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304 Cards in this Set

  • Front
  • Back
parts of a neuron
1. cell body
2. dentdrites
3. Axon
4. Axon collaterals
5. Terminals
6. Varicosities
process from cell body to target
Axon collaterals
branches of axon
Where does release of NT occur on neuron?
nerve terminal
Schwann cells
make mylin sheath for periphery
make myelin for CNS
what are between mylin forming cells
nodes of ranvier
purpose of myelin
accelerates conduction velocity along the axon
what does acceleraton of conduction velocity in a neuron depend on?
size on the axon and mylination
multipolar neuron
has multiple dendritic processes. most tract neurons and neurons with peripheral processes are multipolar
pseudounipolar cell
has single stem that bifurcates to make distal and proximal processes that project to the target organ and the central nervous system. This is cell type in DRG
Unipolar and bipolar cells
have one or two processes. these are associated with special senses
Afferent (sensory) neurons
primary sensory neurons go from body to the CNS
efferent neurons
motor. go from CNS to effectors
local circuit neurons.
connect neurons within the CNS
bundle of axons in peripheral nervous system that contains both afferent and effernt fibers
collection of axons with the orgin (cell bodies) in one area or nucleus that projects to a discrete target
Large collection of axons that may contain multiple tracts with many different terminations, but found wi a defined region. (in SC)
discrete collection of axons, usually in the BS or ventral forebrain that contains axons from multiple sites and interconncets multiple areas (many tracts together)
What makes up largest number of cells in nervous system?
90% are glial cells
function of glial cells
support neurons and maintain ECF
forms mylin sheath around neurons in the CNS
types of glial cells
maintains ECF, supports metabolic activity of neurons, assist in forming BBB
Macrophages that partipcipate in immune fuction
Ependymal cells
comprise lining of cerebral ventricles and regulate CSF
Difference in regeneration of axons in CNS and PNS
severed axon in PNS can regrow to reinnervate the orginal target

Severed axons in CNS do NOT regrow to target; they may sprout new endings, but fuction is not regained
Neuronal cell bodies in periphery
neuronal cell bodies in CNS
Gray matter in SC
central butterfly area

contains cellbodies of neurons and glia, dendrites, axonal processes. Appears gray due to lack of mylin
white matter in SC
surrounds gray matter.

consists of axons; those with myelin give the color white look. White matter connects regions of SC or SC with brain
how does sensory input reach SC?
Dorsal root allows afferents to reach the SC bc DR consists of axons of sensory neurons
contains cell bodies of pseudounipolar sensory neurons
How do efferent leave the cord?
via the Vental Roots with consist of axons of motor neurons
What is ventral SC?
MOTOR is in ventral

dorsal is sensory
how are spinal nerves formed
by joining dorsal and ventral roots
number of Spinal nerves
31 divided into five groups

what does Brainstem consist of?
medulla oblongata, pons, and midbrain
function of BrainStem
responsible for basic mechansisms of life: regualtion of cardiovascular and respiration, sleep and wake, posture, and balance

relays and integrates info from periphery to brain and vice versa

Nuclei of most CN in BS

Central core of BS is reticular formation
reticular formation
in central core of BS it is involved in integrating info from all sensory modalities and affecting motor outflow. Biogenic amine nuclei are in the reticular formation
Function of cerebellum
coordinates ongoing movement and learns new movements

gets input form all muscles, and other brain regions responsible for movement
2 components of cerebellum
cortex: near surface. output cells from here project mainly to the deep nuclei.

Deep nuclei: deeper in cerebellum, neurons in these nuclei provide output from cerebellum
make you, you!
2 parts of forebrain
cerebral hemispheres

cerebral cortex:outer shell of gray matte in each hemisphere, they are about 3mm thick
What connect regions of the cerebral cortex and send info from cortex to other brain regions or SC?
fiber bundles
What conncest the two sides of the cortex?
corpus collsum
Output cells of cortex
pyramidal cells
4 lobes of cortex
3 major regions of input to cortex
other parts of cortex
reticular formation
Major integrating region of brain
cortex; it makes us, us!
Subcortical nuclei
groups of cell bodies deep wi hemispheres; the most prominent are the basal ganglia
Components of basal ganglia
caudate n.
globus pallidus
Function of basal ganglia
help control movement, they cell groups also help with higher cortical function such as cognition and emotion
2 parts of diencephalon
thalmus and hypothalmus
major relay station to cortex

most sensory and motor input from body must relay through thalmus before going to the cortex. The thalmus is also involved in arousal and attention
major endocrine center and is responsible for maintaining homeostatis
limbic system
responsibe for emotional responses, learning, memory, and integratoin of autonaumic responses to emotional stimuli
what does limbic connect to to cause emotion?
cebral ventricles
4 CSF filled interconnected cavities
How are lateral ventricles connected third ventricle and third ventricle connected to fourth ventricle?
they are deep in cortex and connected by foramen Monro to third ventricle wi the diencephalon. the third ventricle is connected by aqueduct of sylvius in midbrain to the fourth ventricle which is between the cerebellum and BS
outer membraneous coverign of brain
layers of meninges
dura matter
thickest and tougest. next to skull.
middle layer of meninge
meninge layer adjacent to brain and SC
where does CSF circulate?
in subarachnoid space between arachnoid and pia
chroid plexus
part of lining of ventricles appears tufted
What cells secrete CSF?
ependymal cells wi choroid plexus
How does CSF return to blood?
by aracnoid villi which are structures that project from the arachnoid to venous sinuses kinda like lymph
total % of body blood that brain gets
What does glucose need for energy?
what does blood brain barrier consist of?
endothelial cells of brain/spinal cord capillaries
Purpose of BBB
prevent large molecules from entering ECF
what can cross BBB?
lipid soluble substances but not lipid insobuble substances

therefore drugs cant cross BBB
3 divisions of gray matter
dorsal horn is sensory

ventral horn is motor

intermediate region is interneurons that connects sensory and motor
what is in the lumbar SC
gracile fasiculus
lateral coricospinal tract
spinocerebellar tract
spinothalmic tract
vestibulospinal and reticulsopinal tracts
gracile fasiculus
in SC on dorsal column. Touch input to lower half of body
lateral corticospinal tract
fine motor control. without this you would be paralyzed
spinocerebellar tract
proprioceptive input from body to cerebellum
spinothalmic tract
pain and temp input from body
vestibulospinal and reticulospinal tracts
postural motor control

found very medial dorsal
what is found in cervical SC?
gracile fasiculus
cuneate fasiculus
lateral corticospinal tract
spinocerebellar tract
spinothalamic tract
vestibulospinal and reticulo.
rubrospinal tract
cuneate fasciculus
touch input from upper half of body; part of dorsal column
rubrospinal tract
motor input of upper limbs
where is vestibulospinal and reticulospinal tracts?
very ventral and medial
where is spinocerebellar tract?
very lateral and ventral to lateral corticospinal tract
Where does corticospinal tract cross over?
at pyramids in BS
where is corticospinal tract
in brain very verntral part
in brain, what is lateral to cuneate n. and fasiculus?
spinal trigeminal n. and tract
medial lemniscus
where aons from gracile and cuneate cross over. Very medial part of brain
olfactory nerve

sense of smell

only sensory
pathway of Olfactory nerve (CN I)
primary sensory neurons in olfactory epithelium in roof of nasal cavity send olfactory info to the olfactory bulb. The fibers are the olfactory n.

the olfactory bulb contains cell bodies of secondary sensory neurons, whose axons comprise the olfactory tract.

the olfactory tract converys olfaction to olfactory cortical areas
optic n.
only sensory
pathway of CN II (optic)
photoreceptors in retina of eye transmit visual info to bipolar cells in the retina, which are the primary sensory neurons

bipolar cells synapse on ganglion cells, whose cell bodies also are in the retina; ganglion cells are secondary sensory neurons

axons of ganglion cells leave eye to form the optic nerve

the optic nerve crosses at the optic chiasm and becomes the optic tract

from the optic chiasm it goes to the lateral geniculate body
occulomotor n.

innervates eye muscles

has both motor and sensory components

exits from the midbrain
what muscles does CN III innervate?
superior rectus
medial rectus
inferior rectus
inferior oblique

levator palpebrae superiosis
what adducts the eye?
medial rectus by CN III
what moves the eye down?
inferior rectus CN III and is helped by superior oblique and CN IV
How does the eye move up?
by superior rectus and inferior oblique both supplied by CN III
what allows you to lift your eyelid?
levator palpebrae superiosis elevates eyelid. It is innervated by CN III
sensory componenet of CN III
contains a few fibers that transmit sensory info from muscle sensory receptors; these exit the motor nerves to course mainly in the opthalmic division of the trigeminal
PS componenet of CNIII
comes from edinger westphal nucleus

preganglionic neurons project to ciliary ganglion

postganglionic fibers inervate constictor pupillaie m. to constrict the pupil, and ciliar muscle to change the shape of the lens
Trochlear n.
exits from caudal midbrain

has afferent and efferent component
What does CN IV do?
innervates superior oblique m

sensory component from m. receptors is similiar to oculomoter
how does superior oblique m. move the eye?
down and lateral, causing inward rotation of the eye
only CN that exits dorsally and the only the one that crosses!
trochlear n. CN IV
Trigeminal n.

both afferent and efferent components

sensory from face and motor to muscles of mastication
where does trigeminal n. arise from?
arises from pons and courses to the trigeminal ganglion, which contains cell bodies of sensory fibers. the three divisions of the trigem leave the ganglion
Three divisions of the trigeminal
opthalmic: sensory input from eye, orbit, forehead, ethmoid, and frontal sinus

maxillary: sensory input from maxilla and overlying skin, nasal cavity, palate, nasopharnx, and some meninges

mandibular: sensory input from mouth, lower jaw, and anterior 2/3 of tongue. motor to mastication m.
4 brainstem nuclei of CN V
1. spinal trigeminal: pain and temp (2ary neurons)

2.Trigeminal main sensory nucleus: touch sensation (2ary sensory neurons)

3. Trigeminal mesencephalic n.: cell bodies of primary sensory neurons that transmit info from the chewing muscles

trigeminal motor n.: cell bodies of motor neurons that innervate chewing muscles
innervates lateral rectus m.

has both motor and sensory component
How does lateral rectus move eye?
innervated by CN VI. moves eye laterally
Where does CN VI exit brain?
pontomedullary junction
sensory of CN VI
sensory from muscle recepters (like occulomoter)
facial n.

motor to muscles of facial expression; taste
Where does CN VII leave the brain?
both motor and sensory components exit at pontomeduallary junction
motor component of CN VII
somatic motor control of muscles of facial expression

visceral (PS) motor control of salivary glands (except parotid), lacrimal gland, and mucus glands
sensory component of CN VII
sensory input from skin on lower part of ear and behind ear

taste buds from anterior 2/3 of tonge. fibers course in solitary tract and terminate in solitary n.
vestibulocochlear n.

auditory and vestibular info

only sensory component
where does CN VIII exit brain?
pontomedullary junction just lateral to CN VII
auditory component of CN VIII
hair cells in cochlea transmit info onto primary sensory neurons

primary sensory neurons exit the cochlea from CN VIII and terminate in the cochear n. in the BS
Vestibular component of CN VIII
hair cells in semicircular canals, saccule, and utricle transmit info onto primary sensory neurons

primary sensory neurons exit the structure from CN VIII and terminate in the vestibular n. in the BS
glossopharyngeal n.

associated with tase and eating

has both motor and sensory
where does CN IX exit the brain?
motor component of CN IX
innervates m. that elevates pharynx during swallowing and speech

PS control of parotid gland
sensory component of CN IX
input from carotid sinus and carotid bodies that monitor blood pressure and blood oxygen levels

sensory input from part of ear and inner ear, and posterior 1/3 of tonge, and upper pharynx(gag)

taste from posteior 1/3 of tongue
most of PS

has both motor and sensory
where does CNX exit?
motor of CN X
smooth m. and glands in pharynx,larynx,thorax,and abdomen(PS)

skeltal m. in pharynx, larynx, and tongue (but not all of em)
sensory of CN X
from all visceral structures innervated by the vagus n; also from BF receptors and chemoreceptors in aortic arch

part of ear,larynx, and pharynx
spinal accessory n

motor to sternocleidomastoid m. and traps in neck

cell bodies of motor neurons are in upper cervical SC; axons emerge from SC to form a trunk that ascends to medulla and then exits the skull with vagus n.
hypoglossal n.

motor control of tongue m.

only motor nerve that exits the medulla
receptor cell
specialized cells that sense the environment and then secrete neurotransmitters to excite nerve ending that are closely associated with the receptor cell.
What does receptor respond to?
only one sensory modality
graded potentials
transduce the stimulus to the neuron
types of graded potentials
generator potential

receptor potential
generator potential
potential caused by stimulus to a nerve ending it will then travel to an axon.

the generator potential has to be big enough to cause an AP
Receptor potential
potential caused by a stimulus to a receptor cell but it must reach AP
describe how the stimulus causes an AP
opening of ion channels, usually sodium, potassium, or and/or chloride, which cuases a change in membrane potential; this is the same as a EPSP
describe graded potentials
decrementing; the amplitude decreases with distance. If the amplitude is hi enough to reach threshold once the potential reaches the first node of Rnavier and AP is generated
What doew frequency of AP depend on?
amplitude of graded potential but the amplitude of AP is constant
A single afferent neuron with all of its branches
sensory unit
why are peripheral afferent neurons called primary afferents?
bc its the 1st neuron in the sensory pathway
where are primary afferents cell bodies?
in DRG or other peripheral ganglia associated w/cranial nerves
describe receptive field
many brances off sensory neurons

the smaller the receptive field, the higher the sensation
what on body has small receptive filds? large?
fingers have small receptive fields while the back has large receptive fields
describe specific ascending pathway
transmits sensation to cerebral cortex

its a 3 neuron pathway usualy
1. primary afferent
2. secondary neuron in SC or BS witch projects to the thalmus
3. tertiary neuron in thalmus which projects to cortex
Describe non specific pathways
used for emotional/autonamic responses

transmits non specific info saying something happened but you dont know what

can have many synapses

usually relays reticular formation; which is an area that integrates input from a wide variety of sensory modalities; one neuron can respond to many sensations

this pathway leads to alternating responses, arousal, and can lead to the affective component of a stimulus (hurts or feels good)
somatosensory cortex
postcentral gyrus, anterior end of parietal lobe
visual cortex
posterior part of occiptal lobe
auditory cortex
superior part of temporal lobe
what signals stimulus intensity?
1.signaled by frequnecy of AP

ex: push down on skin, the harder you push the increase in AP bc its a stronger stimulus

2. signaled by recruitment
describe recruitment of new sensory afferents
stimulus is big enough to excite all of neurons receptive fields and other neurons too bc they overlap so brain sees this as a huge stimulus
two point discrimination
with small rceptive fields it is easir to detect two closely spaced stimuli that it is with large receptive fields

areas with large receptive fields dont have good two pt discrimination(feels like one point instead of two)
in certain receptive field which area has the greatest response to the stimulus
the center of receptive field will generate more action potentials bc of denser innervation
(but this cant distinguish between low intensity stimuli at center vs. hi at edge)
describe lateral inhibition
has an effect to focus the info from a stimulus site. Through inhibitory interneurons,input from the periphery of a stimulus is inhibited, so this will focus input to brain on center of the stimulus. Lateral inhibition occurs at different levels of the brain and SC
what signals stimulus duration?
duration of the firing of the AP
reduction of frequency of AP despite a constant stimulu. There are two major classes of adaptation patterns in sensory fibers
slowly adapting receptors
frequency of AP does not reduce to zero during the duration of a stimulus. theses signal location and intensity of a stimulus
2 types of rapidly adapting recetpors
velocity detectors

vibration detectors
velocity detectors
AP frequency is proportional to velocity of stimulus and frequency is zero once velocity is zero. these receptors signal sensation of flutter, low frequency vibration, and movement across skin
vibration (acceleration) detectors
AP frequency is proportional to acceleraton of stimus, or change in velocity. typical of hi frequency vibration detectors

the bigger the acceleration the more the AP

vibration detectors dont respond to direction or accleration
classification of sensory receptors
superficial: touch,pressure,flutter,
vibration, tickle,warmth,cold,pain, itch

pressure,deep pain

visceral: hunger,nausea,distension,
visceral pin

type of axons, location, and function of free nerve endings
C,A,gamma axons


pain,temp,crude touch
type of axons, location, and function of meissner's corpuscles

on hairless skin

touch pressure
type of axons, location, and function of pacinian corpuscles

subcutaneous tissue,viscera, and skin

deep pressure,vibration
type of axons, location, and function of ruffinis corpuscles

on all skin

stretching of skin
type of axons, location, and function of muscle spindles
Ia,II axons

on muscles

tells muscle length
type of axons, location, and function golgi tendon

on tendon

tells muscle tension
area of skin innervated by a single dorsal root
The dorsal column medial leminscal system
transmits information regarding touch, pressure, and movement of hairs fro mthe body and back of the head
dorsal column medial leminscus pathway
primary afferents enter SC along the whole length and ascend in the Dorsal column on the same side(from lower body fibers make up gracile fasciculus from upper body fibers make up cuneate fasciculus)

ascending fibers terminate in the dorsal column nuclei(fibers in gracile fasiculus synapse on the gracile nucleus, fibers in cuneate synapse on cuneate n.)

the secondary axons exiting the gracile and cuneate cross to the opposite side in the caudal medulla and ascend to the thalmus in the medial lemniscus

fibers in medial lemniscus synaspe in VPL of thalmus

tertial fibers then go and synapse in somatosensory cortx.
what does spinothalmic tract (anterolateral system)transmit?
transmits info reguarding pain and temp
spinothalmic pathway
primary afferents enter SC along its whole length, and synapse on spinothalmic tracts cells in DH of SC

secondary fibers immediately cross to the opposite side to ascend in the ventrolateral part of the SC in the spinothalmic tract to the BS

fibers in spinothalmic tract synapse on cell bodies in the VPL of the thalmus

tertiary fibers ascend to synapse in the somatosensory cortex
describe trigeminal system
kinda like dorsal column-medial lemniscal system and spinothalmic system for face
where do primary afferents enter the BS?
in CN V,VII,IX, and X
trigeminal pathway for non nociceptive (touch) info
primary afferents synapse on neurons in the trigeminal main sensory n.

secondary axons cross to the opposite side and ascend to synaspe on cell bodies in the VPM of the thalmus

teritiary fibers ascend to synapse on cell bodies in the face region of the somatosensory cortex
trigeminal tract for nociceptive info
primary afferents synapse on neurons in the spinal trigeminal. n.

secondary axons cross to opposite side and ascend to synapse on cell bodies in the VPM of the thalmus

tertiary fibers go to synapse on cell bodies in the face region of somatosensory cortex
How is pain sensed?
by hi threshold receptors on bare nerve endings called nociceptors
Two components to pain
short latency prickling pain evoked by noxious stimuli carried by Agamma fibers used for localization of stimulus

long latency pain of burning and less bearable quality carried by C fibers (suffering)
stimuli that excite nociceptors
tissue damaging or potentially damaging stimuli

chemicals can sensitize nociceptors to stimuli
what are some chemicals that can sensitize nociceptors to stimuli
enhanced sensation of pain in response to subsequent stimuli when tissues are damaged
primary hyperglesia
enhanced sensation of pain at the site of tissue damage
secondary hyperalgesia
enhanced sensation of pain in the undamaged area surrounding the damaged area
describe visceral pain
commonly expressed as referred pain where pain is referred to somatic structure

poorly localized
Modulation of pain
pain is VERY subjective. there is a psychological component to pain. There are also delayed responses to pain in emergency situations. so there must be a mechanism for altering and reducing pain signal
The gate Theory
excitation of large diameter fibers (A beta fibers) either directly or through modulatory systems can reduce the activity in the spinothalmic tract neurons therfore reducing pain transmission.

C fibers however inhibit the inhibtor thereby reducing the interneurons inhibitory effect on the STT cells so you feel pain. Both effects of the C fiber faciliate pain transmission
pain descending modulation
periaquductal gray
locus coeruleus
raphe magnus

these things release enkephalins to decrease pain at spinothalmic tract or inhibit the presynaptic inhibition to decrease substance P and decrease STT
when C fibers come in and release substance P to excite the spinothalmic tract, where do ascending tracts go?
sharp pain goes to thalmus

there are collateral branches that go to reticular formation for suffering pain
(thalmus, pons,medulla)
how can pain be prevented
1. altering the transmission of painful information in the periphery at the level of primary afferents (Agamma or C fiber cut)

2. interrupting the ascending transmission of painful infromation and the processing of the painful information in the SC

net effect is to decrease excitation of STT to decrease pain
two major mechanism to activate descending inhibitory pathways
1. brainstem descending pathways excite interneurons in the SC. these interneurons release an opiate NT called enkephalin that inhibits the ascending (spinothalmic tract)

2. some BS descending pathways used enkephalin as their NT. these neurons contatct the presynaptic nerve termainls of primary afferent neurons. substance P is the NT released by primary afferents to excite STT. the release of enkephalin on the presynaptic nerve terminal inhibits the release of substance P, which means that there will be less excitatory input to the STT and therefore less nociceptive to higher centers
what does our rxn to painful stimulus depend on?
1. past experience
2. how other react to pain
3. the emotional content
non opioid analgesics whose mechanism of action is to block prostaglandin synthesis.
Primary use of NSAIDS
treat inflammation,
except for acetominphin of course
Purpose of pain and inflam
protective mechanisms that are essential for survival.

inflammation removes noxious agents from the site of injury to repair tissue damage
prostaglandin synthesis
Tissue Injury

Disturb cell membrane

Release of phospholipids

arachidonic acid

makes both lekotrienes and prostanglandins
how do NSAIDS have antiiflam, antipyretic, and analegic properties?
bc NSAIDS inhibit prostaglandin synthesis by inhibiting cyclo oxygenase

NSAIDS act at the level of the primary sensory neuron (except for acetaminophen)
Two isozymes of COX
COX 1 and COX 2

Cox 1 is made constitutively
COX 2 is induced by cytokines, and other inflam processes but it is expressed constituitively in the brain and kidneys
Only cox in tummy
COX 1 so it would be great if we had a drug that just inhibited COX 2 bc NSAIDS cause GI side effects bc they decrease the mucus cells ability to resist acid
How do NSAIDS block inflam, fever, and pain
the antiinflam and analgesic effects are due to decreased inflam mediators which also reduces the substance the exicites the nocioceptor

prostaglandins reset the hypothalmus to increase set point of body temp causing fever, COX inhibitors block this process and reduce fever
how does aspirin work?
it is a non cometive inhibitor of COX 1 and COX 2 bc it covalently binds to the COX enzyme. It is the ONLY NSAID to do this. Since it binds covalently, it lasts longer.
Effects of Aspirin



NO CV effect at therapeutic dose

GI side effects bc decreases gastric mucosal cells to resist penetration by acid which causes gastrice irritation

Increases bleeding time bc it inhibits platelet aggregation and since plateletts cant make new COX, new platelets must be made fefore bleeding time can return to normal
Therapeutic uses of aspirin
Releve Pain
Relieve inflam
Reduce fever
Describe Acetaminophen (Tylenol)
has both analgesic and antipyretic activites that are equivalent to that of aspirin but it does NOT relieve inflam!!!

Acetaminophen inhibits COX and prostaglandin synthesis but it has more activity in the CNS and less on prostanglins
Therapeutic uses of Acetaminophen
relieve pain
reduce fever
describe pheylpropionic derivitives (Advil, Ibprofin)
largest aspirin alternative.

they have antiinflam, analgesic, and antipyretic action

Fewer GI side effects than aspirin
Celebrex, Vioxx, Bextra

NSAIDS that only inhibit COX 2 so they produce less GI side effects. They are used for treating chronic pain. Very contraversial bc produce sever CV problems.
How do local anesthetics work?
they reversibly block nerve conduction by blocking Na channel at the level of the sensory neuron

causes analgesia , loss of temp, touch, proprioception, and muscle tone
what fibers does local anesthetics work best on? Worst?
Type B and Type C are the best bc they are unmylinated

Type Aalpha,Abeta,Agamma, and Adelta are less susceptible to anesthetic bc of their heavy mylination
what is added to local anesthetic solutions?
vasoconstrictors like epinephrine to decrease systemic absorbtion and prolong duration of action of anesthetic
Adverse effects of local anesthetics.
can be absorbed from site of injection and cause problems, most problems due to ODing pt

Bc its lipid soluble, local anesthetics get into PNS and CNS so get lightheaded, dizzy, numb, and disorieted. If blood levels hi can go into convusions, excessive stimulation of CNS followed by resp and CV depression

with hi conc of local anesthetic it can cause CV depression

Allergic Rxn can occur due to dematitis, asthma, and anaphylactic rxn. allergic rxn occur more frequently with ester local anesthetic
3 FUNCTIONAL classifications of opiates
agonists- opid agonist act on some or all of opoid receptors to produce a biological effect. Examples are morphine, methadone, dermerol, codeine, darvon, hydrocodone

antagonist-opoid antagonists are drugs that bind to all or some of opiate receptors but do NOT produce a biological effect. Examples: Narcan and Trexan

Mixed Agonist/antagonists- mixed activate some opiate receptors and block others. the are partial agonists at kappa and competive antagonists at mu receptors, Examples: talwin, stadol, nubain
3 opoid receptors
Mu-analgesia, sedation,miosis,constipation,respiratory depression, phys dependence, and euphoria

Kappa-analgesia, miosis, dysphoria, and sedation

3 families of endogenous opiates
1.endorphins-neurohormaone that mediates psychologic responses to stress and pain; hi affinity for mu

2.enkephalins-NT that has hi affinity for delta

3. Dynorphins-NT with hi affinity for kappa receptors
opoid analgesics and endogenous opiates 3 primary sites of action
1.SC-opoids inhibit release of NT from primary afferents to inhibit DH neuronal activity

2.Thalmus-Opoids block perception of pain at level of thalmus, reticular foramtion, and limbic to depress pain rxn

3. activation of descending systems: opoids activate descending inhibatory systems which modulate pain transmitted at the level of the SC
what pain is treated best with opiates?
severe dull costant pain is better releived by opoids than sharp pain.
clinical uses of opiates
releave pain

antitussive: supress cough


adjuct with anesthesia bc it is sedative and analgesic
decreased responsiveness to any pharmacolgic drug as a consequence of prior administration of that drug
with opiate use, what can you develop tolerance for?
mental clouding
resp depression
nausea and vomitting
cough suppression
Physical dependence
an abnormal phsyiological state produced by repeated administration of a drug, which then makes its continued use necessary to prevent withdrawl
tough outermost layer of the eye
transpartent surface, major refractive component, continuous with the sclera
opening the controls the amount of light that reaches the retina
2 muscles of iris
inner circular m. and outer radial m.

pupillary diameter depends on activity of these muscles.

eye color is based on pigment in iris
fine tunes refraction for focosing light on the retina (allows accomodation)
Ciliary m.
sphincter like circular m. controls thickness of lens during accomadation
zonular fibers
conncects lens to ciliary m.
what happens to zonular fibers with relax ciliary m?
tension on these fibers is hi and lens is flat

when ciliary m contracts zonular fibers are more relaxed and lens gets more round
highly vascularized between the retina and the sclera
photorecetor area of the ey
center area of retina where light fall if you look straight
center of macula
fovea centalis only cones are found here this is the region of greatest acuity
entrance of optic n.
optic dist aka blind spot
visible spectum
wavlengths in spectrum of 400-700 nm
where does refraction occur in the eye?
cornea and lens

the cornea has 3x the refractive ability the lens does!
how is refraction measured?
in diopters. refractive ability equals 1/focal length in meter.

distance from cornea to retina is 0.024 m so 1/.024= 42 diopters

lens only has 12 diopters
effect of refracton on image in eye
image will be upside down and reversed from right to left on the retina
As an object moves closer, what must occur to eye?
an obj that is closer requires more refraction(diopters) to focus the image on the retina than a far away image. the eye accomodates. the ciliary m, innervated by PS component of CN III contracts releasing stretch on zonular fibers which allows the lens to assume a more spherical shape and increasing its refractive ability
normal vision

lens is flat and the refraction is done mainly by the cornea
far sightedness; eye to short

when looking at a distant image, the images is focused behind the retina. The eye uses the lens to add refractive power to shorten the focal length so that the image falls on the retina. this uses up much of the refractive ability of the lens so that near objects cant be focused
near sightedness; eye ball too long

when looking at a distant object the image is focused in front of the retina. This is no compensatory ability for the eye to increase focal length in this situation so that far objects are ALWAYS out of focus. objects that are closer produce a longer focal lenght bc the light paths diverge rather than stay parallel. this pushes the image back toward the retina so near objects can be focused
with age lens becomes stiffer which prevents it from being able to assume a round configuarion. This reduces accomadation
this is due to uneven curvature of the cornea which has the effect of focusing an object at 2 separate places on the retina, producing blurry vision
what corrects hyperopia
convex lens to increase diopters and refraction. the cornea is also convex and increaes diopters
what corrects myopia
reduce refraction, use concave lens to decrease diopters
What type of lens corrects astigmatism?
cylindrical lens
visual acuity
measure of the ability to distinguish between 2 points. the greater the number of photoreceptors, the better the eye's refractive ability, the higher the acuity
how does a small pupil effect acuity?
increases depth of field of focus bc by allowing less light to reach retina, fuzzy edges of object that is out of focus become darker so object appears to be in focus.
path of light through the retina
in most of retina, light must first pass through regions containing cell bodies and axons of the neurons before reaching photoreceptors

at the fovea, the neurons in front of photoreceptors are pushed laterally so that light has a more direct path to the photorecetprs
2 types of photoreceptor cells
rods; very sensitive to lo light, lo acuity

cones; less sensitive to light, hi acuity, color vision
structure of photoreceptor
outer segment contains light sensing apparatus. infolding of cell membranes make discs; these break off and are free floating in rods, but stay attached to cell membrane in cones
describe photopigments
the photopigment molecules are contained within the disc membrane. there are four photopigments; one for rods and 3 for cones.
What do photopigments consist of?
light absobing molecule called retinal (Vit A derivative) plus a proteins taht spans the membrane 7 times usually called an opsin which is different in each photopigment
What is at the end of the photoreceptor opposite from the photopigments?
machinery for releasing the NT glutamate
ultimate result of phototransduction
biochemical changes alterthe release of NT from the photoreceptor
process in which biochemical events in the photoreceptor alter the electrical properties of the cell
2 major functional groups of brainstem descneding pathways
1. medial systems that primarily influence posture

2. Lateral systems that control fine dextrous movements
2 types of medial BS descending pathways
1. vesibulospinal tracts

2. reticulospinal tracts
vestibulospinal tract
originates in vestibular nuclei and projects to the SC

1. it is ipsilateral
2. it excites extensors and inhibits flexors
reticulospinal tracts
part of medial system

originates in medullary and pontine reticular formation and projects to the SC

1. uncrossed and crossed (contralateral)
2. pontine reticulospinal tract excites extensors and inhibits flexors and medullary reticulospinal tract excites flexors and inhibits extensors
2 types of lateral systems of BS descending pathway
1. corticospinal tract originates in CC and projects to SC

2. Rubrospinal tract originates from red nucleus in midbrain and projects to SC

the function of the 2 are coordinated
Corticospinal tract
from cortex To SC


excites flexors in distal limbs and digits and inhibits extensors
rubrospinal tract
originates from RN in midbrain and projects to SC

excites flexors in proximal limbs and hands, inhibits extensors
what does cerebral cortical motor regions control?
volunary movements
what are areas in cerebral cortex that produce movements when electrically stimulated termed?
motor cortex
2 major conceptual divisions of motor cortex
primary motor cortex

premotor cortex
primary motor cortex
low intensity electrical stimulation produces focal movement
Premotor cortex
consists of lateral convexity of brain and cingulate motor cortices on medial part of brain. in these regions, electrical stimulation produces movements but intensity required to evoke movement is greater that that needed in primary motor cortex and larger muscle grups are excited. these 3 regions have extensive connection wtih the primary motor cortex
Are frontal eye fields motor cortex?
they do not connect with primary motor corex instead they project to regions controlling saccadic eye movements
area 4
primary motor cortex

brodmanns area
where is brodmanns area?
anterior of central sulcus. on lateral convexity of brain cortex is in precentral gyrus

primary motor cortex is located in the anterior portion of the brain the paracentral lobule
how is cortex somatotopically organized?
leg is on medial surface. Arm, hand, and face are represented on the lateral convexity from superior to inferior.

there is a large representaion of fingers and thumb and for muscles used in speech
describe primary motor cortex contralateral representaion of the body
primary motor cortex influences unilateral movement. The primary motor cortex provides input to all body and facial m of voluntary movement it also control distal limbs and digits bc there is no backup control for these if lesioin occurs
what kind of movement is primary motor cortex primarily involved in?
fractionated movement, finely controlled, dexterous movements across single joint.
describe supplementary motor cortex
stimulation on one side produces movements on both sides

it allows coordinated movements of both limbs

it allows you to learn new movement sequence and mentally rehease the sequence. once you learn sequence well, the activity in the supplementary motor cortex lessens and primary motor cortex increases
2 parts of premotor cortex
supplementary on medial brain suface

lateral premotor on lateral brain surface

these take higher intensity to stimulate and allow more muscles to get excited
T or F the supplementary and lateral premotor cortex are both involved in regulating posture
what has major projection to lateral premotor cortex?
parietal lobe
Lateral premotor cortex
outer surface of brain

reacting to environment. Coordinates unilateral movements. posture adjustment is needed for the movement

controls larger muscle groups on contralateral side. Allows reaching movements
somatosensory cortex
recieves somatosensory input and relays info to complementary motor region

modulates sensory input so its appropriate for occasion
posterior parietal lobe
recieves input form somatic sensory areas, visual areas, and premotor areas

coordinates spatial info with movement

input to motor region from posterior parietal cortex allows you to move in relation to objects in environment
lower motor neuron
spinal motorneuron or nerves or CN motor neuron

alpha motor neuron
what happens if damage to lower motor neuron?
decrease m. tone

muscle atrophy

muscle fasiculation

abscence of tendon reflex

no babinski sign
upper motor neuron
refers to corticospinal neurons or other descending neurons above SC
characteristic damage of upper motor neurons
decrease m. tone then becomes increase m. tone (spacticty) over time

affect GROUPS of muscles

enhanced stretch receptors (hyperreflexia)

babinski sign
What is a babinski sign?
stroke lateral foot w/ sharp object:

in normal pt causes flexion toes

w/corticospinal damage, big toe invariable extends and other toes fan out (babinski sign)
functions of cerebellum
to produce coordination of movements

learn new movements


planning and coordination of movement
What seperates anterior and posterior lobe of cerebellum?
primary fissure
What seperates posterior lobe from flocculondodular lobe?
posterolateral fissure
3 major regions of cerebellum
1. vestibulocerebellum which consists of flocculondular and adjacent vermis

2. spinocerebellum which consists of most of vermis and paravermal zone

3. Cerebrocerebellum which consists of hemispheric or lateral zone
Cerebellar deep nuclei
1. Fastigial n.
2. Globose + emboliform n.
= interposed n.
3. Dentate n.
describe vestibulocerebellum
signal in vestibular ganglia -> vestibular n. -> cerebellar fastigial n. -> sends signals to reticular formation and vestibular n. to aid with postural and balance
Problem with vestibulocerebellum
dizzy and when walk drift to that side
Describe spinocerebellum
information from all muscles in body go to spinocerebellar tract to the fastigial n and the interposed n. they compare what the muscles are doing with what the muscles should be doing and controls the ongoing movements. the fastigial n. affects posture via the vestibular and reticular n. The interposed n. sends signals to the Red N. and the thalmus which then sends signal to cortex to move arms/fingers
describe cerebrocerebellum
input and output form cerebral cortex

dentate n. projects to RN and thalmus to cortex. Cortex sends signal to basilar pons which then projects to cerebellum lateral zone. this is how cortex sends message to cerebellum

involved with planning and timing of SKILLED movements
what do cerebellar lesions affect?
ipsilateral side, unless lesion is in middle, then both sides are affected

decomp of movement
intension tremor
inaccurate range and direction of movement
cant perform rapid alternating movements
lose faciliation from deep n.
functions of basal ganglia
initiate movement
permissive effect on movemnt
control gross movement
adjust body position for task
direct pathway of basal ganglia
the cortex activates the putamen which inhibits the globus pallidus allowing the Thalmus to be activated (bc inhibit the inhibitor)

this increases thalmocortical activity increasing muscle excitation by corticospinal tract
indirect pathway of basal ganglia
putamen activates the globus pallidus causing inhibitioni of the subthalmic n. so the globus pallidus is activated and it inhibits the thalmus decreasing thalmocortical activity