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Cell Membrane
- selectively permeable bi-layer
- lipid soluble substances diffuse easily
- otherwise require protein channel
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simple diffusion
ion movement across membrane
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facilitated diffusion
ion movement that requires interaction with a protein to move across membrane
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active transport
- ion movement across membrane that requires interaction with protein and energy
- against the gradient
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Na+/K+ ATPase Pump
pumps Na+ out and K+ in
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How do neurons utilize protein channels in the membrane to create a system of neuronal communication?
Through maintenance of electrochemical gradients and gated channel reactions, action potentials can occur and permit "communication" between cells/neurons.
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Na+/K+ ATPase Pump
 - maintains gradients
- helps produce negative membrane potential
- requires energy
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"membrane potential"
- Electrical difference (voltage) when comparing the outside and inside of the cell membrane (mV)
- refer to the voltage inside the membrane relative to the outside
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Nernst Equation
- calculates electrical potential required to balance a single ion's concentration gradient

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Goldman Equation
The membrane potential of the cell combining information about multiple ions' permeability and concentrations
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Resting membrane potential of most neurons is thought to be approximately...
between -70 and -90mV
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Mechanisms of the Action Potential
- 1. Resting membrane potential
- 2. Depolarizing stimulus
- 3. membrane depolarizes to threshold. Voltage-gated Na+ channels open and Na+ enters cell. Voltage-gated K+ channels begin to open slowly.
- 4. Rapid Na+ entry depolarizes cell.
- 5. Na+ channels close and slower K+ channels open.
- 6. K+ moves from cell to extracellular fluid
- 7. K+ channels remain open and additional K+ leaves cell, hyperpolarizing it.
- 8. Voltage gated K+ channels close, some K+ enters cell through leak channels.
- 9. Cell returns to resting ion permeability and resting membrane potential.
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Relative Refractory Period
Next action potential can being during relative refractory period, but only if there is a more positive graded potential than usually necessary to meet threshold
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Graded Potential
starts above threshold at its initiation point but decreases in strength as it travels through the cell body
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Cell-to-Cell Communication Via Synapses
- 1. action potential depolarizes the axon terminal
- 2. depolarization opens voltage gated Ca2+ channels and Ca2+ enters the cell
- 3. Calcium triggers exocytosis of synaptic vesicle contents
- 4. neurotransmitter diffuses across the synaptic cleft and binds with receptors on the postsynaptic cell
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How is neurotransmitter/receptor coupling "deactivated"?
- 1. NT degraded by enzymes on receptor protein
- 2. NT re-sequestered into presynaptic axon terminal or diffuses away from synapse
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nicotinic cholinergic
found on ion channels
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muscarnic cholinergic
- activate a G-protein complex which results in:
- 1. ion channel opening
- 2. 2nd messenger activation
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What is the difference between an excitatory and inhibitory synapse or stimulus?
Whether the stimulus causes the membrane potential to become more positive (excitatory) or more negative (inhibitory).
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What systems of the body utilize the actions of G-proteins?
- cardiac muscle
- smooth muscle
- retina
- odor receptors
- liver
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G-Proteins bind to? How many subunits does the G-Protein have?
- guanosine nucleotides
- three- alpha, beta, gamma
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What is bound to the G-Protein in the inactive state?
GDP (guanosine diphosphate)
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When the G-Protein couple receptor is bound to its ligand, what happens to the GDP?
conformational change on G-Protein causes GDP to be swapped for GTP and the G-Protein complex is associated with receptor
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What can activated G-alpha subunit do?
- 1. open an ion channel
- 2. affect intracellular enzymes
- a)adenylyl/adenylatecyclase
- b)phospholipase C
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What does adenylate cyclase do?
- converts ATP into cAMP
- cAMPa activates Protein Kinase A (PKA)
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What can Protein Kinase A (PKA) do?
can phosphorylate (activate) a protein
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Stimulatory vs Inhibitory G alpha
- stimulatory- causes adenylate cyclase to increase production of cAMP
- inhibitory- causes adenylate cyclase to decrease production of cAMP
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Phosphodiesterase (PDE)
deactivates cAMP
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When G-alpha-q is activated...
- stimulates phospholipase c (PLC)
- PLC cleaves phosphondylinositol (PIP2) into: diacylglycerol (DAG) + Inositol triphosphate (IP3).
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2nd messengers
cAMP, IP3 & DAG
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Effects of G-Protein Alpha q
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receptors found on the sarcolemma at the NMJ
nicotinic cholinergic
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What happens at the NMJ?
acetlycholine activates nicotinic receptors (opening chemically gated channels on the sarcolemma) leading to sodium influx
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What is triggered on the NMJ once the membrane potential is less negative?
voltage gated Na+ channels open and action potentials move along sarcolemma
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at rest where is the highest concentration of calcium in the muscle?
sarcoplasmic reticulum
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When AP reaches voltage-triggered DHP receptors it leads to...
mechanical change in ryanodine channels on the SR
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Excitation-Contraction Coupling from NMJ to SR
- 1. ACh released from alpha motorneuron at the NMJ
- 2. AP in sarcolemma and T-tubules
- 3. DHP receptors in T-tubules react to depolarization
- 4. open ryanodine Ca2+ channels on SR
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What blocks the myosin head from binding with G-actin at rest?
tropomyosin
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Troponin
- 3 polypeptides
- TnI- binds to actin
- TnT- binds to tropomyosin
- TnC- binds to Ca2+
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What is necessary for sequential myosin head power strokes (muscle contraction) to occur?
- 1. action potential from motor neuron
- 2. calcium released from SR
- 3. available ATP
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Bands/Zones during contraction
- 1. Z-lines move closer together
- 2. sarcomeres shorten
- 3. I bands shorten
- 4. A bands stay the same length
- 5. H bands shorten
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myosin head moves to "cocked" (90 degree) position when...
ATP is broken down into ADP+Pi at the myosin head
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Molecular Basis of Contraction
- 1. rigor state- tight binding between G-actin and myosin
- 2. ATP binds to myosin head - dissociation
- 3. myosin head ATPase breaks down ATP into ADP+Pi
- 4. released energy changes angle between myosin head and myosin filament ("cocked" position)
- 5. power stroke: ADP + Pi are released
- 6. back to rigor state
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spinal cord
two-way highway, plus reflex control
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subcortical
all but cerebral cortex; unconscious control
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cortical
cerebral cortex; thinking & memory integration
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stretch reflex
muscle spindles send action potentials along afferent neurons to synapse at the spinal cord with alpha motor neurons to the agonist muscle
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muscle spindles
- afferent information to CNS regarding
- 1. length
- 2. rate of change in length
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Golgi Tendon Organs
- afferent information to CNS regarding:
- 1. tension
- 2. rate of change in tension
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What are the various aspects of a sensory-motor response that affect time?
- 1. complexity of receptor
- 2. fiber type/size & distance travelled
- 3. number of synapses
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A (I-II) neurons
- large to medium in size
- myelinated
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What allows for better 2-point discrimination on some areas of the skin compared to others?
- size of receptor field per afferent neuron
- receptor density
- "lateral inhibition"
- convergence of first order neurons onto second order neurons
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sympathetic neurotransmitters
achetylcholine, norepinepherine, epinepherine
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sympathetic postganglionic..
- mostly release norepinephrine
- some epinephrine
- few acetylcholine
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what is special about the adrenal gland?
- cells of the adrenal gland originated embryologically as nervous tissue and are rudimentary postganglionic neurons that secrete neurotransmitters into blood
- epinephrine 80%
- norepinephrine 20%
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sympathetic vs. parasympatheic
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muscarinic cholinergic & adrenergic receptors are both...
g-protein couple receptors that open ion channels directly or produce second messengers
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Why is parasympathetic fastest but sympathetic longer in duration of response?
- parasympathetic- long presynaptic neurons are myelinated and fast
- sympathetic- medulla of adrenal glands release epi into bloodstream which takes time to clear
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concussion
neurologic dysfunction from biomechanical force
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diffuse axonal injury
a type of brain injury caused by shearing forces that occur between different parts of the brain as a result of rotational acceleration
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what happens when don't get enough glucose to the brain?
- - inability to clean up excess K+
- - inability to transmit signals
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under normal conditions cerebral blood flow is tightly coupled to
- neuronal activity
- metabolic waste byproducts
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symptoms of reduced CBF
- fatigue
- persisting symptoms
- exertion-based symptoms (headache)
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vision steps (3)
- 1.light enters eye: focused by lens onto the retina
- 2. photoreceptors transduce light energy: change it into electrical signals
- 3. Electrical signals transmitted to brain: eventually allows visual perception.
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light travels...
through retinal cells, is absorbed in posterior layer of eyeball, then stimulates the photoreceptors.
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Rods
dim light, night vision, black & white, dominate periphery of retina
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cones
color vision, mostly cones are found in fovea
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What absorbs the light and prevents reflection within the eye?
Melanin in pigmented epithelium
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First step in the process of transducing light?
- photochemical rhodopsin changes from 11-cis to all-trans
- changes to its activated form
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generic g-protein vs. light g-protein
- ligand - photon
- coupled g-protein receptor - rhodopsin
- g-protein - transducin
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phophodiesterase
- PDE
- breaks down cAMP or cGMP
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what happens to rhodopsin when it absorbs light?
changes shape and activates g-protein transducin
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whats going on in the rod?
- 1. cGMP gated channels = Na & Ca influx
- 2. K leak channels, allowing efflux
- 3. Na/K ATPase pump
- -40mV membrane potential
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when light activates a rod cell does it hyperpolarize or depolarize it?
hyperpolarize
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in darkness...
- rhodopsin is inactive
- cGMP is high
- and ion channels are open
- releases neurotransmitters
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in light...
- light bleaches rhodopsin
- opsin decreases cGMP
- ion channels are open
- hyperpolarization
- does not release NT
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how does hyperpolarization affect glutamate release?
decreases NT release
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vertical circuit synapses
rods and cone synapse with bipolar neurons which synapse with ganglion cells
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optic nerve is made of
ganglion cell axons
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optic neve fibers terminate
in the lateral geniculate nucleus of the thalamus
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pitch
- perception of frequencies
- higher frequency = higher pitch
- normal from 20-20,000Hz
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loudness
- perception of intensity
- normal 0-120 dB
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middle ear gain
- ossicular coupling
- transfers energy from tympanic membrane to the foot plate of stapes
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acoustic coupling vs ossicular coupling
works at low frequencies , works at high frequencies
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round window
dissipate energy
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cells of spiral organ
- supporting cells
- one row of inner hairs
- three rows of outer hairs
- 16,000
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tectoral membrane
covers hairs
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shearing forces caused by
different pivotal points
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deflection of stereocilia
- opens mechanically gated ion channels
- inward K and Ca current causes graded potential and release of NT glutamate
- cochlear fibers transmit impulses to the brain
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deflection away from kinocllium
- close K channels
- hyperpolarization
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deflection towards kinocillium
- depolarization
- opens channels
- increase NT
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at rest stereoclia
- some channels open
- no stimulus
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defelction towards longest cillium
- all channels open
- depolarization
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deflection away from longest cillium
- all channels close
- hyperpolarization
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ribbon
double the ability to perform exocytosis
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what is required for exocytosis
- vesicles
- Ca & Ca channel
- action potential
- NT
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outer hair cells
inervated by efferent neurons
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inner hair cells
send afferent signals
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Low frequency sound causes which portion of the basilar membrane to vibrate?
the portion closes to the apex
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high frequency cause which portion of the basilar membrane to vibrate?
the portion close to stapes
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For both taste and smell what happens prior to the chemicals stimulating the receptors?
disolved in aqueous solution mucus or saliva
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How does a taste cell convert chemical signals into action potentials?
- the taste receptor cell depolarizes when stimulated due to opening of ion channels or 2nd messenger actions
- the taste receptor cell releases a NT onto the sensory nerve fibers, which transmits the signal via action potential
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Which cranial nerves carry info about taste to the brain?
vagus, glossopharyngeal, facial
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afferent info regarding taste continues to which areas in the brain?
- brain stem
- thalamus
- sensory cortex
- gustatory cortex (insula)
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salivation
- taste stimuli produce this reflex
- synapse in the thalamus with efferent neurons to salivary glands
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How is the stimulus from a chemical odorant converted into neuronal signals?
- G-protein coupled receptor in cilia
- activates adenylate cyclase
- increases cAMP
- opens cAMP gated sodium channels
- depolarization of cell beyond -55mV
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in gustatory and olfactory cells, where are the receptors located?
in the membrane of the cilia or hairs
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smell pathways
- reflexes related to salvation- hypothalamus & limbic system
- memory of food likes and dislikes- hippocampus and/or cortex
- analysis of smells- thalamus & frontal cortex
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