protein coupled; muscarinic 2 and 4 act through stimulation of a G protein coupled receptor that is coupled to the alphai subunit (inhibits cyclic AMP and decreases ACh levels); muscarinic 1, 3, and 5 act through stimulation of a G protein coupled receptor that is coupled to the alphaq subunit (results in stimulation of phospholipase C which releases triglycerides which releases DAG (which stimulates PKC) and inositolphosphate (causes the release of intracellular Ca2+)); so 2 and 4 cause inhibitory effect in effector organs and 1, 3, and 5 cause stimulatory effects in effector organs |
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alpha receptors are what |
EXCITATORY everywhere but the GUT where they are inhibitory |
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beta receptors are what |
INHIBITORY everywhere but the HEART where they are excitatory |
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adrenergic neurotransmitter: isoproterenol rank order of potency |
beta1=beta2=beta3>>>>>>>alpha1=alpha2; so a beta agonist primarily |
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adrenergic neurotransmitter: norepinephrine rank order of potency |
alpha1=alpha2=beta1=beta3>>>>>beta2
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adrenergic neurotransmitter: epinephrine rank order of potency |
alpha1=alpha2=beta1=beta2=beta3 |
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adrenergic neurotransmitter: dopamine rank order of potency |
DA1>beta1>alpha1 |
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adrenergic receptors: receptors activated by EPI/NE |
alpha adrenergic receptors (epinephrine>isoproterenol) --> alpha1 adrenergic receptors (phenylephrine>clonidine) or alpha 2 adrenergic receptors (clonidine>phenylephrine); beta adrenergic receptors (isoproterenol>epinephrine) --> beta1 adrenergic receptors (EPI=NE), or beta 2 adrenergic receptors (EPI>NE), or beta3 adrenergic receptors (NE>EPI) |
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signal transduction by alpha1 adrenergic receptors |
stimulation of phospholipase C just like the 1, 3, and 5 of the muscarinic so cause stimulatory effects on effector organs |
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signal transduction by alpha2 and beta adrenergic receptors |
alpha2 inhibits adenylate cyclase and decrease cyclic AMP (just like the 2 and 4 of the muscarinic) so cause inhibitory effects on effector organs; all of the betas stimulate cyclic AMP
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parasympathetic division pharmacology |
lungs= M3; heart= M2; stomach= M3/M1; bladder= M3 |
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ss |
ss |
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interplay of SAS and PNS |
neuromodulation, physiological antagonism, physiological cooperation |
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modulation of neurotransmission= sources of modulators of neurotransmission |
from nerve terminal being modulated (e.g. autoinhibitory feedback), from postsynaptic/postjunctional site (e.g. transsynaptic/transjunctional inhibitory feedback), from nearby nerve terminal (cross talk), and from remote site via circulation (e.g. renin release) |
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mechanisms of neuromodulation |
those autoreceptor and heteroreceptors that we discussed before; so alpha2 receptors that bind norepi/epi are going to decrease the release of NE from a neuron |
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the effect of sympathetic on parasympathetic in the gut |
sympathetic= stimulation of alpha2 receptors on cholinergic nerve terminals to inhibit ACh release so this slows down the gut |
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what are parasympathomimetics |
aka cholinomimetics; drugs that facilitate or mimic some or all of the actions of the parasympathetic nervous system; either direct acting like muscarinic receptor agonists or indirect acting like anticholinesterases (either reversible or irreversible) |
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what are parasympatholytics |
aka anticholinergics; drugs that reduce or inhibit some or all of the actions of the parasympathetic nervous system; muscarinic receptor antagonists or ganglionic blocking drugs |
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what are sympathomimetics |
drugs that facilitate or mimic some or all of the actions of the sympathetic nervous system; either direct acting, mixed acting, or indirect acting |
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2 types of direct acting sympathomimetics |
alpha adrenergic agonists or beta adrenergic agonists |
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2 types of indirect acting sympathomimetics |
drugs that block NE uptake or drugs that facilitate NE release |
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what are sympatholytics |
drugs that reduce or inhibit some or all of the actions of the sympathetic nervous system |
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examples of sympatholytics |
centrally acting sympatholytics; ganglionic blocking drugs; adrenergic neuronal blocking drugs= drugs that inhibit NE synthesis,NE depleting drugs, presynaptic inhibition of release; adrenergic antagonists |
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autonomic control in the eye |
ciliary body produces intraocular fluid which then travels past the lens to the anterior chamber and then through the trabecular meshwork to the canal of schlemm which absorbs it; sympathomimetic drugs can act here for glaucoma
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control of BP |
mABP (mean arterial blood pressure which the brain looks at)=CO x TPR; CO= HR x SV; SV= CF x VR; brain can control the heart (chronotropy and inotropy), the venous system (proload), and the arterial system (afterload) |
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parasympathetic neurons from the spinal cord: pre and post synaptic |
only comes out of the cranium (medulla) or sacrum regions (cranisacral distribution) to innervate cardiac and smooth muscle, gland cells, and nerve terminals; pre terminates close to the effector organ and releases ACh on a nicotinic receptor; post terminates on the effector organ and releases ACh on muscarinic receptors |
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sympathetic neurons from the spinal cord: pre and post synaptic |
comes out of thoracolumbar spine; pre terminates in the sympathetic spinal ganglion close to the spine and releases ACh on nicotinic receptors; post terminates on the effector organ and releases either ACh on muscarine receptors (sweat glands), NE on alpha or beta receptors (cardiac and smooth muscle, gland cells, and nerve terminals), dopamine on dopamine receptors (renal vascular smooth muscle), and ACh on muscarinic receptor (stimulates sweat glands); can also stimulate the adrenal medulla (chromaffin cells) to release the neurohormones epi and norepi (this is only a 1 neuron path with ACh on nicotinic receptors in the adrenal medulla) |
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voluntary motor neurons from spinal cord |
one neuron from spinal cord terminates on effector muscle and releases ACh on nicotinic receptor |