Exam 1 - PSY 220 PDF

↑ -g · ·- U...

↑ -g · ·- U = - = E O E - 8 f e T · · A U - E 8 e e = h· J · O A P & & * o U & & E · · · S - F & f 5 S & = z i I · = & G · T ⑳ E - U > = · 8 - · · T· · E A T o A E I & - ·. · : A U n & · - : 8 & : ↳ U E # ↳ S - · d E T & A & J j = · · & U 6 O · · - & · & G E. D E & & & O & - 1 & - E · = o I A E E G & G ·. E j E · n - E G & - T -. · E T E - ↳ # - N o F ↳ o - T a = · E · O & E · T I A f - u · E - · X & · · = ou : · - Y · & ~ J - E & ↳ : Y Y · O e - & & I : in ~ E : E P - ↳ · E - E N = V - & P  keeping neurons alive NEURON - specialized type of cell - fat layer ↳ Glucose - bounded by lipid bilayer cell membrane > separating inside from ↳ Oxygen (brain 20 % ( includes and outside cell-body , nucleus S classifications ↳ Thiamine (rit. B1) other cellular organelles ↑ Efferent information is EXITING the N S 3. W Interneurons and activating the muscles SOMA ↓ ↓ act locally (within structure) Afferent > information is ARRIVING/detecting bud like extensions on information from the environment an dendrite , where < long projection , only one and bringing them to the N S. synapses are often formed carries neural signal J I X & toward other neurons , organs , sensory (specialized to detect DENDRITIC SPINES AXON muscles certain types of O LIGO DENDROCYTE sensory stimulation ↑ - DENDRITES glial cells that form myelin ↓ in the CENTRAL N.. S Branch off from the AXON HILLOCK cell body , receive signals ↳ where the axon begins SCHWANN I glial cells that form from other neurons and branches from the CELL myelin in PERIPHERAL N S.. Soma START L helps with E MICROTUBULES & NEUROFILAMENTS NODE OF > unmyelinated transportation provide structural support RANVIER > exchange of ions of substances insulating sheat around MYELIN takes place T within the neuron axons that help action SHEAT potentials get transferred more quickly MOTOR NEURONS SYNAPSE AXON > end of an axon , V - receive information on ↓ TERMINAL where it forms dendrites within spinal cord point of a synapse END communication L conduct information along between neurons axon to axon terminal at L ↓ electrical & Muscle - ischemia - infarct , of brain damage Korsakoff's amnesia formed by endothelial cells Blood brain barrier which line brain capillaries, memory impairment due along w/ astrocyte end feet to thiamine deficiency Limits the movement of substances into or medicine works only if chronic alcoholism & out of the brain passed through the BBB poor diet Lipid-soluble (disolve subs · w/high molecular fats) & subs · w/special weight BLOCKED from transport mechanisms entering Can PASS THROUGH  when voltage-gated Nat channels are inactivated no matter the stimulation , only a very strong signal no action potential can can generate an action be generated potential stronger threshold) helps for faster absolute refractory relative refractory conduction of helps conserve period period action potential energy slows down after an action potential , the "jumping" of action conduction the neuron cannot immediately potentials from one damage to of. P a. generate another action potential mode to another myelin sheath Refractory periods saltatory conduction multiple sclerosis Nerve Impulses & Myelin steps : ACTION POTENTIAL. 1 Neuron starts at rest (-10mv. 2 Signals from incoming neurons generate EPSPs and IPSPs in the neuron. 3 If the sum of these postsynaptic potentials surpasses a threshold (becomes depolarized enough) > voltage gated Nat channels open. 4 Nat rushes INTO cell , a rapid depolarization + 5. Nat channels inactivate and Nat cannot enter the cell. anymore The neuron repolarizes as voltage gated K , channels open and kt rushes out the cell. G Voltage-gated + remain open , causing the neuron to hyperpolarize. 7 Voltage-gated K+ channels close and the sodium-potassium pump returns the cell to its resting potential  CHEMICAL SYNAPSE Mitocondria axon voltage gated · Hers cast channels Smi " tran presynaptic neuron neuro ⑪ & M V rescicles i ⑰ Di · % D ⑳ axon terminal A Reuptake Cleft P protein G-protein E dendrite To 8z M metabotropic receptor M m postsynaptic neuron Mu ofchemical on * how are neurotransmitters removed from ionotropic receptor/ - I the synaptic cleft ? ligand-gated ion channels ↳ Enzymes would chop up the neurotransmitters (degradation) I ↳ Reuptake > - recycle the new. back to the presynaptic Difference between - faster open ligand ion , gated ion ↳ Diffusion -> they more away ionotropic and channel , metabotropic effects meta > - chain reaction ,  higher concentration OUTSIDE I ↑ inside is more () charged (+ ) > ( - ) C ) - > (t) X I ↑ I at rest , more sodium higher at rest--TOmV POSITIVE IONS iOnS NEGATIVE # of ions is (Nat) OUTSIDE the cell COMC. INSIDE ↑ toward toward varying I voltage difference between difference in electrical NEGATIVE POSITIVE at rest , more potassium the inside and outside charge between the difference in the (K + ) INSIDE the cell while isn't the neuron firing inside and outside of created by a separation concentration of an action potential a cell of electrical charges charged ions between high concentration the inside & outside to resting potential electrical gradient of a cell low concentration potentials and gradients concentration gradient for balance separates inside and (chemical) 11 outside of a neuron cell membrane Resting & Action Potentials lipid bi-layer w/ protein polarization terminology channels sodium gaining + wants to potassium has opposing depolarization charge sodium-potassium pump enter the cell forces removing It the charge, helps mantain the resting both concentration and less K OUTSIDE , INSIDE cell is becomes less (f/more ( ) + potential of a neuron by electrical gradient attract K + wants to It more , Kt is preserving the concentration Nat INSIDE the neuron exit (t) wants to stay , gradient repolarization INSIDE cell is more INSIDE cell has sodium-potassium pump 3 Nat It Nat (t) Nat Nat brings Kt electrical transports OUT & , is , less , more into charge becomes + wants to enter wants to enter the cell more (t, returns toward 2k IN - - electrical concentration 9 resting potential. 9. going against the hyperpolarization concentration gradient electrical charge becomes even more negative than energy involved the resting potential  closer to the threshold further away from threshold removing (-) ↑ making it ↑ charge more likely it'll reach more (-) less likely it'll action potential reach action potential communicate information , action potential to start I an , to sent down an axon by neurons incoming postsynaptic potential Signals received by a received Signals by a stimulation needs to surpass neuron that slightly neuron that slightly threshold (depolarized enough) rapid conduction of a DEPOLARIZE the cell POLARIZE the cell depolarization down the axon excitatory postsynaptic inhibitory postsynaptic potential potential action potentials wider faster when postsynaptic potentials axon and myelinated axon Resting & action potentials voltage-gated sodium voltage-gated potassium channels channels opens w/depolarization blocks sodium entrance with opens w/depolarization during an action potential , when high depolarization the cell reverses polarity , + now CINACTIVATE) BUT slow Stay open after has both electrical and concentration sodium flows into cell sodium channels gradient pulling K + OUTSIDE toward electrical gradient inactivate Il concentration " leads to slight hyperpolarization exocytosis > how vesicles neurons must be release neurotransmitters communicating slowly Sherrington Concluded adding up signals sum across dif. multiple weak Stimuli fast but slower that happened close locations on the (in time or space than action potential to each other (in time postsynaptic neuron neurons are produced a reflex individual coined sensory Spinal motor temporal spatial cells "synapse" processing cord response summation summation Ramon y Cajal Sherrington reflexes bypass the brain EPSPs & IPSPS discovery of the synapse reflex arc summation of signals Synapses & Synaptic Transmission types of Neurotransmitters IPSPS EPSPS electrical synapse amino acids monoamines slight polarize slight polarization gap junctions of cell glutamate , GABA seretonin dopamine hyperpolarize of , , where direct electrical glycine norepinephrine , cell opens sodium communication between epinephrine opens potassium opens chloride channels neurons take place channels channels acetylcholine Nat enters sodium & others faster than neuropeptides k+ exits Cl-enters pass directly to chemical cholinergic transmission makes neuron postsynaptic synapses make neuron less more likely to neuron endorphins , neuropept likely to fire fire purines Y , substance P ATP , adenosine gases nitric oxide  > molecule that binds to another molecule receptor can trigger ligand-gated< faster than metabotropic ion channels to open cionotropic effect) or a cascade of events follows electrical (metabotropic effect) can down can break down break and concentration monoamine acetylcholine gradient after binding neurotransmitters neurotransmitters enough cast cast rushes into triggers postsynaptic membrane MAO acetylcholinesterase that presynaptic neuron exocytosis has receptors they determine whether neurotransmitters can bind to a cell experiences an neurotransmitters are in depolarization opens them EPSP or IPSP broken down taken back to presynaptic terminal by enzimes presynaptic neuron receptors voltage-gated calcium reuptake channels Synapses & synaptic transmission breakdown of neurotransmitters diffusion SUMMARY of seps : CHEMICAL SYNAPSE neurotransmitter away just goes. 1 An action potential depolarization opens voltage-gated calcium channels. 2 calcium enters the presynaptic neuron. 3 calcium triggers vesicles to release neurotransmitters into the synaptic cleft 4. Neurotransmitters bind to receptors on the postsynaptic neuron certain protein. 5 Receptors on the postsynaptic neuron trigger channels to open Lor cascade of events) resulting , in either EPSP or IPSP at postsynaptic neuron synapse. 6 Neurotransmitters can be broken down , taken back into presynaptic terminal , or diffuse away  Neurotransmitter binds neuromuscular between a motor neuron synapse and a muscle W metabotropic receptor activates g-protein cholinergic ↳ creates other things - when postsynaptic neurons metabotropic slower and neurotransmitters triggered by release inhibits additional release receptors associated with longer-lasting to act on the presynaptic serves as of that neurotransmitter G-proteins and initiate than ionotropic terminal Feedback system a sequence of effects effects receptors on the presynaptic retrograde signaling terminal that respond to metabotropic effects neurotransmitters it releases autoreceptors Synaptic Transmission & Hormones medications & synaptic types of chemical synapses dendrodendritic transmission axodendritic axosomatic dendrite to chemical transmission agonist antagonist dendrite flexibility axon terminal to axon terminal to a chemical that a chemical that binds a dendrite the soma binds to a receptor to a receptor to BLOCK and mimics the others neurotransmitters avoaxonic ability to bring a neuron one effects of a from binding closer or farther away neurotransmitter Neurotransmitter axon terminal to from firing allows from can have axon complex behaviors different functions neuroglandular allows synapse plasticity between a neuron and a gland  Synaptic Transmission & Hormones long-lasting effect hormones types of hormones pituitary gland in brain attached the chemical secreted by one produced by protein peptide g) and the , to part of the body that endocrine hypothalamus , that secretes hormones travels through blood to glands long chains of short chains of affect another part of amino acids amino acids anterior posterior the body pituitary pituitary both attach to cell membrane I have broader impact and activate second can make extension of receptors an than neurotransmitters messengers and release the hypothalamus hormones receives hormones and secretes it into the bloodstream