Term
| Why is the resting membrane potential -65mV and not -95mV? |
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Definition
| B/c it is easy to manipulate -65mV rather than -95mV |
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Term
| How is an action potential triggered in a neuron? |
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Definition
| 1) Start of the action potential 2)Trigger zone/Axon hillock 3) Voltage gated Na+ channel 4) All or none principle |
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Term
| What is the trigger zone? |
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Definition
| Axon hillock- Where graded potentials come together to form an IPSP or EPSP. |
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Term
| NT can open ion channel in Pre-synaptic? |
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Definition
| False, NT's open ion channels in dendrites and cell body (post synaptic cell) not pre-synaptic |
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Term
| What does EPSP's and IPSP's stand for? |
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Definition
EPSP= Excitatory postsynaptic Potential
IPSP= Inhibitory postsynaptic potential |
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Term
| Where are the EPSP's and IPSP's summed? |
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Definition
| Axon Hillock/Trigger zone |
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Term
| Define Graded potentials? |
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Definition
Potentials generated at dendrites and cell body is graded and can decay over distance.
vs. Action potential are generated at axon hillock/trigger zone and have an "All or none effect" (dont decay over distance) |
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Term
| T/F: The decay of graded potential is exponential? |
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Definition
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Term
| What determines if an action potential will occur? |
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Definition
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Term
| What are the two types of graded potential summation? |
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Definition
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Term
| What is the difference between Spatial and Temporal summation? |
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Definition
1) Temporal summation are PSP's (postsynaptic potentials) from one presynaptic neuron. The PSP's are sepreated by time and are fired rapidly one after the other and are summated to reach the threshold to cause an Action potential (AP)
2) Spation summation are PSP's from multiple presynaptic neurons (on the same post-synaptic soma) firing IPSP's or EPSP's and the soma summates these to form an AP. |
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Term
| What do they mean by "all or none" when referring to AP? |
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Definition
| Means that the potential will fire regardless after the threshold is reached (At axon hilloc) and will not decay over time. |
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Term
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Definition
| Rapid change in membrane potential from - to + and back to -; All of none |
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Term
| What are the 4 stages of an AP? |
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Definition
| 1) Resting stage 2) Threshold 3) Depolarization 4) Repolarization |
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Term
| What channels are active in the resting stage? |
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Definition
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Term
| What channels are active during the Depolarization phase of action potential? |
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Definition
| 1) Voltage gated Na+ channels |
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Term
| What channels are active during the Repolarization of AP? |
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Definition
| Voltage gated K+ channels |
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Term
| When does the VG Na+ and VG K+ channel open? |
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Definition
| They both respond at the same time to depolarization but K+ channels have SLOW ACTIVATION, so they don't actually have K+ go down the gradient till +35mV |
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Term
| Why don't AP's decay over time? |
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Definition
| Depolarization of the axon at one point causes voltage-gated Na+ channels to open ahead of this point. Thus the AP migrates down the axon. |
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Term
| List 3 Amino Acid NT and their fxn? |
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Definition
1) Glutamate- Excitatory NT of brain
2) GABA- Inhibitory NT of brain
3)Glycine- Inhibitory NT of spine |
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Term
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Definition
| 1) Serotonin (5-HT) 2)Histamine 3)Dopamine (DA) 4)Norepinehprine (NE) 5) Epinephrine (E) |
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Term
| Name a purine derivative NT? |
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Definition
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Term
| Name 3 types of peptide NT released by the Hypothalamus? |
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Definition
| 1) Thyrotropin releasing hormone 2) Lutenizing hormone releasing hormone 3) Somatostatin |
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Term
| Name 7 peptide NT released by the Pituatary? |
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Definition
| 1) Adrenocortico tropic hormone-ACTH 2)Prolactin 3)Lutenizing Hormone 4) Thyrotropin 5) Growth Hormone 6)Vasopressin 7) Oxytocin |
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Term
| What kind of NT are endorphins? |
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Definition
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Term
| What are 2 types of Peptide NT that are endorphins? |
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Definition
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Term
| Name 3 'other' types of peptide NT? |
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Definition
| Substance P, Andgiotensin II, Bradykinin |
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Term
| Where are peptide NT made? |
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Definition
In the cell body of neuron (and travel all the way down in the terminus of neuron)
-EX. Thyrotropin Hormone, Lutenizing Hormone, Bradykinin, ACTH...etc, |
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Term
| Where are small NT (Dopamine, 5-HT, ATP, Histamine...etc) made? |
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Definition
| Small NT are made in axon terminal? |
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Term
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Definition
| Precursor molecule (tryptophan) with the aid of a synthetic enzyme turns into a NT molecule (seratonin) which gets packed into vesicles with the help of Transporter proteins. |
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Term
| Name 2 gas NT and where are they made? |
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Definition
1) Nitric Oxide (NO) 2) Carbon monoxide (CO)
- Gas NT are not made in cell body or the axon terminal they diffuse right thru the neuron |
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Term
| Name 2 endocannabinoid NT? |
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Definition
| 1) Anandamide 2) Arachidonyl glycerol |
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Term
| How effect does THC have in the neuron? |
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Definition
| THC causes the depression of glutamate (excitatory NT of brain) and decrease the amount of Ca2+ released. So THC (comes from weed) slows neural transmission in brain and slows movement |
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Term
| Name the neuron that releases 1) Ach 2) DA 3)NE 4)Glu 5) GABA 6)Peptide |
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Definition
| 1) Cholinergic neuron 2) Dopaminergic 3) noradrenergic 4) Glutamatergic 5) GABAergic 6) peptidergic |
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Term
| Name 3 types of NT receptors and give examples |
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Definition
1) Transmitter-gated ion channels (aka ionotropic receptors)- Example: Nicotinic receptor and GABA receptor
2) G-protein coupled receptors (aka metabotropic)- ex. Muscarinic receptor 3) Enzyme linked receptor (ex Tyrosine Kinase receptor) |
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Term
| Give two examples of Ach receptors? |
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Definition
| 1) Nicotinic Receptor (Ionotropic receptor) 2) Muscuranic Receptor (Metabatropic receptor) |
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Term
| On the Nicotinic and muscarinic receptors, note what 1) NT acts on it 2) Agonists 3)Antagonists |
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Definition
Nicotinic receptor (Ionotropic receptors)- 1) Ach 2)Ach and Nicotine 3)Curare
Muscarinic (Metabotropic receptor)- 1) Ach 2)Ach and Muscarine 3) Atropine |
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Term
| What type of NT receptor is the GABA receptor? What kind of ion channel is GABA? |
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Definition
| Ionotropic receptor/ Transmitter-gated ion channels and it is a chloride ion channel |
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Term
| What are the 5 things that can bind (agonist) to a GABA receptor? |
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Definition
| 1) GABA NT 2) Benzodiazapine 3) Barbiturate 4) Steriod 5) Propofol |
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Term
| Describe the mechanism of giving a patient propofol? |
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Definition
| 1) Propofol bind to the GABA receptors (Propofol is an agonist for GABA) 2) GABA receptors activate/open and allow Cl- to go down their gradient (inside the cell) which causes the Vm to become more negative (hyperpolarize) thus creating an IPSP 3) The IPSP summate and DO NOT reach threshold and thus do not creat an AP, thus no neuronal transmission is made in the brain (since GABA receptors are found in the brain) |
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Term
| What happend when GABA and a pentobarbital is released as NT on the GABA receptors? |
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Definition
| Giving the barbituate adittionally (since GABA NT is naturally occuring in the brain) opens the channel more frequently thus causing more IPSP's |
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Term
| What are three targets of the activated metabotropic receptors? |
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Definition
| 1) Enzymes (ex. PLC, Adenyl Cyclase) 2) ion channels 3) Gene transcription |
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Term
| What is the fxn of Adenyl cyclase and what is it activated by? |
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Definition
1) Fxn- to make ATP to (secondary messenger molecule) cAMP of GTP to cGMP
2)Activated by diffused G-protein
- Adenyl cyclase is an enzyme that is a targeted by activated G-proteins |
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Term
| What is the fxn of PLC and what activates it? |
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Definition
| 1) Fxn- to make IP3, membrane phospholipid, and DAG by splitting PLC (Phospholipase-C) 2) PLC is activated by Acitvated diffused g-protein. |
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Term
| What type of NT receptor are protein kinases? |
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Definition
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Term
| What is Protein kinase fxn? and what are its indirect effectors? |
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Definition
| Fxn to P-late protein, which changes its conformotion,thus changing the protein's fxn, and the P-lated protein open's ion channels or alters enzyme function. |
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Term
| Name a fast, short acting fast synaptic potential and a Slow synaptic potentials and has long term effects NT receptor? |
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Definition
1) Transmitter gated ion channels (aka ionotropic channels) - Ex. GABA receptors and Nicotinic receptor
2) G-protein coupled receptor (aka metabotropic receptor)- Ex. Muscarinic |
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Term
| What are 3 ways to terminate a transmitter action? and Give description |
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Definition
1) Diffusion- NT can diffuse out of the synaptic cleft
2) Breakdown- Enzyme inactivat NT's (Ex. Actelycholinesterase) 3) Re-uptake- NT can be returned to axon terminals for reuse or transported into glial cells |
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Term
| In Layman terms describe Potentiation of synapses? |
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Definition
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Term
| How does potentiation of synapses work? |
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Definition
1) Increases the release of NT from presynaptic neuron which,
2) Inc. the response in the postsynaptic neuron |
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Term
| during Potentiation of synapses, there is an inc. of NT released but what else can it cause? |
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Definition
| Depression of communication |
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Term
| Describe synaptic fatigue? |
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Definition
| After many, many AP eventually the NT stored in vesicles is depleted. |
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Term
| What can clinically happen in a synaptic fatigue? |
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Definition
| Siezure- NT storage depleted |
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