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PNS Exam2
NWHSU PNS Exam 2 Ch;4,5,6,7
Question | Answer |
---|---|
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 |