neurotransmitters
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| What is the function of AUTORECEPTORS? | Autoreceptors provide a feedback system for Neuron #2.
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| Where are AUTORECEPTORS located? | in the POSTSYNAPTIC DENSITY or RECEPTOR FIELD
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| What happens first once a neurotransmitter is released? | The NT chemicals move across the cleft.
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| What is Neuron #2 waiting for? | Neuron # 2's receptors are waiting to get activated by neurotransmitters.
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| What is EXOCYTOSIS? | The process of releasing NTs into the cleft
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| What is ENDOCYTOSIS? | a process similar to EXOCYTOSIS where we reclaim the empty vesicles so they can be refilled and reused
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| What is the mechanism of an excitatory signal? | When N #1 fires and releases, it is telling N #2 to fire.
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| What is the mechanism of an inhibitory signal? | When N #1 fires and releases, it is telling N #2 not to fire.
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| What does an EXCITATORY signal and an INHIBITORY signal have in commmon? | In both cases, N #1 is firing and releasing a NT.
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| What is a GRAYS TYPE I SYNAPSE? | 1.) almost always associated with an excitatory signal 2.) asymmetrical
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| What is a GRAYS TYPE II SYNAPSE? | 1.) almost always associated with an INHIBITORY signal 2.) symmetrical
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| When pre- and post-synaptic densities are the same, this is almost always indicative of ______________________________. | an inhibitory signal
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| Amino acids are made up of subparts called _______. | amines
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| What are the 3 general families of neurotransmitters? | 1. amino acids 2. (somewhat simpler) amines 3. PEPTIDES (somewhat more complex amino acids that build a polypeptide chain)
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| Where are AMINES and AMINO ACIDS typically found? | in synaptic vesicles
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| Where are peptides usually found, and why? | in secretory granules because they are somewhat bigger structures
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| Receptors are usually found where/when? | postsynaptically
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| An IONOTROPIC RECEPTOR starts its life as ___________________. | an ion channel
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| What is the first difference betweeen an ION CHANNEL and an IONOTROPIC RECEPTOR? | Somewhere on the structure is a little receptor site/a notch/a subunit.
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| How is an IONOTROPIC RECEPTOR gaited? | chemical or LIGAND GAITED
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| It is the job of __________________ to open or close the channel. | the neurotransmitter
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| What flows through the channel? | IONS
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| What does not flow through the channel? | neurotransmitters
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| The chemical key fits in ________________ and unlocks _________________. | the receptor site; the channel
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| What is a CONFORMATIONAL CHANGE? | the twisting open or changing shape of a channel due to neurotransmitters combining with chemicals
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| What happens after CONFORMATIONAL change takes place? | Ions go through the channel.
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| How do we know which ions will go through the channel? | the channel's specificity
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| + charges send ____________ signals to Neuron #2. | excitatory
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| (-) charges send _____________ signals to Neuron #2 | inhibitory
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| When I ask, "What kind of synapse do I have?" I am referring to... | excitatory or inhibitory
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| A GRAYS TYPE I SYNAPSE is associated with _________________. | an ion with a + charge
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| A GRAYS TYPE II SYNAPSE is associated with __________________. | an ion with a (-) charge
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| What is DESENSTITIZATION? | A very dangerous condition in which synapses get clogged and desensitized to new signals
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| Name 3 ways of getting rid of NTs once they are released into the cleft and have done their job. | 1.) DIFFUSION 2.) ENZYMATIC DESTRUCTION 3.) REUPTAKE
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| What is DIFFUSION? | a very passive process in which glial cells communicate and clean up some of the NT like hungry wolves breaking down the NT right away in the cleft
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| What is ENZYMATIC DESTRUCTION? | a very active process that involves the breaking of the NT almost as soon as it is released/NT parts can be brought back into the bouton for reuse/one NT this happens to is ACT
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| What is REUPTAKE? | As soon as NT is released into cleft, it is sucked back into bouton for reuse.
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| What do reuptake inhibitors do? | prevent reuptake so there is more NT bouncing around in the cleft
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| What are the 2 things that can happen when a NT is uptaken for reuse? | 1.) NT can be repackaged for reuse 2.) NT can be enzymatically destroyed presynaptically by monooxidase in the bouton in the wall of the mitochondria
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| What does an MAOI do? | inhibits the enzyme that destroys seratonin
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| What is the name of the enzyme that destroys NT in the wall of the mitochondria? | monooxidase
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| How do nerve gasses work? | by deactivating the wolf-like enzyme that break down ACT
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| What is the most frequently found NT at the NEUROMUSCULAR JUNCTION? | ACT
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| What happens if you destroy the enzymes that break down ACT at the NEUROMUSCULAR JUNCTION? | You can't move and you die; nothing works.
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| What is a disease related too to much of the NT DA? | schizophrenia
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| MAOIs break down ______________, resulting in _______________. | the enzyme that destroys DA; more DA
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| MAOIs increase the amt of which 3 NTs available? | DA, NE, 5HT
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| Is there such a thing as an excitatory or inhibitory neurotransmitter? | No.
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| It is the characteristics of ______________ that determines what happens. | the receptor the NT is opening
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| What is GABA? | an inhibitory NT (in almost every case, it activates inhibitory receptors)
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| We try to increase __________ in seizure disorders. | GABA
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| What do we need to get secretory granules to release NTs? | 1.) a longer amount of time 2.) repeated firings
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| What does the release of NTs from the synaptic vesicles have in common w/ the release of NTs from the secretory granules? | the process of exocytosis
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| Synaptic vesicles contain ______ and ________ which get released every time. | amines; amino acids
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| What is COTRANSMISSION? | a single neuron releases multiple NTs with repeated firings
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| The brain practices its own kind of ________________. | polypharmacy
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| The more specific a drug becomes,the ________________ and ____________. | less effective it becomes; less harmful the side effects (tradeoff in effectiveness_
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| At the cellular level, what is learning? | the breaking down and building of new synapses
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| What is a catecholamine? | a neurotransmitter that is a subset of the monoamine family
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| What are the steps required to build a catecholine structure? | 1. tyrosine 2.) tyrosine hydroxylate 3.) l-doba 4.) dopamine 5.) norepinephrine 6.) epinephrine (adrenaline)
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| What is the function of TYROSINE HYDROXYLATE? | It is an enzyme that breake TYROSINE down/converts it to l-dopa.
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| Describe a rate-limiting step and give an example. | You can feed someone a truckoad of tyrosine, but it won't equal a truckload of l-dopa; the conversion of tyrosine to l-dopa via tyrosine hydroxylate is an example.
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| What does every transition require in the building of a catecholine structure? | an enzyme that makes changes to the previous step
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| Why does the making of a catecholine structure require an enzyme that makes changes to the previous step? | Because certain chemicals such as DA cannot cross the blood-brain barrier
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| What is the importance of DA, and what does too little DA lead to? | movement; Parkinson's-like symptoms
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| What else is too little DA linked to? | mood disorders
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| What happens when you take meth? | DA gets reuptaken/reversal of reuptake pump/reverse direction/goes from sucking in to wblowing out DA into the synapse (blowing DA OUT)
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| What does a person start to resemble as a result of too many amphetamines, speed, etc? | a schizophrenic
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| Where does the transformation from DA to NE happen? | INSIDE a synaptic vesicle; DA gets packaged inside the synaptic vesicle
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| What has to happen to make epinephrine? | You ahve to release NE OUTSIDE the synaptic vesicle. Then enzympes make NE into Epinephrine.
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| What does it usually take to get Neuron #2 to change? | multiple firings on N#2
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| Where is the final place where threshold must be reached if a neuron is to fire? | axon hillock
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| N#2 also has _________ picking up conflicting signals. | dendrites
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| Name the 2 ways in which N#2 makes the decision to fire. | 1.) SPACIAL SUMMATION 2.) TEMPORAL SUMMATION
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| What is SPACIAL SUMMATION? | a widespread summation over space; N#2 takes signals simultaneously from all ifferent neurons giving the same message, saying, "Fire!" (one big shout or signal from other neurons to fire)
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| What is TEMPORAL SUMMATION? | Instead of multiple upstream signals giving FIRE signal, we have neurons going FIREFIREFIRE over time; climbing instead of one big blast
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| What is EPSP? | excitatory post-synaptic potential (likely to excite N#2); the ability of neurons to fire or know when to fire
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| What is IPSP? | inhibitory post-synaptic potential;inhibitory signal is present from another neuron trying to send a message to N#2
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| What is a ZONE OF NEGATIVITY? | It involves a SHUNTING INHIBITION that an counteract all the + charges trying to come through (like a hole in a hose trying to fire)
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| Any place you have a zone of negativity, you have a _________________________________. | shunting inhibition
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| What are AXON COLLATERALS? | multiple branches on an axon that provide a kind of feedback mechanism/can send a signal back to its own dendrites saying, "I'm not going to listen to your msg to fire" an inhibiting the signal.
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| What happens if you release too much NT into the cleft? | The NT reaches out across the active zone and autoreceptors pick up on it and stop the release of NTs.
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| What did Sherrington work with, and what did he want to see? | the REFLEX ARCH; how long a reflex took and what was happening
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| Where do reflexes happen, and why do we have them? | locally in the spinal cord; so we have fast, failsafe movement for survival
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| A NERVE IMPULSE is a ______________ phenomenon that can be observed. | physical
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| What did Sherrington name? | the connection between 2 neurons = the SYNAPSE
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| Sherrington though the connection between neurons was an _______________ phenomenon. | electrical
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| Who implied that the synaptic process is chemical and won the Nobel Prize for it? | Ottolowie
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| Who discovered the first NT, and what was it? | Ottolowie; Acetycholine
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| Any time we have a neuron commanding a muscle to move, we have _______________. | ACT
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| Where is ACT primarily found? | at the NEUROMUSCULAR JUNCTION
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| What happens at the neuromuscular junction? | nerves enervate muscles
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| What else is ACT very important for? | learning & memory in the brain
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| Where do we normally get rid of ACT, and what happens? | in the cleft; it gets released by a neuron onto a muscle
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| How and where is ACT destroyed? What destroys ACT? | enzymatic destruction; in the cleft; AChE ESTERASE
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| Why must we get rid of ACT? | so it does not clog the signal
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| How do nerve gasses work? | They bind to and block out AChE, preventing it from destroying ACT, ACT builds up and clogs signal
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| What is NE important for? | overall state of arousal
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| NE deficiencies are mostly associated with _________________. | depression
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| Too much NE is sometimes associated with _______________. | mania
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| Adrenaline is important to ____________. | the sympathetic nervous system (fight or flight/gets you ready for action
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| What does the parasympathetic nervous system do? | calms you back down
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| The sympathetic and parasympathetic nervous systems are _____________________________. | always moving back and forth/balancing out.
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| What has been shown to prevent PTSD? | beta blockers to trauma victims within a few days of the trauma
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| Seratoninn (5HT) is a ______________ and is associated with ______________. | monoamine; melatonin
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| What is 5HT derived from? | an amino acid: triptophan
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| Why are drugs like meth and coke so addicting? | They mess w/ dopamine levels/reward system/hijack the anterior part of the cingulate gyrus
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| What is the most common excitatory (+) NT in the brain? Clarify what this means. | GLUTAMATE; Most of the time the receptors the GLUTAMATE is activating are excitatory.
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| What can be released in large quantities if you damage a brain area? | GLUTAMATE
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| What is it called when neurons surrounding an injured area of the brain are overstimulated by damaged nerves? | a glutamate storm
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| A lack of ____ results in seizures. | GABA
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| Alcohol has its own little site on ____________ receptors. If alcohol is present and ______________ gets released, the ________________ might stay open twice as long a it normally does. | GABA; ion channel
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| Describe DOWNREGULATION | a way in which neurons are changing number of receptors; neuron GETS RID OF receptors to reestablish equilibrium (In alcohol addiction, the neuron gets rid of 1/2 its GABA receptors... results in nowhere near the Cl- ions you need
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| What is UPREGULATION? | The brain builds back receptors (In the case of alcohol, it builds back GABA receptors.)
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| What is a RECEPTOR ANTAGONIST? | a drug that blocks/keeps receptor from being activated. It is like a cover over the receptor site that prevents that receptor from being activated for awhile.
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| What is a RECEPTOR AGONIST? | a drug that activates the receptor
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| What is it called when several repeated firings are needed to bring a neuron to threshold? | TEMPORAL SUMMATION
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| The effect of cotransmission can be likened to ____________________________. | polypharmacy
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| When a G-Protein center gets activated, it activates the ____________, which then _______________________________. | ALPHA SUBUNIT; detachesa dn moves along the membrane until it activates something
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| What is the effect of the G-Protein on the other receptor? | The G-Protein unit modulates the activity of the other receptor.
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| The G-Protein receptor is _______________. | metabotropic
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| the G-Protein is inddirectly coupled to the _________________. | ion channel
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| The brain fires more frequently when ________________________________. Secretory granules release __________________ then the _____________________ gets activated, which strengthens connections. | something is novel or important; peptides; ionotropic receptor
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| Once connections are strengthened, it takes _________________ from now on to activate the _________________. | less firing; ionotropic receptor
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| the first messenger is the ____________. | neurotransmitter
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| Sometimes what the G-Protein activates is an ______________. | enzyme
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| A msg that says, "Tear down some receptor sites bc we're bombarded with msgs from above" would result in ________________. | downregulation
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| What kind of receptor is an autoreceptor? | a G-Protein
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| When a G-Protein gets activated it, ______________________________. It hits an ______________________. | revs up and moves across the membrane; effector protein
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| And effector protein could be an ______________ or an _________________. | enzyme; ionotropic receptor
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| What is the G-subunit able to do? | modulate the normal behavior of the receptor
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| ________________ make it very difficult for bad stuff to get into the brain. They are, in effect, the _________________. | TIGHT JUNCTIONS; blood-brain barrier
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| What can get around the blood-brain barrier? | usually only small, uncharged, lipid-based particles
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| Why is it a problem that most things cannot pass through the blood-brain barrier? | b/c a lot of very useful drugs have a hard time getting across the blood-brain barrier
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| What exists in the capillary wall or _____________________ that can bring food, remove waste, etc. from bloodstream to brain? | endothelial cells; active transporter proteins
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| What is the 2nd layer of the blood-brain barrier/another layer of protection? | astrocyes pseudopodia
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| Astrocytes pseudopodia are a subtype of ________________ that put out___________ and seem to be a 2nd layer of barrier from thing sbeing able to get in and out of brain thru the bloodstream. | glial cell; false feet
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| To get through the blood-brain barrier PASSIVELY, something must be _________________. | a small, uncharged, lipid-based particle like oxygen
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| how much blood does the brain consume? | 1.5 pints per minute
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| The brain requires __x the amount of fuel as any other body part | 10
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| The brain uses about __% of the oxygen you breathe in even though it accounts for __% of body weight | 20%;2%
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| How much of the brain's energy is consumed getting the neuron to rest? | 80%
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| Can the brain store fuel? | No. There's no storage for oxygen or glucose in the brain; brain needs constant circulation or flow of such things.
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| There is a redundancy of arteries brining the blood into the brain. They are ____________ and ____________ arteries. If you blow out or clog up one system, ______________________. | vertebral; cartoid; there is a backup
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| What happens 5-10 seconds after the brain runs out of oxygen? | lose consciousness
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| What happens 20 seconds after the brain runs out of oxygen? | twitching/convulsions/brain starts to shut down
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| What happens 4 min after the brain runs out of oxygen? | permanent damage
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| What happens 10 min after the brain runs out of oxygen? | death or severe, lasting brain damage
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| What is the first process of vision? | attention/focusing
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| Regardless of sensory modality, we have to __________ (change the energy from one form to another). in this case, we're turning data into action potentials so __________________________. | transduce; our nervous systems can handle the data
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| Rods handle | black & white
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| cones handle | color
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| Where does transduction in the visual system take place? | in the rods and cones
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| area in each eye that doesn’t have room for any rods and cones = | the blind spot
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| What exists at the OPTIC CHIASM? | a partial decussation/a partial crossing over of information
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| Which eye fields cross over? | the nasal eye fields
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| Which eye fields stay on the same side/don't cross over? What is this called? | the temporal eye fields; ipsolateral
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| If you cut thru the optic chiasm, you would have __________________. | just central vision = BITEMPORAL HEMIANOPIA.
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| What is it called when you lose vision in a single eye? | monocular blindness
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| What happens when there is a lesion of one optic tract? | lose an entire hemi-space/HOMONYMOUS HEMIANOPIA
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| Some of the info from each eye goes to which part of the brain? | hypothalamus
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| Only a relatively small # of neurons actually produce essential NTs like... | SE, DA, NE
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| What are DIFFUSE MODULATORY SYSTEMS? | systems in the brain not handling the ON/OFF of the brain but modulating/fine-tuning/moving u back and forth between things)/diffusely spreading important NTs throughout the brain
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| 4 different diffuse modulatory systems/one for each of... | SE, DA, NE, ACT
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| Describe DA's diffuse modulatory system | DOPAMINERGIC: SUBSTANTIA NIGRA… if SN gets hit, lack of DA in basal ganglia will result in a movement disorder: Parkinson’s.
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| What is transduction? | Changing energy into one form to another; turning environmental energy into action potentials
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| When do ganglion cells come into play? | Once bipolar cells see something consistent happening between rods and cones
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| Ganglion cells are a kind of ____________ system. | intermediary
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| Ganglion cells push out a long axon. All these long axons converge in a single place and exit the eye. Once they leave the back of the eye, these axons are known as _________________. | the optic nerve
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| What does each eye get that the other doesn't? Or, what is lost to the opposite eye? | the periphery
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| The middle part of the world (in vision) is handled by __________. | both eyes
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| The peripherals of the world (in vision) are handled by __________________. | one eye or the other
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| Name the 3 areas of vision. | midline; right hemi-space; left hemi-space
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| Only PART of the visual information that is handled by each eye crosses over to the opposite eye. Where does it cross over? | at the optic chiasm
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| From ganglion cells through the handling of information, there is __________________. | no new synapse; no handing off of information
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| What happens if you lose one optic tract? | everything from the opposite visual hemi-space is gone
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| About 10% of all ganglian cell info that’s coming out of eye is going into... | the superior colliquii.
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| Describe the 5HT diffuse modulatory system. Specifically, what is it called? | SERATONERGIC – little nuclei on seam all the way down the 2 hemispheres called RAPHE NUCLEI. These are the nuclei from which long projections come out and bathe brain in serotonin; RAPHE NUCLEI are the diffuse modulatory system for serotonin.
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| What gives itself feedback and changes itself so it stops releasing so much NT? | an autoreceptor, which is a G-Protein
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| Where are peptides normally packaged? | secretory granules
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| Where are amines usually packaged? | synaptic vesicles
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| Where are amino acids usually packaged? | synaptic vesicles
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| Where is the first visual synapse located? | betw. rods and cones and bipolar cells
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| Only _________________ can activate the G-Protein receptor. | PEPTIDES
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| What is an Electrical Synapse, you bitch? | AKA Gap Junction, which is very fast, very reliable, and very simple. Physical connection between two neurons in some places. Electrotonically- mediate escape reflexes
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| What are the ions that connect neurons? | Connexons
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| First vision process involves________________. | rods and cones
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| Where does transduction take place? | Retina
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| What is the blindspot? | This is where the ganglion cell axons are pushing out of the eye to form the optic nerve; there are no rods or cones in this part.
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| Where is the next synapse located after the synapse between bipolar and ganglion cells? | Thalamus
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| What is the thalamus? | sensory relay system
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| The thalamus is made up of lots of little structures scrunched together, known as _______________________. | Lateral Ganiculate Nuclei
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| Once the information hits the primary visual cortex in the occipital lobe ________ or ________ can said to have taken place. | vision or sensation
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| If you have any lack of raw visual sensory information, you have _________. | Blindness
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| What are the three places that a small amount of info coming out of each eye goes to? | hypothalamus, midbrain and into cranial nerves, and superior coliculi
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| In order to perceive visual sensation, you need to push that information back to the front of the brain by two different perceptual streams. what are they and what is their purpose? | Ventral stream- leaves occipital lobes and goes back into temporal lobes to give it perceptual meaning, the "What" pathway; Dorsal/parietal stream- leaves occipital lobes and goes into the parietal lobes to givess us the "where"
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| Special part of Thalamus known as... | LGN (Lateral Geniculate Nucleus).
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| Describe the 1st perceptual stream... | info leaves occipital lobes and returns to temporal lobes, where the brain perceives/sometimes known as VENTRAL STREAM or "WHAT" pathway
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| Describe the NE diffuse modulatory system | NORADRINERGIC/arises out of an area in the brainstem in a blue-colored spot/LOCUS CERULEUS (“the blue spot”); the actual neuron bodies are located in the blue spot in the brainstem; those neurons reach out their axons and bathe the brains in NE.
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| ACH diffuse modulatory system | cells send out long axons and bathe bigger areas of the brain w/ NT; neurons are in discrete, small locations. CHOLiNERGIC (influenced by ACT). BASAL NUCLEUS of MEYNERT = tiny nucleus of ACT-releasing neurons/imp. to learning and memory.
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| Describe the 2nd perceptual stream | dorsal pathway or parietal pathway, goes up into parietal lobes from occipital lobes, gives us the WHERE of something, keeps track of motion and direction
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| Bizarre perceptual distortions can occur if... | strokes, tumors, infections, etc
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| Where is the 2nd visual synapse located? | bet. bipolar cells and ganglion cells
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| Final visual synapse is located... | in the THALAMUS
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| The thalamus uses a lot of ______________. | seratonin
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