Exam 2 Flashcards
Declarative memory
facts, events, places; made possible by hippocampus
Procedural memory
aka non-declarative memory, how to do motor actions
Association cortex
short term memories from the hippocampus go here after about a month
Cerebrum lobes
frontal, parietal, occipital, temporal
Hippocampus
temporal lobe structure, found in medial temporal lobe, has connections with other regions of the brain that hold visual and auditory information, crucial for declarative memory, name derived from sea horse’s genus name
Limbic system structures
sit above the brainstem and between other cerebral structures, memory and emotion
How to keep a group of neurons active for a longer period of time? Is this excitotoxicity?
cell should keep action potential depolarization longer by modifying voltage gated potassium channels so that they are harder to open. Not excitotoxicity because it’s only sustained for a very small amount of time
Short term memory vs long term memory when keeping nerurons active for a longer period of time
working memory requires changes in proteins that are already present; long term memory requires the synthesis of new proteins (ie/ long term potentiation)
membrane channels and learning and memory
either channels are blocked or channels are opened for a longer period of time
Configural learning system
all sense information comes to the hippocampus and then the hippocampus will determine if it will be remembered or not
Entohinal cortex
corticol area which receives sensory information, it will then send it to the configural learning center, associated with the hippocampus but not a part of it, has large cell bodies referred to as pyramidal cells
Perforant path
axons from the entorhinal cortex that synapse onto the dentate gyrus
Dentate gyrus
a part of the hippocampus, looks like a row of teeth or a bite mark, cells are referred to as granule cells due to very small cell bodies
CA1,2,3,4
CA stands for Cornu Ammonius, cells curl around like a ram’s horn, other regions of the hippocampus
Mossy fibers
axons from the dentate gyrus that will synapse on CA3
Schaffer collaterals
axons from CA3 that will synapse with CA1
CA3
sends information to septurm and mammillary bodies, primary output region
Mammillary bodies
a part of the hypothalamus, associated with the hippocampus, damage to the mammilary body cells and hippocampus can be seen with chronic alcoholism and stroke
CA1
communicates with the hippocampus on the other side of the brain
Lomo and Bliss experiment
used rabbit brains to stimulate the performant path and measure the activity of cells in the dentate gyrus
Lomo and Bliss experiment results
low frequency stimulation will lead to low activity in the dentate gyrus (some action potentials, doesn’t depolarize membrane sufficiently), high frequency stimulation of path leads to high activity in dentate gyrus (many action potentials, leads to threshold for which LTP can occur), high frequency of the path wait for a while (1hr, 2hr, 1wk, 1month) and come back with low frequency leads to high activity in the dentate gyrus
Long term potentiation (LTP)
model for change in connection between neurons in the brain, how memories are formed
Which neurons in the brain undergo LTP
all of them
Long term depression (LTD)
process of forgetiing
Threshold for LTP and action potentials
is no the same
Hebb’s law
neurons that fire together wire together, neurons that produce action potentials at the same time will increase their strength of connection
Doggie mice
discovered in 1992, mice that overexpress NMDA receptors, this illustrates how important NMDA is to LTP
> quanta amount of glutamate released
glutamate could still bind to all three of its receptors but it doesn’t mean that enough sodium will enter through AMPA in order to open NMDA, AMPA needs to be open long enough for a depolarization that will open NMDA to allow calcium to enter
Calcium calmodulin complex
protein regulated by calcium, it will take the inactive form of calcium calmodulin kinase 2 and activate it, leads to the activation of adenalyl cyclase
CAM Kinase 2
will autophosphorylate, enzyme
CAM Kinase 2 and AMPA
CAM Kinase 2 will lead to phosphorylation of mechanisms that will insert AMPA receptors into the post synaptic dendrite membrane such that the next time the presynaptic neuron produces an action potential glutamate will bind to more AMPA receptors because the synapse has already been potentiated
Adenalyl cyclase
will take ATP and convert it to cAMP
Kreb
will be activated by a series of enzyme activations of cAMP, will serve as a transcription factor for a multitude of things and increase expression of them
cAMP
cyclic AMP, response element binding protein
BDNF
product of Kreb, brain derived neurotrophic factor, produced by the cell and will make its way to the synapse to bind with TrKB in pre and post synaptic neuron, acts in autocrine and paracrine way to increase the size of the synapse
TrKB
tyrosine kinase B, increases activity/production of F actin
F Actin
main cytostructural protein of a dendrite, will polymerize and increase the surface area of pre and postsynaptic cell
Actin and presynaptic cell
increases the surface area so that there’s an increase in the amount of vesicles that can attach to the presynaptic membrane to release more neurotransmitter
Actin and postsynaptic cell
increase the surface area to increase the amount of receptors on the dendrite membrane
Protein Kinase C
will lower the threshold/sensitivity of calcium channel so that it can easily open; this and the metabolic glutamate transporter will also lead to an increase concentration of calcium
Nitric Oxide synthase
activated by calcium to produce nitric oxide which will diffuse into presynaptic cell from the post synaptic dendrite (retrograde)
Presynaptic cell and nitric oxide
nitric oxide will increase the activity of VGlut
VGlut
vesicular glutamate transport, the channel of the vesicles in the presynaptic cell that glutamate will enter in order to be recycled
VGlut increase activity
the quanta amount of glutamate will then increase within the vesicle such that next time the presynaptic cell reaches an action potential more gluatamate will be released
LTP mechanisms with Glutamate
Calcium and nitric oxide synthase, Calcium calmogulin complex, CAM Kinase 2, Adenalyl cyclase
Names for end of axon
axon terminal, synaptic end knob, synaptic bouton
Why is the end of the axon wider than the rest of the axon
there’re a lot of mitochondria due to high need for energy production, there’re a lot of vesicles which contain neurotransmitters
Vesicles
made by the golgi apparatus in the neuron cell body and they “walk” down the axons of the neuron with the help of microtubules
Synaptic clef
space between neurons, a few nanometers in distance
Presynaptic neuron
cell that releases the neurotransmitter
Vesicle docking site
proteins that will grab onto vesicles in the high density area
Perforated synapse
synapse splits initially due to neurotrophic factor BDNF working through TrKB increasing the size of the synapse by polymerization of F actin and once it reaches a certain size it will split into two axon terminals
Active zone
portion of the end of the presynaptic neuron where axons fuse and exocytosis of neurotransmitter occurs
Perforated synapse and AMPA
all perforated synapses have AMPA receptors
Chemical tag
activity regulated cytoskeletal associated protein attaches to elements like F actin so that BDNF knows which synapse to move to
Hippocampus death and LTP
if the hippocampus dies the ability to undergo LTP also goes
How does the hippocampus die
it’s usually the first structure to go if there’s any damage to the brain due to how vascularized it is and it shows the most default activity within the brain active even when asleep, diseases like viral encephalitis leads to the hippocampus dying
Long term glucocorticoid exposure
cortisol acts in the hippocampus which allows us to remember stressful events better by making LTP easier by increasing calcium levels
Chronic stress
is excitotoxia as prolonged increase of calcium levels in the cell cause apoptosis, this is why a symptom of PTSD is memory loss
Glial scar
when the cells of the hippocampus die a combination of connection tissue and neuroglial cells will fill in
Aplysia californica
marine sea slug about the size of a fist, model system used to study neuroscience
Gill withdrawal reflex
contact to the siphon on the dorsal side will lead to the muscles contracting and skin forcefully closing over it, it’s a two neuron circuit consisting of a sensory neuron and a motor neuron
Neurons of the gill withdrawal reflex
the sensory neuron will send information from the skin to the motor neuron who will move the skin and muscles to protect the siphon
Habituation
decrease in responding after continual stimulation
Sensitization
increase in responding to non-noxious stimulus following a threatening stimulus
Aplysia californica experiment
done by Eric Kandel; touched the siphon with a nonthreatening stimulus such as touching it with glass rod or a little jet of water and after a while the withdrawal relfex would not happen and habituation would occur. they then delivered a shock to the snail at a random location of the body and then touched the siphon with a non threatening stimulus and the snail responded with the gill reflex
Aplysia californica experiment results
the shock modified the activity of the sensory neuron through an axoaxonic synapse on the sensory neuron such that anything that activates the sensory neuron associated with the siphon will activate the motor neuron
Mechanism of gill withdrawal reflex
found by Eric Kandel; the sensory neuron releases glutamate onto the motor neuron and it will be activated causing it to undergo an action potential and contract the muscles.
Sensitization of the gill withdrawal reflex mechanism
serotonin is being released by the facilitating interneuron onto serotonin receptors of the sensory neuron. after serotonin binds to one receptor PLC will cleave PIP2 to make DAG and PIP3. DAG will activate PKC which will lower the threshold of L type voltage gated calcium channels increasing neurotransmission. PKC will also move vesicles containing glutamate closer to the active zone. Serotonin will also bind to another receptor which will activate adenylyl cyclase to make cAMP which will activate cAMP dependent PKA. PKA will lower the threshold of L type voltage gated calcium channels as well as move vesicles closer to the active zone. PKA will act on the potassium channel to make them stay inside the neuron longer to maintain depolarization longer and open voltage gated calcium channels
Serotonin receptor types
g protein coupled receptors
Sensitization of the neurons leads to
next time the sensory neuron is activated by any stimulus it will release glutamate and therefore keep activating the motor neuron leading to the circuit being sensitized
Experiment of giving aplysia californica infections of prozac results
make sensitization of the circuit easier as fluoxetine prevents reuptake of serotonin leading to serotonin being in the synaptic clef
Neurogenesis
neurons are born all the time and most of them come from the hippocampus
Lateral ventricles
are lined by progenitor cells which give rise to amount 1 million new neurons per day and sits next to the hippocampus
How new neurons incorporate themselves into circuits
reinforcement of circuits, reconnections to the other parts of the brain, neurons are born into a spot if it’s needed there
Exercise and hippocampal neurogenesis
exercises leads to the increase of neurogenesis due to an increase of cerebral blood flow and increase insulin sensitivity in the brain
Cerebral blood flow and hippocampal neurogenesis
due to an increase of cerebral blood flow there’s more oxygen and glucose going to the brain
Insulin sensitivity and hippocampal neurogenesis
it’s easier for brain cells to bring in glucose also limiting the chance of type 2 diabetes
Type 2 diabetes and alzheimers
there’re many links between the two, type 2 can cause the blood brain barrier weaker such that infections can easily come in and the immune reaction and inflammation could lead to alzehimers, daily brisk walks appear to reduce alzheimer’s incidences
Exercise and memory
exercise has a lot of protective effects on the brain
Post synaptic neuron
cell that receives the neurotransmitter
Post synaptic density
seen via electron microscopy, a high concentration of proteins within the membrane or waiting to be inserted into the membrane
Neuron parts
cell body, axon, split into collaterals with thousands of axon terminals, thousands of dendritic spines which has branching dendrites
Dendrite
receiving part of the neuron
Synapsis in the body
found in neurological but also in meiosis 1 prophase 1 with gene exchange
Mechanism of neurotransmitter release
action potential reaches axon terminal, voltage gated calcium channels with open in response to about +30mv, calcium will move into the cell and the channel closes, neurotransmitter is diffused into synaptic clef, neurotransmitter binds to receptors located in postsynaptic membrane, neurotransmitters are removed just as soon as it binds, presynaptic neuron will either reuptake or the neurotransmitter will undergo enzymatic degradation by enzymes of postsynaptic neuron
Voltage gated calcium channel types and characteristics
F,L,N, and T; N are open for a normal amount of time, L is open longer, and T are open for a short amount of time, F are open when cell membrane is hyperpolarized
Calcium concentration of neurons
there’s 10000x more concentration of calcium outside than inside the cytosol
Calcium
important second messenger than changes protein conformations, moved out of cytosol by calcium ATPase which is powered by ATP from the mitochondria
Synaptotagmin
protein within the synaptic vesicle membrane, only found in the presynaptic neuron
Synaptotagmin and SNARE
synaptotagmin will change conformation due to calcium and interact with SNARE proteins to pull the vesicle open so that the contents are exposed to the extracellular space (exocytosis)
Ionotropic
receptors that have to be associated with an ion channel, leads to a graded potential
Metabotropic
receptors that aren’t directly linked to an ion channel, leads to receptor tyrosine kinase or G protein coupled receptors
Synaptic delay
from the point of release of neurotransmitters in presynaptic cell to the indication of change of membrane potential in the postsynaptic cell takes about 0.2 milliseconds, this is due to the rate of diffusion and binding to the receptors and incorporation of transmitter into postsynaptic neuron
Excitatory neurotransmitters
increase chance action potential will be produced by postsynaptic cell; does not cause action potential; moves the positive charges towards the axon hillic to increase the likelihood of reaching threshold
Inhibitory neurotransmitters
decrease the change action potential will be produced by postsynaptic cell; does not prevent action potential; draws positive charges away from the axon hillic decreasing the chance of reaching threshold
Monoamine hypothesis of depression
there isn’t enough neurotransmission involved with serotonin (5-HT)
Serotonin and depression
low levels of serotonin transmission leads to depression
Risorine
drug designed to increase the amount of serotonin in the synaptic clef in both the central and peripheral nervous system to lower blood pressure, it was reported that people wouldn’t feel as sad when taking the drug
Serotonin and peripheral nervous system
causes vascular smooth muscle to relax decreasing blood pressure
Tricyclics
three drug classes that treat depression, prevents reuptake of 5HT by inhibiting the transporter protein which would reuptake 5HT increasing the time 5HT was in the synaptic clef and increasing transmission
Tricyclics side effect
also prevents the reuptake of norepinephrine
Norepinephrine
created by the locus ceruleus and is transported everywhere in the brain in response to epinephrine, causes corticol arousal and increases alertness
Locus ceruleus and sleep cycle
the activity of the locus ceruleus decreases as the phases of sleep continue
MAO
monamine oxidase, found generally in postsynaptic membrane to break down serotonin
MAOi
monamine oxidase inhibitor, inhibits enzymatic degradation of serotonin by binding to MAO
MAOi side effect
inhibits the breakdown of norepinephrine leading to more alertness and disturbed sleep cycle
Fluoxetine
reported to be a selective serotonin reuptake inhibiter (SSR), blocks only serotonin transporters
Postsynaptic potentials
are graded potentials
IPSP
inhibitory postsynaptic potential leads to hyperpolarization
EPSP
excitatory postsynaptic potential leads to depolarization; when EPSP reaches threshold action potential will occur
EPSP and IPSP over time
the potential of the membrane over time will fluctuate between IPSP and EPSP
Quanta
the amount of neurotransmitter released by a neuron, under normal circumstances it will be the same amount and the same type of neurotransmitter released by a neuron
Amount of receptors on the postsynaptic membrane
is always the same leading to the same change of membrane
Summation of graded potentials
if a neuron fires once and then again but before the first graded potential is over the second graded potential will begin leading to the graded potentials being summed, allowed because the mechanism for graded potentials is a ligand gated ion channel which is dependent on the concentration of the ligand
Summation of action potentials
cannot happen due to the refractory period which allows for propagation and prevents cytoxicity
Temporal summation
successive firing of an excitatory neuron causing graded potentials to be summed
Spatial summation
more than one neuron firing at the same time interacting with different spots on the postsynaptic membrane leading to graded potentials being summed
IPSP and EPSP firing together
can lead to a lack of net change in the membrane
Temporal and spatial summation
can lead to reaching threshold and an action potential
Axoaxonic synapse
synapse between a presynaptic neuron and a facilitating interneuron which will change whether or not the presynaptic neuron will release neurotransmitters
Autorecetpros
presynaptic neurons have receptors for the neurotransmitter they release so that it is able to detect if it released the neurotransmitter and has a negative feedback response
Agonist
will bind to a receptor and have the same effect as the normal neurotransmitter
Antagonis
binds to a receptor but doesn’t activate it, it will bind to the side or sit in the channel to block it
Drugs and autoreceptors
there’re drugs that will interact with autoreceptors so that the autoreceptor doesn’t tell the neuron that it is releasing the neurotransmitter leading to a break in negative feedback loop
Neuromodulator
molecule released by a neuron that acts on multiple cells through diffusion
Adenosine
is a neuromodulator, binds to receptors and shuts down neuroactivity around it, levels of adenosine build up due to higher metabolism of ATP
Caffeine
antagonist for adenosine receptors, keeps cAMP in neurons by inhibiting phosphodiesterase
Acetylcholine
exciatatory neurotransmitter, when released by motor neurons onto skeletal muscle cells it will cause skeletal muscle contractions
Fostridium tetni
tetanus produces a toxin which leads to tetanic paralysis, this suggest that the toxin facilitates the interaction between SNARE and synpatotaged without the need of calcium leading to a high amount of acetylcholine release, effects the masseter causing lock jaw
Tetanic paralysis
sustained muscle contraction
Botulinum toxin
causes flaccid paralysis by preventing the release of acetylcholine by locking SNARE proteins leading to them unable to react with synaptotagmin, can be used medicinally for chronic cramping or cosmetically to prevent contraction of muscles leading to less pronounced wrinkles
Flaccid paralysis
inability to have muscle contractions
Black widow spider
produces a venom which leads to motor neurons getting rid of all acetylcholine at once so that the stores of acetylcholine are lost, initially causes tetanic paralysis then flaccid paralysis
Blow darts
have curare on the tips of the darts which is a fast acting antagonist for the acetylcholine receptor causing flaccid paralysis
Nicotine
agonist for acetylcholine receptors in the central nervous system, leads to increase of alertness
Nicotinic acetylcholine receptor
controls sodium channel
Sarin nerve gas
inhibits acetylcholinesterase which breaks down acetylcholine leading to an increased expression of acetylcholine causing tetanic paralysis
Myasthenia gravis
antibodies are made against acetylcholine receptor leading to flaccid paralysis, almost always starts on the left side of the face, will eventually lead to suffocation due to the diaphragm being effected
Glutamate
derived from glutamic acid, excitatory neurotransmitter, all vertebraet species use this as a primary excitatory neurotransmitter
Glutamate receptor
AMPA, NMDA, metabotropic glutamate receptor
AMPA
ligand gated, ionic tropic, channel for sodium
NMDA
ligand and voltage gated, there has to be a depolarization of 20-30mv, magnesium sits in the pore of the channel, once it’s released calcium will enter, there have to be enough sodium ions to have entered through AMPA to cause depolarization
Metabotropic glutamate receptor
G protein coupled receptor, glutamate will bind, then the alpha subunit will activate phospholipase C which will break down a the membrane phospholipid PIP2 into DAG and IP3, DAG will stay in the membrane and activate protein kinase C which will lower the threshold of voltage gated calcium channels making it easier for calcium to enter, IP3 will move to the cell body and act as a ligand for calcium channels in the ER
DAG
diacylglycerol
IP3
inositol tris phosphate
Dopaminsergic
neuron that produces and releases dopamine
Dopamine
involved in modd, effects learning and memory processes, culprit in parkinsons, reinforces and reward system
Ventral tegmental area
holds a lot of dopaminergic neurons which will release dopamine on o the nucleus accumbous ending to the reward and reinforcement circuit
Olds and Milder
operantly conditioned rodents pushed down a bar in order to receive an electrical stimulation of the nucleus accumbous to lead to an action potential mimicking dopamine, the rodents eventually disregarded the need for food, water, and reproduction
Opiods
resembles dopamine and leads to a sense of euphoria
GABA
gamma amino butyric acid, released by a facilitating interneuron onto the presynaptic dopaminsergic neuron, primary inhibitory neurotransmitter, opens channels for chloride at the presynaptic neuron which will lower membrane potential and lower the amount of dopamine being released
Opioid receptors
Delta or Kappa receptors, are on the facilitating interneuron, when an opioid binds it shuts off the neurotransmission of GABA and lead to the presynaptic neuron releasing dopamine in higher amounts due
Endorphins
natural effect of shutting off GABA release
Tolerance and downregulation
if the body anticipates something there’s downregulation and inactivation of the receptors which bind to that thing
Downregulation of Delta or Kappa receptors
leads to the need for taking more of an opioid, the higher concentration of the substance for a fewer amount of receptors
How drugs affect neurotransmission
increase leakage of neurotransmitter from vesicles in the cytoplasm lead to breakdown, increase transmitter release into the clef (tetanic tetni), block transmitter release (botulinum toxin), inhibit transmitter synthesis (amino acids, proteins which are made), block transmitter reuptake (SSRI, tricyclics), block clef enzymes that metabolize transmitter (MAOi, serin nerve gas), bind to receptors on postsynaptic membrane lead to antagonis to agonist transmitter action (nicotine: agaonist, curare: antagonist), inhibit or stimulate second messanger activity within postsynaptic cell (caffeine with cAMP)
