• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/103

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

103 Cards in this Set

  • Front
  • Back
Concentration Gradient:

always more Na+, K+, Cl- ions
in or outside the cell?
more Na out of cell

more K inside cell

more Cl out of cell
voltage (V) (membrane potential)
separation of charge across a membrane
current
flux or flow of and ion

-ampheres (I)
Hyperpolarization
when Voltage in cell becomes more negative

happens when cell membrane becomes more permeable to K+
Concentration Gradient is maintained by:
Na/K pump (uses ATP)
Depolarization
When voltage in the cell becomes more positive

happens when cell membrane becomes more permeable to Na+
Goldman-Hodgkin-Katz Eqn:
60mV log *
[Pna[na]o+Pk[k]o+Pcl[cl]i]
-----------------------
[Pna[na]i+pk[k]i+Pcl[cl]o]

takes into account concentration of ions
and permeability of membrane to ions
voltage gated ion channels
are ion specific, throughout length of axon
K leaky gated ion channel
k leaks out of cell, according to concentration gradient

are open at rest only
2 Na+ voltage gated ion channels
and
1 K+ voltage gated ion channel
Na+ activation gate (m3)

Na+ inactivation gate (h) = plug

K+ activation gate (n4)
scorpion and snake venom
prevents Na+ inactivation gate (h) from closing.
Bee sting
blocks K+ activation
Action potential:
REST
Vm at rest= -70mv
m3 is closed
h is open
n4 is closed

K+ leaky gates are open
so K+ exits the cell
and cell is close to Vk (hyperpolarized)
Action Potential:
UPSTROKE
depolarization to threshold
m3 open
h open
n4 closed

so now Na goes in cell and it becomes more + (depolarized)
The highest (most depolarized) the cell can get =
Vna
Action Potential:
DOWNSTROKE
Hyperpolarization
m3 open
h close
n4 open

K leaves cell and cell hyperpolarizes (becomes more negative)
Action Potential
ABSOLUTE REFRACTORY PERIOD
from undershoot to Vrest
m3 close
h close
n4 close

no AP possible because all are closed

can go as low as Vk

But leaky K+ gate open so goes back to Vrest
scorpion venom
and snake
keeps h open
so upstroke plateau
seizures
TTX from pufferfish
permanently blocks Na+ channels
Frontal Lobe function
personality
motor
LTM
Parietal Lobe
somatosensory
pain temp taste pressure touch vibration
occipital
vision
temporal
hearing
STM
insular
olfaction
limbic
Longitudinal Fissure
separates L and R hemispheres
Central Sulcus
separates Frontal and Parietal
Pre-Central Gyrus
Primary Motor Cortex
Post-Central Gyrus
Primary Somatosensory Cortex
Lateral Sulcus
separates temporal from frontal and parietal lobe
superior temporal gyrus (STG)
primary auditory cortex
ie transverse gyrus of Heschl
Uncus/ Piriform cortex
primary olfactory cortex
gray matter v.s. white matter
gray = collection of cell bodies

white = collection of axons
Subcortical Structures on caudal aspect
optic nerve, chiasm, tract
pituitary gland
mamillary bodies (limbic system)
oculomotor nv
cerebral peduncles/ crus cerebri
pons
big flat area on Ventral side
Medulla Oblongata
precursor to spinal cord

pyramids
inferior olives (next to pyramids)
thalamus
on Dorsal side
filters all sensory info
Dorsal Aspect
*pineal gland/body
*sup colliculi (secondary vision- coordinates head and eye movement)
*inferior colliculi (secondary hearing)
*trochlear nv
Main Blood Supply
2 vertebrals
and
2 internal carotid arteries
Blood Supply from Vertebrals
1 anterior spinal aa
2 dorsal spinal aa
2 PICA (post cerebellar aa)
to Basillar
Blood Supply from Basilar
(at beginning of PONS)
2 AICA (ant inf cerebellar aa)
2 CN III
2 PCA (post cerebral aa)

* 2 post comm aa come of PCA
Internal Carotid aa
become MCAs (middle cerebral aa) which follow the lat sulcus and supply the lat aspects of the brain.
Circle of Willis:
1 ant communicating aa
2 ACA (ant cerebral aa)
2 internal carotid aa
-opthalmic aa comes off
2 Post Comm aa
2 PCA (Post cerebral aa)
-off Basilar aa
Which lobes do the cerebral arteries supply/:
ACA
MCA
PCA
ACA- medial aspects of all lobes but occipital

MCA- lateral aspects of all lobes except occipital

PCA- occipital

*MCA and ACA anastamose
Opthalmic artery
- comes off
- supplies
comes of internal carotid artery (MCA)

supplies the eye ball
Radicular arteries:
1 ant spinal a and
2 post spinal aa
anastamose
action potential is faster if
axon has larger diameter
and
axon is myelinated
Multiple Sclerosis
autoimmune d/s: attack your oligo's in CNS (not schwann in PNS), so slows conduction of APs, and since ions leak out of axon there isn't enough voltage change to activate m3 channels once gets there.
CNS neurons can't regenerate
astrocytes inc in # (proliferation)
astrocytes in in size (hypertrophy
astrocy secrete more growth factor
BUT there is permanent astroglial scarring so cell dies!
PNS neurons can regenerate if cell body still intact
schwan cells proliferate, hypertrophy, secrete more growth factor too.

but they also create collagen and remylinate the axon

and the macrophages eat debri
ACh (acetylcholine)
- chemical pathway
mitochondria make Acetyl CoA

acetyl co-a + choline ---acetylcholine transferase--->
ACh ---acetylcholinesterase--->
choline + acetate
ACh
- limiting factor
- nucleus in brain
-important for
- choline
- Basal Optic Nucleus of Meynert
-important for LTM and NMJ
-also leads to NE which is important for STM
Myesthenia Gravis
ACh receptors don't work
so give meds to block acetylcholinesterase so ACh doesn't get broken down and Post synaptic receptors that do work have more time to get ACh.

*in a healthy person the med's would cause spasms
Fast and slow receptors for ACh
fast = nicotinic (fires EPSPs)

slow = muscarinic (agonist)

*shrooms are permanent muscarinic
Altzeimer's
lack ACh production so give them choline. the choline binds to Acetyl Co-A to make ACh
Dopamine
- is an "Amine" b/c is derived from an Amino Acid
tyrosine---tryrosine hydroxylase--> L-Dopa --> DA --> NE --> epinephrine (adrenaline)
Parkinson's
give L-Dopa b/c DA doesn't travel through BBB
Dopamine
-location
-important for
released by Pars Compacta of the Substantia Nigra
- Parkinsons
- addiction (cocaine increases DA)
Serotonin
tryptophan--5 hydroxy tryptophan (5HT)-->histadine-->histamine
Glutamate and Asparate
excitatory NTs
-too much glutamate causes adult seizures
GABA
an inhibitory NT in adults
but excitatory in babys
-causes seizure in baby's
-prevents unwanted motor in adults
How does GABA prevent unwanted motor in adults?
it is released by the Striatum (caudate and putamen) and travels to pars reticulata of the substantia nigra
Supstance P
is a peptide PT occuring in the substantia nigra that is used for SLOW PAIN
Nucleus Basalis of Meynert
In the forebrain (frontal lobe)
- for long term memory
- releases ACh
- altzeimer's
Pars Compacta of Substantia Nigra
in midbrain (where colliculi are)
- releases DA
- parkinson's
- addiction
Locus Coerulus
found in M.O. and Pons
- NE
- important for STM
Raphe nucleus
found in M.O. and Pons
- 5HT (which leads to serotonin)
- consciousness
- sleep d/o
- depression
Telencephalon
5 lobes
Diencephalon
Thalamus and Hypothalamus
Mesencephalon
Midbrain: pineal gland, crus cerebri, mamillary bodies, colliculi, optic nv/chiasm/tract
Hind Brain/ Brainstem
Pons, M.O.

* cerebellum is here but separate anatomically/functionally
3 layers of Meninges
Dura matter
Arachnoid matter
Pia matter
Denticulate Ligaments
anchor the pia matter to the spinal cord (throughout the length of the S.C.)
Filum Terminale
pure pia matter
prevents
Rexed Lamina I
marginal nucleus
for fast pain
R.L. II
substantia gelatinosa
for slow pain
R.L. III
nucleus proprius
for fast pain
R.L. IV
nucleus dorsalis
for slow pain
R.L. V, VI
interneurons
R.L. VII
clarke's nuc
coopersharington nuc
centrobasal nuc
intermediate lateral horn (IML)
R.L. VIII, IX
motor nuclei
R.L. X
central gray nuclei
Dorsal Horn

Intermediate Horn

Ant Horn
R.L. I-IV

R.L. V-VII

R.L. VIII-IX
Epicritic
-dorsal column
sensory system for fine touch:
Nucleus Gracilis and
Nucleus Cuneatus
Travel in the Medial Lemniscus
to the VPL of the Thalamus
Protopathic
- ALS (anterolateral column)
sensory system for pain and temp:
Spinothalamic and Spinoreticular
RL interneurons
decussates at AWC
to thalamus (VPL or nonspecific)
DCST (descending corticospinal tract)
LSCT (80%)
VSCT (20%)

LCST decussates at pyramids
VCST decussates at AWC
AWC
spinoreticular
DCST
DCRST
descending corticoReticularSpinal Tract
post limb IC
decussates to R.F.
reticulospinal tract to Ant to Ant column
RL 8 and 9 to NMJ
mm spindle fibers
and
GTO fibers
Ia and II

Ib

contain alpha, beta and gamma motor neuron signals
Signs of LMN lesion
hyporeflexia
mm atrophe
hypotonia
flacidity
eg polio
(ALS is both LMN and UMN)
Signs of UMN lesion
hyperreflexia
mm bulk preserved
hypertonia (stiff)
spasticity
eg. stroke, multiple sclerosis, parkinsons
fibrillation
UMN problem
single m fiber
can't see
fasciculation
UMN problem
motor unit
can see twitching
clonus
UMN problem
muscle firing on own because unwanted motor is not being dampened by CNS
chorea
UMN problem
whole body moving like snake
eg. huntington's (autosomal dominant)
Left Hemisphere
secondary ctx problem
affected by L MCA
Aphasia: Brocca's or Wernicke's
(both = global aphasia)
Alexia- reading
Agraphia- writing
Dyscalcula- math
L and R Hemisphere
secondary ctx problem
Amnesia - MCA or ACA
Apraxia- ACA- Corpus Collosum- problem following directions
Agnosia: tactile - ACA
auditory- MCA
Amnesia
- anterograde
- retrograde
anterograde- hippocampus- cant remember new memory

retrograde- frontal lobe- cant remember old memory
3 Retinal layers
1) Photoreceptor- secrete NT
2) Bipolar cell - secrete NT
3) Retinal Ganglion layer - sends AP down CN 2
Fovea (visual macula)
cones only, sharpest vision
Photobleaching
in dark: depolarized b/c cGMP props Na channel open
light: rhodopsin --photon--> opsin and trans retinal
energy released activates cGMP phosphodiesterase wich removes cGMP from Na channel, so becomes HYPERPOLARIZED and releases NT
opsin vs retinal
opsin = genetic
retinal = from diet (retinol from carrots easily converted to retinal)
cuneus ctx

calcarine fissure

lingual ctx
inf visual field

sup visual field
Fibers in Lissaure's Zone
A delta
C
Ia/II
Ib