NEUROCHEMISTRY & NEUROTRANSMITTERS. NEUROCHEMISTRY IS A SUB-SPECIALTY OF BIOCHEMISTRY THAT DEVELOPED...

NEUROCHEMISTRY &NEUROTRANSMITTERS

NEUROCHEMISTRY IS A SUB-SPECIALTY OF BIOCHEMISTRY THAT DEVELOPED RAPIDLYIN THE 1950’S. IT DEALS PRIMARILY WITH THE CHEMISTRY OF THE BRAIN AND NERVOUS SYSTEM.

A VERY IMPORTANT PART OFTHIS DISCIPLINE DEALS WITHSO-CALLED “NEUROTRANSMIT-TER SUBSTANCES” WHICH ARE SIGNALING CHEMICALS SENT BETWEEN NERVE & NERVE AND NERVE & MUSCLE. THESE SUBSTANCES ARE CLOSELYRELATED TO HORMONES. OTTO LOEWI

ANOTHER WAY OF LOOKING AT HORMONES, NEUROTRANMITTERS AND RELATED MOLECULES IS SIMPLY TO LABEL THEM AS SIGNALLING DEVICES, BUT THAT IS A BIT OF AN OVERSIMPLIFICATION.

OUTLINE:

1)REVIEW OF NERVOUS SYSTEM; TRANSMISSION2)GATED PROTEINS OF NERVOUS TRANSMISSION3)THE PRESYNAPTIC AREA OF NEURONS4)NEUROTRANSMITTERS & SYNTHESIS5)THE SYNAPTIC AND POSTSYNAPTIC AREAS6)RECEPTOR PROTEINS7)SURVEY OF NEUROTRANSMITTER DISEASES

THIS IS AN INTRODUCTION TO NEUROLOGY & PHARMACOLOGY.

WHAT DO WE REMEMBER FROM UNDERGRADUATE STUDIES ABOUT COMPONENTS & FUNCTIONS OF THE NERVOUS SYSTEM? (REVIEW OF THE NERVOUS SYSTEM & NEUROTRANSMISSION)

NERVE (aka NEURON) IS A CELL TYPE THAT COMMUNICATES INFORMATION BY ELECTRICAL AND CHEMICAL MEANS. THE INFORMATION, TYPICALLY (BUT WITH EXCEPTIONS), TRAVELS FROM THE DENDRITE THROUGH THE CELL BODY AND THE AXON TO THE AXON TERMINALS.

JUST LIKE HORMONES, THE COMMUNICATION (OR SIGNALLING) IS MEANT TO COORDINATE THE ACTIONS OF HIGHER ORGANISMS, BUT IN A MUCH MORE RAPID MANNER THAN IS COMMON TO HORMONES. TYPICALLY THE RATE OF NERVE CONDUCTION TAKES PLACE AT 1 TO 100 meters/ second FOR UNMYELINATED NERVES [WE’LL TAKE UP THE SUBJECT OF MYELINATION A LITTLE LATER]. THE RATE OF CONDUCTION ALSO INCREASES WITH THE DIAMETER OF THE NEURON ITSELF.

1) NEURONS SERVE THE CNS

2) SEVERAL KINDSARE REQUIRED

IN ORDER TO OPERATETHE COMPLETE NERVOUS SYSTEM,OTHER NEURON TYPESARE NECESSARY –SUCH AS MOTOR &SENSORY NEURONS.

WHILE THE MOTORNEURON SENDS SIGNALSTO MUSCLES, THE SENSORY NEURONTRANSDUCES SIGNALSSUCH AS HEAT AND PAININTO SIGNALS AND SENDSTHEM TO THE BRAIN.

THE IMPORTANT DIFFERENCE IN THESENERVES IS THE PRESENCEOF MYELINATION.

THE CONDUCTION PROPERTIESOF NERVES -

IN AN UNMYELINATED NERVE, AT REST,THE POTENTIAL ACROSS THE NERVEMEMBRANE IS ~ -60mV. WHEN A WAVEOF DEPOLARIZATION TRAVELS DOWNTHE NERVE, THE NERVE POTENIALINCREASES TO ~ +30mV, THEN RAPIDLYHYPERPOLARIZES BEFORE RETURNINGTO THE RESTING POTENTIAL IN ABOUT3.8 msec.

THIS IS ACCOMPANIED BY TWO EVENTS AT THE NEURAL MEMBRANE, 1st AN INCREASE IN Na ion PERMEABILITY, THEN AN INCREASE IN K ion PERMEABILITY.

WHAT CAUSES THESE EVENTS?

REMEMBER THAT, NORMALLY, POTASSIUM IS HIGHER IN CONCENTRATIIONINSIDE THE CELL WHILE SODIUM IS HIGHER OUTSIDE THE CELL. ANY CHANGE IN MEMBRANE PERMEABILITY SPECIFIC FOR THESE IONS WILL CAUSE THEM TO FLOW INWARD FOR SODIUM – OUTWARD FOR POTASSIUM. IF SODIUM IS ALLOWED TO FLOW INWARD, THE POTENTIAL BECOMES MORE POSITIVE. IF POTASSIUM IS ALLOWED TO FLOW OUTWARD, THE POTENTIAL BECOMES MORE NEGATIVE. THE FLOW IS CONTROLLEDBY “GATED” ION CHANNEL PROTEINS. THESE MEMBRANE PROTEINS AREAFFECTED BY LOCAL VARIATIONS IN ION CONCENTRATION AND POTENTIAL.

= -60mV (negative inside)

SODIUM CHANNEL PROTEIN

THE STRUCTURE AND OPERATION OF THE POTASSIUM GATED CHANNELPROTEIN IS SIMILAR TO THAT OF THE SODIUM GATED CHANNEL PROTEINWITH SOME ESSENTIAL DIFFERENCES:

1)THERE IS A MOLECULAR FILTER THAT PREVENTS THE PASSAGE OF SMALLER SODIUM IONS THROUGH THE CHANNEL. WHY IS SUCH A FILTER NOT NECESSARY FOR SODIUM GATED CHANNEL PROTEINS?

2)THE OPENING OF THE POTASSIUM GATED CHANNEL IS DELAYED IN TIME BY THE LOCAL VOLTAGE CHANGES SO THAT: AS THE POTASSIUM CHANNEL STARTS TO OPEN, THE SODIUM CHANNEL STARTS TO CLOSE.

SODIUM CHANNEL TOXINS: TETRODOTOXIN (puffer fish) AND SAXITOXIN (plankton species)BIND WITH HIGH SPECIFICITY TO SODIUM CHANNELS (KD = <1 nM). THESE ARE USEDIN RADIOACTIVE FORMS TO PURIFY SODIUMCHANNEL PROTEINS AND MAP THEIR LOCATIONS ON AXONS. SAXITOXIN IS FOUNDIN SOME FORMS OF THE “RED TIDE” FAMILIARTO PEOPLE WHO LIVE ALONG SEA COASTS.

SAXITOXIN

LOOKING AT THE ACTION POTENTIAL IN MOTION:

TIME = 0

TIME = 1 ms

TIME = 2 ms

THIS SHOWS HOW THEACTION POTENTIALMOVES ALONG THE AXON WITH TIME. THEOPENING AND CLOSINGOF GATED CHANNEL PROTEINS IS ONLY SHOWN FOR Na+ IONSFOR SIMPLICITY.

HYPERPOLARIZATIOINGUARANTEES THAT THEWAVE OF DEPOLARIZATIONIS UNIDIRECTIONAL. AT TIME= 0 (e. g., WHEN ACTIVATEDBY A STIMULUS) A GIVENAREA (DISTANCE) OF MEMBRANE IS IMMEDIATELYDEPOLARIZED.

MYELINATION: WHAT IS IT AND WHAT DOES IT DO?

MYELINATION IS THE ADDITION OF CONCENTRIC PLASMA MEMBRANESAROUND THE REGULAR PLASMA MEMBRANE OF A NEURON. THE MYELINIS PRODUCED BY A GLIAL CELL KNOWN AS A SCHWANN CELL.

NODES OF RANVIER

MYELINSHEATH

AXON

MYELINLAYERS

SCHWANN CELL

THE COMPOSITION OF THE MYELIN LAYERS ISSIMILAR IN LIPID TYPES TO THOSE OF THE PLASMAMEMBRANE. HOWEVER, 2 PROTEINS ARE UNIQUETO THE MEMBRANE: (PO IN THE PNS) AND PROTEOLIPID (IN THE CNS). THE ROLE OF THESE PROTEINS IS TO BIND TO THEMSELVES AND HOLD THE LAYERS TOGETHER.

NOTE THAT THESHEATHS ARESEPARATED BYSHORT NON-MYELINATED SPACES.

MYELINATED NERVES HAVE THE ADVANTAGE OF ALLOWING CONDUCTIONTO OCCUR AT 10x THE RATE OF UNMYELINATED NERVES. THIS IS VERYIMPORTANT FOR COMMUNICATING WITH MUSCLES (FROM THE CNS) ANDSIGNALLING THE RECEPTION OF PERIPHERAL PAIN, PRESSURE, ETC. (TOTHE CNS).

SINCE THE VELOCITY OF NERVE CONDUCTION IS PROPORTIONAL TONERVE CROSS SECTION, IT ALSO MYELINATED NERVES ALLOW THE EXISTENCE OF THINNER NERVES. FOR EXAMPLE, A 12 m DIAMETER MYELINATED NERVE WILL CONDUCT AT A RATE OF 12 m/s. THE COMPARABLE CONDUCTING UNMYELINATED NERVE MUST BE 600 m INDIAMETER.

IN PRACTICAL TERMS, WE WOULD HAVE TO HAVE SPINAL CHORDS AS THICK AS TREE TRUNKS TO CARRY OUT OUR NORMAL,HUMAN NEUROLOGICAL FUNCTIONS!

unmyelinated

myelinated

HOW MYELINATED NEURONS WORK:

MYELINATED NEURONS CONDUCT BY THE PROCESS OF SALTATORY(LATIN – SALTARE “TO JUMP”) DEPOLARIZATION. IN THE MYELINATED NEURON, NEARLY ALL OF THE SODIUM ION GATED CHANNEL PROTEINS ARE LOCATED AT THE NODES OF RANVIER. CONSEQUENTLY, DEPOLARI-ZATION OCCURS AT THE NODES AND JUMPS FROM NODE TO NODE ATA HIGHER RATE THAN SIMPLE DEPOLARIZATION ON AN UNMYELINATEDNERVE.

a)CONCENTRATED VOLTAGE GATED Na+ CHANNELS DEPOLARIZE A LOCAL AREA.

b)DEPOLARIZATION MOVES RAPIDLY DOWN THE INSIDE OF THE AXON (JUMPS) TO THE NEXT NODE.

c)AT THE NEXT NODE, THE CHANNELS OPEN AND CAUSE THE NEXT WAVE OF DEPOLARIZATION.

THE PRESYNAPTIC AREA

WITH THE ARRIVAL OF THE DEPOLARIZED SIGNAL AT THE PRESYNAPTICAREA A NUMBER OF EVENTS OCCUR THAT MUST BE CONSIDERED SEPARATELY AND TOGETHER :

1)THE TRANSDUCTION OF THE SIGNAL IN THIS AREA

2)THE SYNTHESIS OF NEUROTRANSMITTERS

3)THE MECHANISM(S) OF TRANSMITTER RELEASE

4)THE KINDS OF NEUROTRANSMITTERS THAT EXIST

5)HOW A SUBSTANCE CAN “QUALIFY” AS A NEUROTRANSMITTER

6)THE SEQUENCE OF EVENTS THAT CAUSE TRANSMITTER RELEASE

ARRIVAL AT THE SYNAPSE

WITH THE ARRIVAL OF THE DEPOLARIZED SIGNAL AT THE SYNAPSEA NUMBER OF EVENTS OCCUR THAT MUST BE CONSIDERED SEPARATELYAND TOGETHER :

1)THE TRANSDUCTION OF THE SIGNAL






THE PRESYNAPTIC AREA (aka AXON TERMINAL) IS A VERY BUSY LOCATION.THE ELECTRON MICROGRAPH SHOWS THE PRESENCE OF MANY VESICLESAND FIBERS. THE AREA IS TYPICALLY WIDER THAN THE AXON TO FACILITATERAPID COMMUNICATION WITH THE POSTSYNAPTIC CELL.

WHEN THE WAVE OF DEPOLAR-ZATION ARRIVES AT THIS AREA,Ca+2 IONS PLAY AN IMPORTANTDOUBLE ROLE IN THE TRANSDUCTION OF THE SIGNAL THAT CAUSESTHE RELEASE OFNEUROTRANSMITTERS. DEPOLARIZATION AT THIS POINT CAUSES THE OPENING OF VOLTAGE GATED Ca+2 CHANNEL PROTEINS.

THE FIGURE SHOWS TWO STAGESOF THE ROLE OF Ca+2 IN THIS PROCESS.

A)THE Ca+2 CHANNEL PROTEIN (GREEN) IS CLOSED WITH HIGHER CONCENTRATIONS OF Ca+2 IN THE SYNAPTIC CLEFT.B)UPON DEPOLARIZATION, THE CHANNEL PROTEIN OPENS AND ADMITS Ca+2 (RED DOTS) TO THE PRESYNAPTIC CYTOPLASM. THIS CAUSES: 1. TRANSPORT OF THE SYNAPTIC VESICLE TO THE SYNAPTIC MEMBRANE, FUSION & 2. OPENING OF THE SYNAPTIC VESICLE TO THE SYNAPTIC CLEFT.

NOTE: A NUMBER OF PRESYNAPTIC PROTEINS ARE INVOLVED IN THIS TRANSPORT AND FUSION PROCESS.

SYNAPTIC CLEFT

SYNAPTIC CLEFT

THE SYNTHESIS OF NEUROTRANSMITTERS AND THEIR STORAGE TAKESPLACE IN THE PRESYNAPSE. EVEN THOUGH WE HAVE NOT YET CONSIDERED NEUROTRANSMITTERS -- EXCEPT TO SAY THAT THEYARE BIOCHEMICALS THAT CONVEY SIGNALS FROM NEURON TO NEURONOR NEURON TO MUSCLE – LET’S LOOK AT THE SYNTHESIS OF TWO COMMON NEUROTRANSMITTERS: ACETYLCHOLINE AND NOREPINEPHRINE.

ACETYLCHOLINE IS MADE FROM ACETYL-CoA AND CHOLINE (DIETARYSOURCE):

THE SYNTHESIS IS ENTIRELY WITHIN THE PRESYNAPTIC CYTOPLASM.

BELOW YOU SEE THE DIAGRAM OF SYNTHESIS AND STORAGE OF ACETYLCHOLINE

NOTE: THE REUSEOF THE SYNTHETIC BIOCHEMICALS –ACETYL CoA AND CHOLINE.

AFTER SYNTHESIS, THENEUROTRANSMITERIS TAKEN UP INTO THEPRESYNAPTIC VESICLE AND THE VESICLE ISUSUALLY TAKEN TO THEVICINITY OF THE PRESYNAPTIC TERMINAL (OR MEMBRANE). EACHVESICLE CONTAINS ABOUT10,000 ACETYLHOLINE (Ach)MOLECULES.

THE SYNTHESIS OF NEUROEPINEPHRINE IS MORE COMPLEX.

NOTE THE FOLLOWING:

1.THE SYNTHESIS MAY CONTINUE ON TO EPINEPRINE. IT BEGINS WITH TYR.

2.NOREPINEPHRINE IS USUALLY A NT WHILE EPINEPHRINE IS A HORMONE – THE ROLES MAY BE REVERSED.

3.TYROSINE HYDROXYLASE IS THE RATE LIMITING ENZYME.

4.AROMATIC AMINO ACID DECARBOXYLASE IS AN ENZYME IN THE PATHWAY OF OTHER NT SYNTHESES (PINK SQUARE).

5.DOPAMINE IS FORMED IN THE CYTOPLASM AND THEN ENTERS THE VESICLES FOR THE FINAL REACTION(S).

*DOPA = 3,4-DIHYDROXYPHENYLALANINE.

*

SO FAR WE KNOW THAT Ca+2 IONS INDUCE THE TRANSPORT AND FUSIONOF VESICLES CONTAINING NEUROTRANSMITTERS TO THE PRESYNAPTICMEMBRANE THAT BORDERS THE SYNAPSE.

WHAT HAPPENS NEXT?

A REFERENCE WAS MADE TO PROTEINS THAT ARE PROMPTED BYCa+2 IONS TO CAUSE FUSION OF VESICLES & PRE-SYN. MEMBRANES.THIS IS ACCOMPLISHED WITH A PROTEIN COMPLEX OF SYNTAXIN-SYNAPTOBREVIN-SNAP25 MOLECULES. THESE MOLECULES HAVEBEEN PROPOSED TO ALSO CONTINUE IN THE FORMATION OF PORESIN THE FUSED MEMBRANES EITHER BY “FULL COLLAPSE” OR “KISS-AND-RUN” MECHANISMS. THE FULL COLLAPSE MECHANISM CAUSESTHE COMPLETE EMPTYING OUT OF THE NTs IN THE VESICLE. THEKISS AND RUN MECHANISM FORMS A TRANSIENT HOLE AND THENCLOSES LEAVING SOME OF THE NTs IN THE VESICLE. THE VARIATIONALLOWS FOR CONTROL IN THE AMOUNT OF NT RELEASED INTO THESYNAPTIC CLEFT.

PROTEIN COMPLEX AT THEFUSED MEMBRANES FORCINGTHE MEMBRANES OPEN AS ARESULT OF Ca+2 BINDING.

SNAP-25

SYNTAXIN

SYNAPTOBREVIN

SNAP = Synaptosome associated protein is Ca+2

ion sensitive (25kD)SYNTAXIN = 35 kDSYNAPTOBREVIN = ~19 kD

NEUROTRANSMITTER S ARERELATIVELY SIMPLE, SMALLMOLECULES

PARTIAL LIST:

CHOLINERGIC – e. g., ACETYLCHOLINECATECHOLAMINES – e. g., NOREPINEPHRINEAMINO ACID/DERIVATIVES – e. g. GLYCINE, AMINOBUTYRIC ACIDSOME HORMONES- e.g., EPINEPHRINENEUROMODULATORS- e.g. ENDORPHINS (NOT TRUE NTs)

NOTE THAT ONE END OF THE MOLECULE HAS A POSITIVE CHARGE

THIS IS A GENERAL LIST THAT INVESTIGATORS HAVE COME TO AGREE UPON FOR A SUBSTANCE TO BE CONSIDERED AS A NEUROTRANSMITTER:

1)SUBSTANCE MUST BE PRESENT IN THE PRESYNAPSE.

2)SUBSTANCE MUST BE RELEASED WITH NEURAL STIMULATION.

3)EFFECTS OF SUBSTANCE, WHEN APPLIED TO A POSTSYNAPTIC AREA, MUST BE IDENTICAL TO THE PHYSIOLOGICAL EVENT CAUSED BY THE PRESYNAPTIC DEPOLARIZATION.

4)THE EFFECTS MUST BE PHYSIOLOGICALLY PROPORTIONAL TO THE PRESYNAPTIC STIMULUS.

5)THERE MUST BE A LOCAL MECHANISM TO INACTIVATE THE SUBSTANCE.

EXPERIMENTALLY SOME OF THESE CONDITIONS ARE DIFFICULT TOOBTAIN DATA FOR.

A QUICK REVIEW AND LEAD IN TO WHAT OCCURS AT THE POSTSYNAPSE

WHAT WE NOW WANT TO COVER ARE A FEW DETAILS ABOUT THESYNAPSE, RECEPTORS AND INACTIVATION

THE SYNAPTIC CLEFT

THE SYNAPTIC CLEFT IS A COMPARTMENT THROUGH WHICH NEUROTRANSMITTERS TRAVEL FROM THEIR RELEASE AT THEPRESYNAPSE TO A RECEPTOR AT THE POSTSYNAPTIC MEMBRANE.THE NTs MOVE BY DIFFUSION TAKING ABOUT ½ msec TO ARRIVE ATTHEIR RECEPTORS. AFTER BINDING TO THEIR RECEPTORS, NTsMAY BE ENZYMATICALLY BROKEN DOWN (e.g. ACETYLCHOLINE BYTHE ACTION OF ACETYLCHOLINESTERASE) OR TAKEN BACK UPAGAIN BY THE PRESYNAPSE (e.g. NOREPINEPHRINE IS TAKEN BACKUP BY A TRANSPORT PROTEIN).

FROG NEUROMUSCULAR SYNAPTIC CLEFT. CLEFTS ARE TYPICALLY~200 ANGSTROMS WIDE.

PRESYNAPSE

POSTSYNAPSE

VESICLE

POSTSYNAPTIC RECEPTOR PROTEINS

THE RECEPTORS THAT BIND WITH NEUROTRANSMITTERS MAY BEDIVIDED INTO TWO MAIN FAMILIES AND SERVERAL SUB-FAMILIES:

VOLTAGE GATED CATION Na+ CHANNELS (e.g. ACETYLCHOLINEM ) (USE G PROTEINS) K+ CHANNELS (e.g. THE SAME) Ca+2 CHANNELS

TRANSMITTER GATED ION ACETYLCHOLINEN CATION ex (LIGAND GATED) GLUTAMATE GATED Ca+2 ex SEROTONIN GATED CATION ex ABA GATED Cl- in GLYCINE GATED Cl- in

IN ADDITION, ACETYLCHOLINE RECEPTORS ARE ALSO DIVIDED INTOTYPES THAT ALSO BIND TO EITHER NICOTINE OR MUSCARINE:

IF WE CONSIDER ACETYLCHOLINE, IT WILL BIND TO EITHER A NICOTINICOR A MUSCARINIC RECEPTOR. A NICOTINIC RECEPTOR HAS THE APPEARANCE SHOWN HERE:

THIS RECEPTOR OPENS A PASSAGE (HOLE) FOR Na+ ENTRY. NICOTINEALSO BINDS TO THE RECEPTOR. THIS TYPE OF RECEPTOR IS FOUNDON MUSCLE TISSUES (NEUROMUSCULAR JUNCTION).

TWO RATHER WELL-KNOWN SUBSTANCES: CURARE AND COBRATOXINALSO BIND TO THE NICOTINIC ACETYLCHOLINE RECEPTOR TO CAUSEPARALYSIS.

ORIGINALLY, CURAREWAS PLACED ON ARROWSAND DARTS FOR HUNTING.IT KILLED ANIMALS BYPARALYSIS OF LUNGMUSCLES. THE WORD ISDERIVED FROM THE SOUTHAMERICAN INDIAN WORD:WOORARI “POISON”.

MUSCARINIC ACETYLCHOLINE RECEPTORS MAKE USE OF G PROTEINSTO ACHIEVE A POSTSYNAPTIC EFFECT WHICH MAY CAUSE DEPOLARI-ZATION OR HYPERPOLARIZATION (INHIBITION). HERE IS AN EXAMPLEOF ONE RECEPTOR THAT CAUSES HYPERPOLARIZATION.

AFTER ACETYLCHOLINEBINDS TO THE RECEPTORIT ACTIVATES A G PROTEIN(TOP PICTURE). IN THISCASE THE G sub and subSUBUNITS (RATHER THANTHE sub subunit) DIFFUSETO A POTASSIUM CHANNELPROTEIN AND CAUSE IT TOOPEN.

THIS CAUSES K+ TO FLOWOUT OF THE POSTSYNAP-TIC CELL AND HYPER-POLARIZE (IT BECOMESMORE NEGATIVE AS SHOWNON THE BOTTOM). THIS IS A MECHANISM USED IN HEART TISSUE TOSLOW DOWN THE HEART RATE.

AN EXAMPLE OF TREATING PARKINSON’S DISEASE BY USING NEUROTRANSMITTER REPLACEMENT – ALLEVIATING NEUROPATHOLOGY

PARKINSON’S DISEASE AFFECTS PATIENTS BY ADVERSLY AFFECTINGVOLUNTARY MOVEMENT (e.g. WALKING) AND PRODUCING INVOLUNTARYTREMOR. THE DISEASE IS RELATED TO A DEGENERATION OF NEURONSTHAT PRODUCE DOPAMINE AS A NEUROTRANSMITTER (SEE THE SYNTHETIC PATHWAY FOR NOREPINEPHRINE). THESE PATIENTS CAN BETREATED WITH AN AGONIST (REPLACEMENT THAT STIMULATES THEDOPAMINE RECEPTOR) KNOWN AS BROMOCRIPTINE. THIS IS AN ARTIFICIALWAY OF SUPPLEMENTING THE LOSS OF DOPAMINE IN THE CNS THAT ISNEEDED FOR NORMAL MOTOR (MUSCLE) FUNCTIONS.

WHAT IS IMPORTANT TO KNOW?

1) THE CONDUCTION PROPERTIES OF UNMYELINATED AND MYELINATED NERVES.2) HOW DOES A GATED SODIUM CHANNEL PROTEIN WORK?3) WHAT ARE SODIUM CHANNEL TOXINS? (WHAT DO THEY DO?)4) WHY WOULD OUR SPINAL CHORDS BE AS BIG AS TREE TRUNKS WITHOUT MYELINATED NERVES?5) WHAT HAPPENS IN THE PRESYNAPTIC AREA TO VESICLES WHEN CALCIUM CHANNELS OPEN?6) WHAT IS DOPA? WHAT DO NOREPINEPHRINE AND EPINEPHRINE HAVE IN COMMON?7) WHAT IS A “KISS AND RUN” MECHANISM FOR VESICLE OPENING?8) WOULD YOU CONSIDER ENDORPHINS TO BE NEUROTRANSMITTERS ACCORDING TO THE CRITERIA THAT QUALIFY SUBSTANCES TO BE NTs?9) WHAT ARE THE TWO GENERAL KINDS OF ACETYLCHOLINE RECEPTORS AND WHAT MECHANISM DO THEY USE TO ACHIEVE A POSTSYNAPTIC EVENT (EFFECT)?10) WHAT IS BROMOCRIPTINE AND WHY IS IT USED?

NEUROCHEMISTRY & NEUROTRANSMITTERS. NEUROCHEMISTRY IS A SUB-SPECIALTY OF BIOCHEMISTRY THAT DEVELOPED...

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