PGY300 Test 1 Review PDF

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PGY300 Test 1 Review: Lecture 1: CNS Intro CNS: brain & spinal cord Diff meninges: protect CNS; spinal cord and brain -Pia Mater, Arachnoid Membrane, Dura Mater Inside  Outside -Meningitis: inflammation of meninges -Spinal cord – Gray Matter: Central Synaptic Region -Afferent/ Sensory: cell bodies in dorsal root then dorsal horn where they may synapse with motor neurons that r leaving thru dorsal horn back out into periphery -Efferent/Motor: neurons that lave the spinal cord from the ventral horn

-White Matter: myelinated fibers going up to brain and down -Ascending Tract: carry neurons to the brain -Descending Tract: carry neurons from the brain -CSF provides nutrients for brain and cushion -Made in Choroid Plexus -Blood Brain Barrier -Prevents things from getting from blood to brain -Formed by tight junctions and astrocytes (glial cell) -Medulla: lowest part of brain, Cardiac & Respiratory function; Involuntary -Cerebellum: Motor control; half of neurons in whole brain -Pons- Relay area from cerebellum to cerebrum -Cerebrum- Thinking -Primary sensory and association areas -Motor association and Motor cortex areas -Sensory information: Thalamus (except in olfactory system) > Primary Somatic Area > Association Sensory Area > Motor Association area > Motor primary area -Cerebrum- body represented by Homunculus- shows diff parts of body represented to greater or lesser extent along surface of cerebrum -Association areas: -Wernickes- Sensory

-Brocas- Motor -Corpus Callosum- send information from hemisphere to other -Info from left side of body goes to right hemisphere and vice versa -Right Hemisphere : sense of self -Basal Ganglia: Parkinson’s; involved in controlling motor activity by disinhibition until you actually want to use a function -Limbic System: -Thalamus- relaying sensory info to the cerebral cortex -Hippocampus- convert short to long term memory -Amygdala-memories associated w strong emotional content -Hypothalamus- homeostasis function -MRI: imaging of brain; magnetic fields) -advantage: skull doesn’t interfere with image -good for anatomical imaging of brain -FMRI: look at function of brain by looking at blood flow movement to evaluate which parts of brain are active -PET: positron- positive electron to produce signal; combines with electron and annihilate an electron to produce signal -EEG- electrode over skull measures electrical activity across skull -small signals -sleep behavior, localizing seizure site LECTURE 2: The Neuron -Neuron: input to dendrites, to soma, down axon -A.P generated in axon (initial segment), goes down axon quickly because it’s myelinated -when A.P reaches the terminal, large depolarization activates voltage sens Ca channels, Ca flows in and stimulates N.T release -G.P in dendrites that travel down and if they’re big enough to reach threshold, A.P produced -Schwann cells (in periphery) and Oligodendrites (CNS) myelinate cells -Schwann wraps around cell -Multiple Sclerosis(M.S)- lose the myelin wrapping so A.P and signal slows down -Variety of diff types of neurons -Sensory and Motor neurons

-Astrocytes- BBB formation and N.T uptake (removing neurons from synapse) -1 millimeter long glial cell wrapping -1 micrometer – Node of Ranvier: A.P is reboosted as it travels down axon -Charge: pos and neg ions -Current: ions/sec, rate of flow of ions -Voltage- driving force to move ions -Conductance- how easy it is for ions to move through; dependent on size of channel or how many channels are open -Depolarization/Excitation/more positive or Hyperpolarization/Inhibited/more negative -For a cell to become negative inside and positive outside, to develop a resting membrane potential things that must occur: 1. must create imbalance of ions in and out of cell 2. for resting membrane potential, K+ is important so you create high K inside of cell compared to outside; require energy from ATP 3. NAK pumps uses energy to depletes sodium from in cell and high potass in cell and low Na in cell 4. Once u have that concentration diff, the cell is negative bc once you create the imbalance of ions, if you open channel that lets one type ion go through, potass will leave cell, depleting cell of pos charge and that flux continues until cell becomes so negative that acts as another force Equilibrium Potential: -each ion has diff equilibrium; +60mV for N; -90mV for K; -63mV for Cl -the more K+ channels opened, closer to -90mV cell will become -more Na channels opened, closer to +60mV -once equilibrium potential is met, that ion stops flowing Lecture 3: Membrane Proteins Cell Membranes: Lipid bilayer -impermeable to ions -need Carrier or Channel to get ions past membrane -Carriers: slower because needs to change direction -Advantage: can move against concentration gradient Primary or Secondary Active Transport (using energy from high concentration of sodium outside to move something in through a carrier, not directly using energy) -Uniport(1 thing) vs Symport (2 things in same direction) vs Antiport (2 things in opposite direction) (ex: NAK pump)

-NaKpump- faces in one direction and binds Na and then binds phosphate group, changes confirmation and faces outside of cell bc phosphate allows it to change its confirmation, releases Na, accepts some K; phosphate falls off and now faces back inside -Net result: 3 Na out and 2 K in -Electrogenic bc every cycle youre short one pos charge inside cell

-Channels: pores -Facilitated Diffusion -Channel Properties: Selectivity Conductance, Gating- Voltage, Ligand(N.T), Mechanical (auditory system) -Voltage: Na channel; structure: Long Protein -4 domains -Cross membrane 6x per domain -s4: voltage sensor bc has positive amino acids so it’s sensitive when inside of cell changes its voltage so when inside is very negative its pulling s4 down and when cell depolarized it’s no longer pulled down as much and protein changes confirmation -s5 and s6 are the activation gate; linked by P loop; determines selectivity - Inactivation gate- in between 3rd and 4th domain (not all Na channels are voltage sensing channels- Ex: salt channels in gustatory system and glutamate gated channels)

Ionotropic Receptors: -Ligand: ACh (excit), GABA (inhib), Glycine (inhib) -5 separate proteins -each of those 5 cross membrane 4x -M2 faces pore and determines Selectivity -Glutamate (excit) : AMPA and NMDA -4 subunits -crosses membrane 3x Lecture 4: Action Potentials -G.P- open channels, not voltage sensitive, open by ligand or N.T, slow, variable size, can sum them up, don’t travel very far, get smaller as they travel through nerve, analog -A.P- fast, fixed size, digital -at some point for G.P to turn to A.P must reach threshold at trigger zone -Height of G.P > stronger stimulus > higher frequency A.P

Action Potential-Na channels activated, at threshold, some Na channels activated which depolarizes cell, more Na channels open which further depolarizes cell (regenerative- chain reaction event) leads to rapid activation of Na channels and Positive charge coming into cell then this is followed by rapid decline of A.P which is based on 1. Na channels inactivating and 2. K channels start to activate which hyperpolarizes cell, the K channels close slowly so there is an after polarization where voltage is below original baseline bc some K channels that haven’t closed yet -Inactivation mechanism of Na channels is a separate gate -Activation gate opens because depolarization in cell -Inactivation gate closes channel shortly after -Absolute Refractory Period: cant produce an A.P, which prevents A.P from going back and forth, impossible because Na channel inactivation ex. A fuse -Relative Refractory Period- for certain amount of time, it is harder to produce A.P, but if stimulus is strong you could, Na recovered but still K channels hyperpolarizing cell -Myelin; formed by layers from glial cells, if reduced, speed of A.P reduced Nodes of Ranvier- where A.P is regenerated -excess K outside of cell will depolarize cell bc some pos charge coming into cell, makes cell more excitable- Hyperkalemia -if K outside cell is low, some K comes out which hyperpolarizes cell, harder to produce another A.P Lecture 5: The Synapse -Synapse: key events- A.P travels down to synaptic terminal where it activates voltage dependent Ca channels causing vesicles fuse with membrane, releasing N.T travel through cleft to diffuse quickly to bind to postsynaptic receptors which can be ionotropic or metabotropic -SNARE proteins between the vesicle and membrane to help position vesicle to be ready to release N.T -Botulinum Toxin- food poisons, interfere w interaction with SNARE proteins so vesicles aren’t properly placed, don’t get N.T release -Uptake Mechanism: N.T has to be removed after its released -Secondary active transport or Broken down by enzyme (Ach esterase) -Myasthenia Gravis: lose some of Ach receptors because autoimmune disease, treatment trying not to break down Ach by inhibiting the Ach esterase -Cocaine enhances dopamine release by reduces dopamine uptake; sense of euphoria and reward

-2 types of receptors: Ionotropic and Metabotropic (G-protein coupled receptor, 7 transmembrane receptor) -Metabotropic: slower, but a lot of amplification -Second messenger systems: -Ca -cAMP- olfactory -IP3- olfactory -cGMP- visual -GPCR release cAMP in olfactory system, which can stimulate more enzymes producing more second messengers -IP3 system- olfactory system -Olfactory system: detection of odorant causes increase in cAMP that opens a channel -Visual system: light activates a G-Protein system that causes decrease in cAMP closing a channel -Ach- ionotropic, somatic motor neurons, muscarinic -Dopamine involved in Parkinson’s disease -Serotonin- SSRIs, inhibitors of serotonin uptake in depression; aplhesia- sensitization mechanism -Glutamate- AMPA and NMDA receptors- memory mechanisms -GABA and glycine- inhibitory -Nitric oxide- Gas, Enteric Nervous system Lecture 6: Memory Mechanisms -Memory mechanism, a hundred billion neurons, each neuron gets about 1000 synapses so many many synapses -Divergence- Input to one neuron spreads out to many neurons; used for adaptations mechanisms, not specific info, more general info -Convergence important for amplifying and being able to detect weak signals ex rod system -many neurons collect the info and then they all send that info to one neuron, allows for very high sensitivity of that final neuron; the final cell will be very responsive -Summation: postsynaptic -Spatial-2+ diff inputs coming in at same time from diff synapses -Temporal- one synapse, stimuli quickly coming one after another summing together

-Presynaptic Facilitation-mechanism: Paired Pulse Facilitation: 2 stimuli occurring in rapid succession and at synapse, first stimulus causes increase in Ca and N.T release and second stimuli opens Ca channel again so influx of Ca builds off of leftover Ca in cell causing more N.T release -NMDA receptor –type of glutamate receptor so activated by glutamate, glutamate can open channel but might not allow ions go thru bc susceptible to Mg block bc inside of cell is so negative, can unblock by slightly depolarizing cell -ex combo of glutamate opening NMDA and AMPA receptors where glutamate first opens all the AMPA receptors very briefly but its enough to depolarize postsyn cell so NMDA receptors are no longer subjected to Mg block -Long Term Potentiation: glutamate gets released, activated AMPA receptors, allows NMDA receptor to work, NMDA receptor has not only depolarizes cell but also brings in Ca so next time you activate synapse, allow for bigger response, increase in AMPA receptors -Long Term Depression; AMPA receptors are removed from postsyn membrane, causes more difficulty depolarizing cell bc synapse doesn’t work as well -Novel Object Retention Test: mice test; young mice remembered object, adults didn’t -NMDA receptors can have 2A or 2B subunit 2B-young 2A-older If you prevent animal from switching from 2B to 2A, by knocking out the gene for 2A, older animals perform better -shows NMDA receptors very involved in memory -Aplysia neurons: Habituation: system habituates or no longer responds to stimulus if we repeatively stimulate bc presyn Ca channel was suppressed, not allowing as much Ca influx, reducing N.T release -Sensitization- stimulate facilatory neuron on head, bang head once causing serotonin release enhancing presyn release, enhance Ca release, suppress K channels, reducing depolarization presynaptically and overall Lecture 7: Sensory Systems -Receptive field: the smaller the receptive field, the higher the acuity bc looking at a smaller area -Convergence: increases sensitivity, decrease resolution -Lateral Inhibition: enhance resolution by suppress spurious responses around the area

-Phasic Receptors- very large response to small stimulus; sensitive -Tonic Receptors- tell u about properties of stimulus, not as sensitive bc they tell you about the whole range of stimuli -Gating Theory of Pain- u can regulate an inhib interneuron, which normally is suppressing pain signals, but inhib interneuron can be suppressed by pain pathway -Auxillary pathway can reinvingoarete the inhib interneuron so you don’t feel as much pain ex: rubbing the area you hurt makes it feel better -Olfaction- hundreds of receptors (GPCRs), activate G protein causes production of cAMP, opens a channel causing depolarization by cAMP, second effect Ca comes thru channel which activates Cl channels, and one depolarization by Cl channel; 2 depolarizations, 1 by cAMP channel, 1 by Cl channel -Gustation- 3 receptors activated by G proteins, 2 more channel like, 5 in total -Sweet, Bitter, Umami (all GPCR activated, cause increase in IP3 and Ca, activates TRP channel which depolarizes cell by Na influx) -Sour- acid- protons that run thru channels itself or binding to K channel causing it to close, causing depolarization -Salt- sodium running through Na channel causing depolarization -Bitter-poison; you want the GPCR because it’s sensitive to small amounts -Umami- glutamate in food, indicator of how much protein -Sweet- carbs -Sour- spoiled food -Salt Auditory-Sound waves: pressure waves detected as vibrations in ear shaking tectorial and basilar membranes -Hair cells (sensory cells for auditory system) connected between membranes and they vibrate (stereocilia) back and forth in response to physical vibration -as they vibrate distant in between cilia either increase or decreases; open and closes channel -when they become greater, tip link pulls open channel and vice versa -sense of frequency of pitch of a sound is based where on basilar membrane there is max vibration -part furthest from oval window vibrates more with low freq sound -part closest to oval window vibrates more with high freq sound -Hair Cells Adaptation- once hair cell is stimulated and Ca flows in, that causes one of anchors for tip link to move down a little bit, creating less tension between two cilia, meaning channel doesn’t open as much -receptor cells constantly reset based on environment

Visual System: -fovea- area of retina that is highest density of photo receptors, specifically cones, very little convergence, high and small receptive field, highest visual accuity -Rods: sensitive to dim light but don’t convey color info to you -Rhodopsin – protein in rods and cones, GPCR that binds light photons and become activated by photons leading to breakdown of cGMP to close a channel, you are hyperpolarizing the cell -when u activate it, u r suppressing channel and N.T release -diff from olfactory system where you are making cAMP to open a channel Lecture 8: Skeletal Muscle Contraction -skeletal muscle is the fastest, all or none response, complete contraction or no contraction -fast twitch response -smooth muscle u can contract muscle a little bit or a lot -Sarcoplasmic Reticulum- part inside cell containing Ca involved in muscle contract -Antagonistic Muscles -Motor Unit- a nerve and how many muscle that motor neuron/ muscle cells supplies -Innervation Ratio – a count of that -High Innervation Ratio- supply a lot muscles with one neuron, not such good motor control -Contraction: A.P on surface of membrane travels down T-tubule system, reaching area near sarcoplasmic retic, Ca channel in the T tubule get activated by A.P, it changes confirmation and instead of letting Ca in, it yanks on another Ca channel and opens that (this channel is on membrane of sarcoplasmic retic) Ca coming out of sarcoplasmic retic, binds to Troponin that pulls on tropomyosin out of the way letting actin and myosin overlap -Sarcomere-functional contractile unit in muscle cell -single muscle fiber will have rows and rows of sarcomeres -cycle where myosin head group can be at 45 degree angle (where it is when it pulls actin toward center; not binding ATP, rigor mortis) or at 90 degree angle (addition of ATP allows myosin to unbind from actin and move other, when it’s reaching out for another actin) -Power stroke: when phosphate falls off, confirmation changes, power to move actin -ADP still lingering, then it falls off and back in rigor mortis state -this interaction between myosin and actin occurs spontaneously as long as ATP is around, doesn’t occur spontaneously in muscle bc tropomyosin blocking ability of actin to bind o myosin, only relieved if Ca is around (form stimulation of sarcoplasmic retic) to bind to troponin to remove tropomyosin -Phosphate in: 90 degree

-Phosphate out: 45 degree -Neuromuscular Junction: (aka Endplate) Ach release by presyn terminal, produces large G.P called endplate potential (EPP), guaranteed to produce A.P because way above threshold which travels down T-Tubule System activating Ca channel which is physically connecting to the Ryanodine (RyR) channel (Ca channel) which allows Ca to come out and cause muscle contraction Lecture 9: Reflex Circuits -Monosynaptic Reflex Circuit: sensory neuron directly connects to motor neuron -Polysynaptic Reflex Circuit: intervening interneurons -Muscle Spindle- inside reg muscle, whenever muscle is stretched, it is stretched, sensory neuron will increase firing rate thru monosyn reflex will go back to main muscle contracting it -sometimes u don’t want this reflex, so muscles of spindle counteracts whatever the main muscle is doing Ex: if we want to contract the main muscle, the spindle will get shorter also which will send feedback to stop contracting the main muscle but you don’t want that, you want to prevent the muscle spindle form knowing u contracted main muscle so u contract spindle muscles to stretch out this sensory area so the main muscle contracts -Net result: sensory area doesn’t change shape at all so it doesn’t tell main muscle to stop what it’s doing IN SHORT-In main muscle contracts, sensory area will contract but you don’t want it to contract so you pull on it so it doesn’t change shape, intrafusal muscle contract making sensory area longer net result: no change (All for VOLUNTARY contractions) -Passive contraction- not involving the brain, just engaging monosynaptic reflex, not the gamma motor neurons, sensory system senses something sends signal back to motor neuron ex. Patella reflect -Reciprocal Inhibition: when u activate one set of muscles, u automatically inhibit motor neuron to opposing muscle through polysynaptic reflex pathway, u don’t have to think about this, working through interneuron to inhibit opposite muscle -Crossed Extension Reflex- doing one thing on one side of body and the reverse on the other side of the body -Renshaw cells- cells that motor neurons in spinal cord r activating so motor neurons are sending signal to muscle but also sending Ach signal to these interneurons (Renshaw cells) within, which release glycine that inhibits motor neuron that stimulated it, prevents motor neuron from overreacting -Strychnite: poison that inhibits these glycine receptors, motor neurons are firing too actively, muscle contracting too much, tetanus response, fatal

Lecture 10: Autonomic Nervous System -Efferent Nervous System: 1. Somatic Nervous System 2. Autonomic Nervous System Sympathetic- fight or flight, when you get agitated or nervous Parasympathetic- eating/digesting or relaxing Enteric -Parasympathetic: originates at either brain or very bottom of spinal cord, nerves come out of th...