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PNS Exam2

NWHSU PNS Exam 2 Ch;4,5,6,7

QuestionAnswer
Electrical synapse are excitatory or inhibitory? Excitatory
Why is there no synaptic delay exhibited by electrical synapses? Bc cells are connected physically by the gap junction
When is the membrane most excitable? Bw -70 & -55
Which synapse is more common in the nervous system? Chemical synapse
Chemical synapse are excitatory or inhibitory? Both
Which synapse exhibit longer lasting effects and adapt to changes in behavior transmission? Chemical synapse
F EPSP result from binding that causes? Depolarization
F EPSP's ion channels are usually specific or non-specific? NON-specific
What is the limit of summation in a F EPSP? Threshold
F IPSP result from binding that causes? Hyperpolarization
F IPSP's ion channels are usually specific or non-specific? Specific for either K or Cl or BOTH
What is the limit of summation in a F IPSP? The equilibrium potential for the ion (K or Cl) whose conductance increased
What happens to the threshold potential in F IPSP? INCREASE threshold potential making the cell LESS excitable
Why do EPSP's recover faster than IPSP's? Bc Na/Kpump's rate of exchange is based on the intracellular concentration of Na
Why are EPSP's shorter than IPSP's? Rate of exchange of the Na/Kpump is based on the concentration of Na inside the cell...so more Na inside the rate of exchange increases
Define first messenger? Anything that binds a receptor on the cell membrane
First messengers could be? Neutotransmitters, hormones, immune modulators, drugs, natural compounds
Fast potentials occur when? First messengers bind receptors that are part of an ion channel (maybe be non-specific or specific)
Examples of non-specific channels? Na or K
Examples of specific channels? K or Cl
Activation of non-specific channels results in? Depolarization = F EPSP
Activation of specific channels results in? F IPSP
What kind of potentials occur when a second messenger is involved? Slow potentials
Do slow potentials require a 1st messenger? Yes. The first messenger binds to the receptor but the receptor is not coupled to the channel
Slow potentials use a transducer called? G-protein
Job of G-protein? Activates a membrane enzyme system that activates the 2nd messenger
Slow potentials can be generated by? Activating channels by phosphorylation, G-protein as 2nd messenger
Define Chemical inactivation? The simplest way to stop the action of substance is to chemically break it down
Chemical inactivation is primarily used by? ACh system
The most common way messenger action is stopped is by? Reuptake
How is acetylcholinesterase produced? By the Postsynaptic membranes of cells expressing both nicotinic and muscarinic cholinergic receptors
When acetylcholinesterase is released, it breaks down? ACh down into acetate ions and choline molecules..this stops the action of acetylcholine
Choline undergoes what process? Undergoes secondary reuptake by Presynaptic cell
Increased phosphorylation by PROTEIN KINASE (PK) activity causes? Slow IPSP
Decreased phosphorylation by PHOSPHOPROTEIN PHOSPHATASE (PPP) causes? Slow EPSP
S EPSP can also be initiated by closing? K channels
Chronic pain is due to what? Slow EPSP
When you decrease threshold potential? You increase excitability by making cells easier to fire
Define Agonists? Considered to be substances whose molecular structure is similar to the known endogenous (naturally produced and secreted substance)
T/F: The agonists MUST exhibit the same function or effect as the endogenous NTX. True. The agonist may be natural substance or synthetically produced, more or less potent at the receptor, may have stronger affinity for receptor, or may bind competitively
What are the two major agonists of AcH? Nicotine and Muscarine
Nicotine binds where? Specifically at AcH receptors on skeletal muscle and dendrites of Postganglionic autonomic neurons
Muscarine (from mushroom) binds where? Specifically to both cardiac and smooth muscle as well as secretory elements of certain glands
Ligand binds? Binds and activates Agonist
Endogenous is made where? INSIDE the body
GABA is a Neruotransmitter that? Binds and activates its own channel= AGONIST
Define temporal summation? Frequency of EPSP activity occurs at a rate such that another EPSP is generated before the previous EPSP has completely degraded
Define spatial summation? When several synapses proximal to each other are fired simultaneously. Each taken separately would create small EPSP but take together would create a wave of depolarization great enough to reach threshold
What are the primary agonist of M-ENK? Derivatives of the opium poppy
Define antagonist? Chemical substance whose molecular structure is very similar to the naturally occurring substance
What happens with an antagonist? The similar structure may allow to bind but the structure being different such that the receptor is not able to carry out the activity...the effect is BLOCKED
What exogenous substances are the antagonists for the nicotinic and muscarinic cholinergic receptor sites? Curare and Atropine
Action of Curare? To bind specifically and competitively to nicotinic cholinergic receptors and cause flaccid paralysis
Action of Atropine? It counteracts the effects of the parasympathetic nervous system by blocking the postganglionic effector receptors on the cardiac and smooth m and glands
What enzyme is used to make ACh? Choline Acetyl Transferase
What breaks down ACh? ACh-E
Define Modulators? Cofactors - cant do job on their own (Ex BDZ)
Define Mediators? Neurotransmitters - can do job on their own (Ex GABA)
What are the 3 nicotinic sites? (1)neuromuscular junction (2)ALL of pre to post gel GVE sites (para& simp) (3) CNS sites
Result of nicotinic cholinergic binding? Fast EPSP
Agonists of nicotinic sites? Endogenous agonist - ACh Exogenous antagonist- Nicotine
Antagonist of nicotinic sites? Endogenous agonist - Curare Exogenous antagonist- Rabies
Nicotinic receptors are found where? Found at neuromuscular JXN and all pre to post gel autonomic synapse
Muscarinic receptors are found where? Found at post gang parasympathetic sites as well as two sympathetic sites
Where is ACh excitatory? Neuromuscular JXN where ACH released from GSE terminals ->F EPSP
Where is ACh inhibitory? On SA node of heart, ACh released from post gang PARAsympathetics terminals ->S IPSP
Define agonist? Binds receptor channel activated right away
Define antagonist? Binds and BLOCKS the activation
Define Potentiator? Substance that enhances the action of the agonist
Define Inhibitor? Substance that detracts the action of the agonist
What is black widow spider venom to ACh? Is a release potentiator of ACH
What is botulin toxin> Release inhibitor
Excitatory amino acids include? Glutamate, Aspartate, cysteic acid, homocysteic acid
Inhibitory amino acids include? GABA, glycinem taruine, beta alanine
Where is GABA in high concentrations? CNS
GABA is synthesized from the amino acid glutamate via the enzyme? Glutamuc acid decarboxylase with a cofactor B6 (pyndoxyl phosphate)
What does a lack of GABA cause? Seizures
Most common BDZ agonist? Valium and librium
What does BDZ do to GABA sites? POTENTIATES the effects of GABA biding causing increased frequency of Cl channel opening
What type of NTX at GABA-A sites? A FAST inhibitory (BDZ)
What type of NTX at GABA-B sites? A SLOW inhibitory (baclofen agoinst at pre-synaptic GABA-b site)
What kind of axons ALWAYS use ACh as their NTX? PREggl para GVE, PREggl symp GVE, Postggl para GVE
What kind of axons ALWAYS use ACh as their NTX at muscarinic cholinergic receptors? ONLY POSTggl para GVE
What axons make up white ramus? PREggl symp GVE
Created by: wizdumbslp