Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
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 |
Created by:
wizdumbslp
Popular Chiropractic sets