Anatomy final Flashcards
(29 cards)
Pathway to Sympathetic trunk
- preganglionic fibers that originate at spinal cord exit the spinal cord via ventral root
- preganglionic fibers pass through white ramus com (which allows fiber to enter trunk)
- Fibers enter sympathericc trunk gaglion. this is where the pregaglionic fibers synpase with postganglionic fibers
At sympathetic trunk ganglion, preganglionic and postganglionic fibers can form synapses 1 of 3 ways
- Preganglionic and postganglionic neurons synpase at same level (the preganglionic fiber travels straight out, not up or down, and post. travels to effector)
- Preganglionic and post ganglionic neurons synpase at up or down level
- Preganglionic and post ganglionic neurons synapse at distant collateral ganglion in abdoman and pelvis
Pathways with synapse in Trunk Ganglia
if synapse forms here–> postganglionic fibers travel through grey rami to leave trunk, which communicates to enter ventral or distal ramus of adjoining spinal nerve.
grey rami communication: carry postganglionic fibers from sympathetic trunk ganglion to periphery
from here it travels to effector organs
Pathway to head (uses Pathways with synapse in Trunk Ganglia)
found at top of thoraxic portion of sympathetic division
-preganglionic fibers emerge from T1-T4, synapse with postagnglionic fibers at superior cervical ganglion of sympathtic trunk
-servs skin and blood vessles of head, stimulates dilator muscles of eyes-gets bigger (smooth muscle tissue control size of pupil), inhibits nasal and salivary glans, innervates muscle to upper eyelid, sends branches to heart (to increase heart rate)
Pathway to thorax (Pathways with synapse in Trunk Ganglia)
-preganglionic fibers emerge from T1-T6-run tandom with plexus in parasympathetic division
-most postganglionic axons pass through cardiac(increase heart rate), pulmonary(dilation of airways-lets more oxygen into lungs), and esophageal plexus (less active) to effector organ
Pathways with synapse in Collateral Ganglia
-preganglionic fibers from T5-L2 synapse
-form splachnic nerves:
–greater, lesser, least, lumbral, and sacral splanchnic nerves
–function: serve abdominal viscera and inhibit function to slow it down
Pathways to abdoman (Pathways with synapse in Collateral Ganglia)
-Fibers T5-TL innervate abdoman
-function: serve to slow down stomach, most intestines, liver, spleen, and kidney
Pathways to Pelvis (Pathways with synapse in Collateral Ganglia)
-Fibers T10-L2 inervate pelvis
-function: serves to slow down bladder, reproductive organs, distal half of large intestines
Process for focusing light for close vision
- Accommodation of lens: contraction of ciliary muscles–causes lends to bulge
- Constriction of pupils
–prevents divergent rays from entering eye
–pupil is smaller in diameter overall, so limiting ho much light rays enter eye - Convergence of eye-medial roation of eyeballs
–keeps objects focused on fovea centralis–>higher resolution
–closer the object, more eyes must converge
Info processing of Retina In Dark
- Ion channels open, Na+ enters and photoreceptors depolarizes to -40mV
- Ca2+ channel opens in terminal–> neurotransmitter released b/w photoreceptors and bipolar cells
- Neurotransmitter causes bipolar cell to hyperpolarize–>IBSP
- No neurotransmitter released b/w bp cell and ganglion cel–> no ap generated by ganglion cell bc Ion channels open
Info processing of Retina In Light
- Light stimulus causes ion channels to close, Na+ doesn’t enter and photoreceptors hyperpolarize to -70mV
-Ca2+ channels close–> neurotransmitter not released b/w photoreceptor and bp cells - Bp cell depolarizes in absence of neurotransmitter–>EPSP
- Ca2+ channels open, neurotransmitter released b/w bipolar cell and ganglion cell
- ganglion cell generates ap–>sent via optic nerve
G-Protein signaling system for Phototransduction
(in first step of info processing of Retina In Light)
- Retinal absorbs light and changes shape
- visual pigment activates transduction (g-protein)
- Transducin activates phosphoisterie
- PDE converts cGMP using causing cGMP levels to fall
- As cGMP levels fall, cGMP gated cation channels close, resulting in hyperpolarization
For smell to occur
- Activation of sensory neurons
–oderant dissolves in mucus
–oderant binds receptor proteins in olfactory cilium membrane - transduction of smell–>binding created graded potential by sensory neuron
–if strong enough, mitol cells generate an action potential.
–Na and Ca2+ influx depolarizes sensory neurons and creates graded potential
–continious refux causes adaptation
Activation of taste bud receptors
-chemical tastant must dissolve in saliva
-tastant binds epithelial cell–>graded potential occurs
a) salty–> na+ influx through Na+ channels directly depolarizes gustatory epithelial cells
b)sour–> H+ acts intracellulary to open ion chennels and create graded potential
c) bitter/sweet/umami– G-protein gustducin activation leads to opening of ion channels to depolarize membrane
–neurotransmitter release of sensory dendrite elicts action potention
Pathway to cortex
Facial nerve-2/3 of tongue
glossophargeal-1/3 of tongue
most fibers travel to primary gustatory cortex
others travel to limbic system and hypothalmus
brain combines infro from smell and taste to produce a more refined taste
portection method- can induce fight or flight
transmission of sound to inner ear
1) sound waves vibrate typmanic membrane(same vibration as sound waves)–> transfered to inner ear
2) malleus vibrates in response to typmanum
–incus and stapes vibrate to
–medial portion of stapes vibrates to oval window that divides middle ear from inner ear (starts tranmission of sound to inner ear)
3) movement of oval window caues perlymph fluid of scala vestibuli to move as pressure wave towards helicotrema
–round window rleases pressure in inner ear so parlymph can move
4) once perliymph moves, 1 of 2 paths are taken
–a) basilar membrane path soun waves trnasmitted through scala media
–pressure waves vibrate it and hair cells stimulated
–b)heliocotrema path(low frequnecy)
–doesnt stimulate sensory receptors
–creates small wave of paralympth that cant bend basilar membrane.
sound transduction
movement of basilar membrane stimulaets inner hair cells
-inner hair cells have sterecillia
–tallest sterecillia embedded in tectorial membrane which doesnt moves in response to bending
-sterecillia joined by tip-links; which open mechanically gated ion channels
when basilar membrne at rest, no sound is carrying. some tip links open and hair cells are slightly depolarized
Stereocillia pivot towards tallest hair
all tip links open so all ion channels open
-K+ and Ca+ enter cell
inner hair cells depolarize creating a graded potential
-neurotrasmitters from inner ear cell released to cochlear nerve and produce action potential
Stereocillia pivot towards shortest hair
all tip links closed
-no K+ and Ca+ enter cell
-inner hair cells hyperpolarize and no graded potential created
-neurotrasmitters dont creeate atp
Outer hair cells
cange flexability of basilar membrane
1) increases responsivness of inner hair cells
2)protection–> stiffens in response to loud sound–> stabalizes basilar membrane
Linear head and acceleration of head position In Utricle
maculae orineted horizontally in head and hair cells are verticle (back and forth movement)
Linear head and acceleration of head position In Saccule
maculae oriented vertically and hair cells are horizontal
Stimulation of muscle fibers to occur
1) Events at neuromuscular junction
–motor neurons release ACh at neurotransmuscular junction
–ACh binfs chemically gated ion channels on Sarcolemma
2) Generation of EPP and AP across sarcolemma
–ACh opens ion channels on sarcolemma to create end plate potential (EPP)
–EPP is graded potential specific to muscle tissue
–EPP depolarizes sarcolemma and if strong enough can generate ap
3) excitation contraction coupling
–ap spreads from sarcolemma to T-tubles. when ap arives Ca2+ channels are forced opem and Ca2+ is released
4) cross bridge formation and muscle contraction
Cross bridge formation
A) ca2+ bonds troponin and it changes shape
B) after shape is changed, it rolls to the side
C) once it moves, myosin binding site on actin exposed
D) myosin head spilts ATP into ADP Pi
E)ADP Pi released from myosin head, causing myosin head to change shape increasing bend–myosin head pulls actin filament to center of sarcomere (power stroke)
F) myosin head binds to another ATP–> myosin head detaches from actin binding site
steps D-F occur along length of actin filament until muscle contraction ends or ATP/Ca2+ run short