Psych 115 Midterm 1 UCLA Exam Questions and Answers 100% Pass

Psych 115 Midterm 1 UCLA Exam Questions and Answers 100% Pass What are the three layers of protective layer called? Meninges - Dura Mater (thick outer layer) - Arachnoid (Spongy middle layer) - Pia Mater (thin inner layer) What is the organ that constantly manufactures the CSF? choroid plexus, which resides in hollow tubes and cavities called ventricles Where does the action potential originate? Integration zone (or active zone) What are the three types of neurons? Multipolar - with multiple dendrites coming off the soma Bipolar - just 2 processes sticking off soma Unipolar - just one extension form soma that branches off into two How do excitatory, inhibitory, and modulatory neurotransmitters differ? excitatory - depolarize post synaptic neuron and increases likelihood of post synaptic action potential inhibitory - hyperpolarize post synaptic neuron and decreases likelihood of AP modulatory - has multiple effects on post synaptic target What is the difference between efferent and afferent? efferent - output afferent - input What is the potential equation for a voltmeter? V = C+ - C- What is the driving force on a molecule and when is it zero? - Sum of both electrical force (determined by charge of membrane & ion) & chemical force (determined by concentration gradient) acting on ion - its zero either when both forces are zero OR when they are equal and opposite What are the approximate equilibriums for each molecule? Ek = -80mV ENa = +60 mV ECl = - 90 mV ECa = +120 mV How do IPSPs work? Inhibitory Post-Synaptic Potential - when an inhibitory transmitter such as GABA is released from synapse and binds to receptors such as ligand gated chloride channels which make membrane potential more negative which leads to hyperpolarization of membrane preventing it from making an action potential How do EPSPs work? Excitatory Post Synaptic Potentials - when the excitatory neurotransmitter (glutamate or acetylcholine) is released & binds to ligand gated sodium ion channels which depolarizes cells and makes it more likely to fire AP What is the passive propagation of the EPSP? When the EPSP gets smaller as it travels from the synapse to the axon hillock (integration zone) How can spatial summation and temporal summation help with the passive propagation of the EPSP? Spatial summation - if two presynaptic neurons fire simultaneously the two EPSPs will sum to create a larger EPSP Temporal Summation - creation of large EPSP from two smaller EPSPs occurring in rapid succession at a single synapse Why is an AP called an "all or none" phenomenon? As soon as membrane is depolarized above spike threshold, an AP will occur. - This is because opening voltage gated sodium channels will allow sodium to enter and depolarize membrane, which opens ever more channels (positive feedback cycle) How do the 4 protein subunits that make up the voltage gated sodium channel influence its 3 different states? Physical configurations of subunits change for each state Closed - Na+ cannot pass through pore, when cell is hyperpolarized Open - Na+ ions can flow freely, happens when depolarization occurs, but quickly switches to inactive after millisecond Inactive - Na+ cannot pass through pore, channel cannot be opened even if depolarized, must go back to closed state through hyperpolarization before another AP What is the role of the delayed rectifier channels? Open at -45mV to help potassium ions get out faster, they open slowly to allow spike to reach its peak -only has 2 states, open (when membrane depolarized above delayed rectifier threshold) and closed (when below threshold) After sodium moves into cell and potassium moves out because of the AP, how do they go back to equilibrium? Na-K ATPase Pump which ejects 3 sodium ions for each 2 potassium ions imported, which repolarizes membrane at the end of AP What is the difference between active and passive transport? Active - required ATP an pushes ions in the direction it wants REGARDLESS OF DRIVING FORCES Passive - ion channels open or close to allow ions to flow according to electrochemical gradient in direction of driving force Which factors contribute to the ending of the action potential - Na-K ATPase Pump -Delayed Rectifier K+ channel - Inactivation of Sodium channels - Leak K+ channels What is the difference between the central and peripheral nervous systems? Central Nervous System - includes brain and spinal cord, group of neurons in CNS called nucleus Peripheral Nervous System - includes spinal and cranial nerves that relay sensory & motor info to & from CNS, group or cluster of neurons on PNS called ganglion What is the role of the Dorsal root ganglion? DRG unipolar neurons in PNS whose job is relay somatosensory information from skin to spinal cord How do local anesthetic drugs work? They block somatosensation by blocking active zone sodium channels in skin What does active propagation look like? And where does it occur? IT happens in unmyelinated axons and they have sodium and delated rectifier channels all the way down axon so there is a repeated AP all down axon, but very slow What is saltatory conduction? and Where does it occur? Happens in myelinated axons which reduces passive attenuation (reduction of AP), have gaps in myelin called nodes of Ranvier which have high density of active sodium and delayed rectifier channels in membrane, which gives it a boost to get to the next node What is passive propagation and where does it occur? It happens in axons without active channels and the AP propagates very fast but not very far Where does myelin come from? Myelin Sheath made by glial cells -in PNS made by Schwann cells -in CNS made by Oligodendrocytes where dense population of myeline called white matter, with little myelin called gray matter What is multiple sclerosis caused by? loss of myelin in CNS, cause is unknown but theorized that is autoimmune or apoptosis of oligodendrocytes What happens in the synaptic bouton? Voltage gated calcium channels opened by AP which causes calcium to flow (into cell?) How does the presynaptic action potential cause vesicles to fuse with membrane? 1. neurotransmitter manufactured by neuron 2. NT pumped into vesicles by vesicular transporters 3. Filled vesicles move toward cell membrane and waits for AP 4. When AP occurs, calcium enters synaptic bouton and causes vesicle to fuse with membrane and dump NT into synapse 5. Clathrin coat forms on inner surface of membrane and pinches a new empty vescile from cell membrane 6. New vesicle sheds its coat and starts filling up with NT again What are the steps in chemical neurotransmission? -NT travels to postsynaptic target cell & binds to receptors -NT unbinds to receptor and is degraded (catabolized) or reabsorbed into cell (reuptake) What are the two major categories of neurotransmitters? 1. Small molecule NT are modified amino acids (also includes choline) 2. neuropeptides which function as hormones to send signals over long distances are small protein molecules What are some examples of small molecule neurotransmitters? Amino Acids: GABA - inhibitory Glycine - inhibitory Glutamate - excitatory Aspartate - excitatory Biogenic Amines: Dopamine - modulatory Adrenalin/Noradrenaline - modulatory Seratonin - Modulatory Histamine - Modulatory NOT synthesized from Amino Acids: Acetylcholine - excitatory/modulatory What is glutamate? Dominant excitatory neurotransmitter in brain Synthesized from AA glutamine by enzyme glutamine aminohydrolase What is GABA? Gamma-amino-butyric Acid is dominant inhibitory neurotransmitter in CNS Synthesized from Glutamate by enzyme glutamate decarboxylaze (GAD) by removing CO2 Which neurons produce glutamate, inhibitory or excitatory? BOTH! the only difference between them is whether they express gene for GAD Why does glutamate excite while GABA inhibits? They bind to different receptors What is the difference between metabotropic and ionotropic receptors? Ionotropic - ligand gated channels that are opened by neurotransmitter binding to make membrane more permeable to ions Metaotropic - G-protein coupled receptors that are activated when neurotransmitter binds to extracellular domain which causes linked G-protein to be released from intracellular domain of receptor protein & float through cytoplasm until it binds to various targets What are examples of Glutamate receptors being both ionotropic and metabotropic?