CNS/PNS
DESCRIBE THE LOCATION OF THE MEDULLA RELATIVE TO THE CEREBELLUM.
THE MEDULLA IS ROSTRAL/ ANTERIOR TO THE CEREBELLUM
WHAT IONS AND ION CHANNELS ARE RESPONSIBLE FOR THE RELEASE OF NTS AFTER AN AP?
CA++ IONS AND ION CHANNELS
WHAT IS AN IONOTROPIC RECEPTOR?
AN IONOTROPIC RECEPTOR IS ONE THAT HAS AN ION CHANNEL EMBEDDED IN IT, WHEN AN NT BINDS, IT ALLOWS FOR IONS TO EITHER FLOW IN OR OUT OF THE NEURON.
DESCRIBE HOW NTS CAN BE REMOVED FROM THE SYNAPSE AFTER BEING RELEASED?
(1) REUPTAKE, TRANSPORTERS ARE EMBEDDED IN THE PRESYNAPTIC MEMBRANE AND WHEN AN NT COMES IN CONTACT WITH THEM THEY CAN BE SUCKED BACK INTO THE PRESYN MEMBRANE. (2) DEGRADATION, ENZYMES FLOAT AROUND THE SYNAPSE AND BREAKDOWN NTS WHEN THEY COME IN CONTACT WITH THEM.
DESCRIBE THE DIFFERENCE BETWEEN AGONIST AND ANTAGONIST DRUG EFFECTS.
AGONIST FACILITATES INTENDED NT ACTION VERSUS ANTAGONIST WHICH INTERFERES WITH INTENDED NT ACTION.
THE DEGRADATION OF _________ IN THE _____________ IS COMMONLY ASSOCIATED WITH PARKINSON'S DISEASE.
DOPAMINE; SUBSTANTIA NIGRA
WHAT ARE EPSPS VS. IPSPS AND HOW DO THEY AFFECT THE POSTSYNAPTIC NEURON? (MENTION ION MOVEMENT)
EPSPS RESULT FROM NTS BINDING TO RECEPTORS AND EITHER ALLOWING FOR NEGATIVE IONS TO LEAVE THE NEURON OR POSITIVE IONS TO ENTER. IPSPS RESULT FROM NTS BINDING TO RECEPTORS AND EITHER ALLOWING FOR POSITIVE IONS TO LEAVE THE NEURON OR NEGATIVE IONS TO ENTER.
WHAT IS A METABOTROPIC RECEPTOR?
A METABOTROPIC RECEPTOR IS A RECEPTOR THAT DOES NOT HAVE AN ION CHANNEL EMBEDDED IN IT. IT IS NORMALLY COUPLED WITH A G PROTEIN. WHEN AN NT BINDS TO THE RECEPTOR IT ACTIVATES THE G-PROTEIN THAT GOES ON TO DO, VAGUELY PUT, OTHER STUFF. SOMETIMES THIS INCLUDES THE OPENING OF A DISTANT ION CHANNEL
WHY ARE INHIBITORY RECEPTORS (LIKE GABA) IMPORTANT?
WITHOUT INHIBITION, THERE WOULD BE AN OVERWHELMING AMOUNT OF EXCITATION WHICH CAN LEAD TO A LOT OF NEGATIVE SIDE EFFECTS LIKE SEIZURES, ANXIETY, ETC. OVER-EXCITATION OF NEURONS CAN ALSO MAKE THEM DYSFUNCTIONAL.
BMAA (a neurotoxin found in marine environments, and again just an example of a drug, don’t waste time memorizing the synaptic action) binds to the glutamate binding site on the NMDA receptor keeping the Ca2+ channel open for longer. Is this an agonist or antagonist?
A CAT'S CEREBELLUM IS RELATIVELY LARGER COMPARED TO THE REST OF IT'S BRAIN THAN A SHEEP'S CEREBELLUM IS IN RELATION TO THE REST OF ITS BRAIN. WHAT DOES THAT BEHAVIORALLY SAY ABOUT A CAT AND A SHEEP?
CATS ARE MUCH MORE DEXTEROUS, FAST, AND HAVE BETTER FINE MOTOR CONTROL THAN SHEEP. THE SIZE OF THE CEREBELLUM PREDICTS THESE QUALITIES OF THE ANIMAL.
HOW DOES A NEURON REACH AP THRESHOLD?
A NEURON REACHES THE AP THRESHOLD DUE TO THE RELEASE OF NTS BINDING TO RECEPTORS CAUSING EPSPS AND IF THE EPSPS "OUTWEIGH" IPSPS THE NEURON'S VOLTAGE RISES TO -55MV (AP THRESHOLD)
ARE RECEPTORS, NEUROTRANSMITTERS, OR BOTH INHIBITORY/ EXCITATORY? EXPLAIN.
RECEPTORS. NTS CAN'T "DECIDE" WHETHER THEY SEND AN IPSP OR EPSP THEY CAN JUST ACTIVATE THE RECEPTOR THAT ITSELF CAN EITHER SEND AN EPSP OR IPSP DEPENDING ON THE CHARGE OF THE IONS IT LETS IN.
WHAT IS THE PRIMARY FUNCTION OF GLYCINE?
GLYCINE IS RESPONSIBLE FOR INHIBITION PRIMARILY IN THE SPINAL CORD.
WHY ARE MAOIS OUTDATED? (EXPLAIN IN DETAIL)
MAOIS INHIBIT ENZYMES THAT BREAKDOWN A LOT OF DIFFERENT TYPES OF NTS, SINCE MAOIS INHIBIT MAO WITHOUT BEING PICKY THIS LEADS TO A LOT OF SIDE EFFECTS. IN SIMPLE TERMS, THEY ARE NOT SELECTIVE ENOUGH.
SALLY HAS DAMAGE TO HER OLIGODENDROCYTES AND GERRY HAS DAMAGE TO HIS SCHWANN CELLS. WHO HAS WORST COG/BEH OUTCOMES AND WHY IS THAT THE CASE?
SALLY MAY HAVE WORSE OUTCOMES BECAUSE OLIGODENDROCYTES EXIST IN THE CENTRAL NERVOUS SYSTEM AND ARE NOT ABLE TO REPAIR NEARLY AS WELL AS SCHWANN CELLS THAT ARE IN THE PNS. MYELIN BEING DAMAGED IN THE BRAIN COULD RESULT IN MUCH MORE SERIOUS COG/BEH DEFICITS DUE TO SLOWER PROCESSING OR DAMAGED AXONS
DESCRIBE THE PROCESS OF DEPOLARIZATION. (MAKE SURE TO MENTION CHANNELS AND ION MOVEMENT)
ONCE AP THRESHOLD IS REACHED, NA+ CHANNELS OPEN ALLOWING FOR A RUSH OF NA+ IONS INTO THE NEURON, CAUSING A SPIKE IN VOLTAGE (HENCE DEPOLARIZATION).
WHAT RECEPTORS ARE WITHIN THE ACH NT SYSTEM? WHAT TYPE OF RECEPTORS ARE THEY?
NICOTINIC (IONOTROPIC) MUSCARINIC (METABOTROPIC)
WHAT ROLE DOES ACH PLAY IN THE PNS?
IN THE PNS, ACH ALLOWS FOR CONSCIOUS MUSCLE CONTRACTIONS, THE SYMPATHETIC NS ALSO RELEASES ACH AT BOTH THE PREGANGLIONIC SYNAPSE AND POSTGANGLIONIC.
DRUG X BINDS TO MU-OPIOID RECEPTORS INHIBITING THE RELEASE OF GABA IN THE MESOLIMBIC SYSTEM. THIS ALLOWS FOR A MASSIVE RELEASE OF DA INTO THE MESOLIMBIC SYSTEM. IS THIS DRUG AN AGONIST OR ANTAGONIST?
THIS DRUG IS AN AGONIST, ALTHOUGH IT IS TECHNICALLY AN ANTAGONIST FOR GABA ITS PURPOSE IS TO ALLOW THE FLOOD OF DA THROUGH THE MESOLIMBIC SYSTEM AND IT HELPS FACILITATE THAT ACTION WHICH MAKES IT AN AGONIST.
BILLY USED TO LOVE PLAYING BASKETBALL BUT NOW HAS TROUBLE BEING ABLE TO THROW A BALL. BILLY HAS DAMAGE TO THE .........?
MOTOR (EFFERENT) NERVES
DESCRIBE THE PROCESS OF REPOLARIZATION. (MAKE SURE TO MENTION CHANNELS AND ION MOVEMENT)
AT ABOUT +30MV K+ CHANNELS BECOME FULLY OPEN ALLOWING K+ TO SHOOT OUT OF THE CELL CAUSING A CRASH IN VOLTAGE (HENCE REPOLARIZATION)
ARE GABA RECEPTORS GENERALLY INHIBITORY OR EXCITATORY? WHAT HAPPENS IF THEY DON'T WORK PROPERLY (BEHAVIORALLY SPEAKING)?
INHIBITORY. SEIZURES/ ANXIETY AS A RESULT OF OVERFIRING OF NEURONS
WHAT ARE THE THREE DOPAMINERGIC SYSTEMS AND WHAT ARE THEY RESPONSIBLE FOR?
MESOCORTICAL (COGNITION), NIGROSTRIATAL (MOTOR), MESOLIMBIC (REWARD)
EXPLAIN HOW ALZHEIMER'S MEDS WORK.
AD MEDS NEED TO BE ACH AGONISTS. (1) INHIBIT ACHE (2) INHIBIT ACH TRANSPORTERS (3) PROMOTE THE RELEASE OF ACH