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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)


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) )

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)

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)

the 3 autonomic neurotransmitter divisions

cholinergic, adrenergic, and NANC

cholinergic autonomic neurotransmitters include

acetylcholine


adrenergic autonomic neurotransmitters include

norepinephrine, epinephrine, dopamine, and acetylcholine

NANC autonomic neurotransmitters include

ATP, nitric oxide, dynorphin, neuropeptide Y, substance P, vasoactive intestinal peptide

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)

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)

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

termination of neurotransmission through what

degradation (ACh through AChase), diffusion (like norepi), reuptake (like norepi)

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

nicotinic receptors

ion channel (ionotropic) that allows sodium to go through when two ACh bind to the channel

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

alpha receptors are what

EXCITATORY everywhere but the GUT where they are inhibitory

beta receptors are what

INHIBITORY everywhere but the HEART where they are excitatory

adrenergic neurotransmitter: isoproterenol rank order of potency

beta1=beta2=beta3>>>>>>>alpha1=alpha2; so a beta agonist primarily

adrenergic neurotransmitter: norepinephrine rank order of potency

alpha1=alpha2=beta1=beta3>>>>>beta2

adrenergic neurotransmitter: epinephrine rank order of potency

alpha1=alpha2=beta1=beta2=beta3

adrenergic neurotransmitter: dopamine rank order of potency

DA1>beta1>alpha1

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)

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

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


parasympathetic division pharmacology

lungs= M3; heart= M2; stomach= M3/M1; bladder= M3

ss

ss

interplay of SAS and PNS

neuromodulation, physiological antagonism, physiological cooperation

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)

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

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

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)

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

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

2 types of direct acting sympathomimetics

alpha adrenergic agonists or beta adrenergic agonists

2 types of indirect acting sympathomimetics

drugs that block NE uptake or drugs that facilitate NE release

what are sympatholytics

drugs that reduce or inhibit some or all of the actions of the sympathetic nervous system

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

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

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)

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

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)

voluntary motor neurons from spinal cord

one neuron from spinal cord terminates on effector muscle and releases ACh on nicotinic receptor