NEU Quiz 4/6 - Hearing and Plasticity Flashcards
Neuroplasticity and Synaptic strength definiton
Ability of brain to form or change synaptic connections
- Our brain’s ability to change with experience
- Do not have static brains, can alter connections
- Synaptic plasticity leads to changes in circuit function
- Observed at both Pre and Postsynaptic (number of receptors that NT binds to can change, and how long ion channels stay open) locations
Number of neurons don’t change after born but explosion of synapses that you can refine over your lifetime
Synaptic strength: Average amount of voltage produced in a postsynaptic neuron by an AP in a presynaptic neuron. Takes less input from pre to have a response in the post. Way to increase the amount of action potential in the post.
Various temporal components of synaptic plasticity, long vs short
Short term
- Seconds to minutes
- Post-translational modification of existing proteins (add a group like methylation to make it an active protein)
Long term
- Hours to days to years
- Changes in gene expression (increase of transcription)
- Protein synthesis
- Growth of new synapses
In mammals, what is the typical brain area that is studied when examining synaptic plasticity? Why is this a particularly interesting area? How, in a brain slice with this area present, do researchers elicit long term potentiation?
Synaptic plasticity is change that occurs at synapses, the junctions between neurons that allow them to communicate.
Process by which neuronal activity results in changes in the strength of connections between neurons, and it is important for learning and memory within the hippocampus
Long-term plasticity can bidirectionally modify synaptic strength—either enhancing (LTP, long-term potentiation) or depressing (LTD, long-term depression).
Hippocampus Functions: Role in memory (spatial, facts, events) (episodic memory) AND role in learning — Spatial navigation → place cells
Dentate gyrus and olfactory bulb → new neurons can possibly be made here –> Excite a pathway to elicit a long term potentiation
C1 measure changes in synaptic strength
Easy circuit to manipulate and examine changes in synaptic strength
Neuronal plasticity is frequently studied in “hippocampal slices”
In such slices, several intra-hippocampal circuits remain intact
In layman’s terms, what is Donald Hebb’s rule?
Cells that fire together, wire together” and, more formally, “any two cells or systems of cells that are repeatedly active at the same time will tend to become ‘associated,’ so that activity in one facilitates activity in the other”.
When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.
More simply: Neurons that fire together, wire together
Cell A and Cell B is strengthen together
Glutamate Receptors and Mechanism of LTP Initiation
AMPA (open active state) - glutamate binds
Ionotropic
Ligand gated
Allows Na+/K+ to pass
Causing depolarization whenever AMPA is open
NMDA - glutamate binds
Ionotropic
Ligand AND voltage gated
Mg2+ blocks
Allows Na+/Ca2/K+ to pass
Membrane needs to become positive enough to repel the magnesium block
Calcium - intracellular second messenger leads to increase in gene transcription
Because magnesium ions are dislodged from the NMDA receptor’s pore when the postsynaptic cell is strongly depolarized
Easier for postsynaptic cell to be depolarized and unblocks magnesium from the NMDA receptor more quickly and that increase depolarization to where you could reach reach threshold for a AP in a postsynaptic cell more easily
When neurotransmitter molecules bind to receptors in the plasma membrane of the receiving neuron, the receiving neuron becomes more negative inside. the receiving neuron becomes more positive inside. ion channels in the plasma membrane of the sending neuron open.
dendrites
Effect of Glutamate release on dendritic spines of postsynaptic neurons
LTP → Increase spine growth
The stabilization of LTP requires protein synthesis
At least some of this protein synthesis may occur in the dendrites, as suggested by the presence of dendritic ribosomes
Dendritic protein synthesis is needed for hippocampal LTP
Blocking protein synthesis with emetine blocks LTP stabilization but not its induction
What is necessary to elicit long-lasting LTP?
Long-term sensitization requires the transcription factor CREB
- Transcription Factor = protein that helps start transcription
- CREB activated after serotonin received
- CREB binds CRE near various genes (DNA)
- New proteins made: increase axon terminal size AND sprout new synapses
- Lasts hours-days
Long-term potentiation, or LTP, is a process by which synaptic connections between neurons become stronger with frequent activation. LTP is thought to be a way in which the brain changes in response to experience, and thus may be an mechanism underlying learning and memory.
The type of receptor that is critical for the induction of hippocampal LTP, admitting calcium into a dendritic spine, is called a(n)
NMDA receptor
Which statement about LTP is false?
LTP involves an enhancement in synaptic efficacy that can last for hours, days, weeks or even longer.
If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and another nearby synapse (B) on the same dendrite is weakly stimulated at the same time, then the second synapse (B) will also show LTP.
If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and a nearby synapse (B) on the same cell is weakly stimulated a few seconds later, then the second synapse (B) will also show LTP.
The requirement for coincident pre- and postsynaptic activity was predicted by Donald Hebb in 1949.
If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and a nearby synapse (B) on the same cell is weakly stimulated a few seconds later, then the second synapse (B) will also show LTP.
Which molecule binds NMDA receptors and prevents the flow of ions at resting and hyperpolarized membrane potentials?
Glutamate
What is the immediate consequence of Mg2+ blockade removal from the NMDA receptors?
Ca2+ influx into the post synaptic terminal
LTP represents a lasting increase in the size of EPSP
following a high frequency train of stimuli
Which condition(s) must be met to induce LTP?
Glutamate must be released from the presynaptic terminal.
Glutamate must open the postsynaptic AMPA receptors.
The postsynaptic membrane must be depolarized for a period of time.
Mg2+ block must be expelled from NMDA receptors to allow Ca2+ influx.
What triggers LTD
Low frequency stimulation followed by slow or small increase in Ca2+
Which mechanism used in hippocampal LTD is not part of the hippocampal LTP mechanism
Calcium dependent activation of protein phosphatases
What would happen if Mg2+ was not expelled from NMDA channels?
LTP would not occur
What is the mechanism of LTP expression?
Increase in the number of postsynaptic AMPA receptors
which brain area is important for memory?
hippocampus
What are the two main qualities of sound? How are they measured?
Sounds are audible variations in air pressure. Properties are frequency and amplitude. Units are Hertz (Hz) which is cycles per second. Pitch is determined by frequency. Intensity/amplitude determines loudness.
Sound waves have frequency; that is, the pitch of sounds goes up or down. The amplitude of a sound determines its volume (loudness). Tone is a measure of the quality of a sound wave.
Outer ear
Outer ear:
Auricle: Funnels sound wave
External auditory meatus: Connects auricle with eardrum, Contains cerumen from ceruminous glands (earwax), Wax traps foreign bodies and repels insects, Carries sound to eardrum
Tympanic Membrane : Eardrum, Between outer and middle ear, Vibrates in response to sound waves
Order of Events in Hearing
- Sound wave travels through external auditory meatus (ear canal)
- Tympanic membrane vibrates (ear drum)
- Auditory ossicles vibrate – (transferring sound from air medium to liquid medium –> increase the power of the sound)
- Stapes vibrates oval window, causing vibration of fluid
- Frequencies that are outside of our hearing end up traveling all the way through the cochlea and not activating any hair cells
- Frequencies within the hearing range activate specific parts of the pathway –> sound waves of high freq maximally cause vibration/movement of the base of the basilar membrane. Sound waves of low freq maximally cause vibration/movement of the apex of the b.m.
- Basilar membrane movement causes the organ of corti (has the hair cells) to move upward, this upward movement causes the hair cells to move/shear against the tectorial membrane
- The stereocilia, which are stuck into the tectorial membrane, are bent towards the tallest stereocilium at the peak waveform
- Bending of the stereocilia causes the tip links to stretch, opening in the hMET channels (mechanically gated cation channels)
- K+ and Ca2+ enter through the channels on the stereocilia, depolarizing the membrane (K+ is high in endolymph,
enters stereocilia with its conc gradient) - VG calcium channels in the hair cell body open, calcium rushes in, vesicles fuse with membrane
- (AT THE SAME TIME: K+ in the hair cell body leaves with its concentration gradient (which is low extacell in the
perilymph) through the K+ leak channels located in the cell body) - Glutamate is released onto the peripheral process of the spiral ganglion cell
- If reaches threshold, spiral ganglion cell sends action potentials through auditory nerve
- Auditory n –> ventral cochlear n. –> left and right SOC –> left and right inferior colliculus –> left and right medial geniculate nucleus –> left and right A1
Cochlea: Organ of Corti
inner ear
receptor of the ear and does electrical impulses
Within scala media → has organ of corti in this chamber
Sits on basilar membrane
Vibration of membrane moves hair cells
Hair cells = sensory/afferent receptors for sound
Inner afferent send signals to brain
Efferent help sculpt activity
Stereocilia – stick out of top of cells
Connected by tip links – open/close channels
Primary Auditory Cortex – A1 is major target at ascending axons from MGN with conscious sound perception and recognition of speech sound and music
Primary Auditory Cortex also called core region
Superior gyrus of temporal lobe
Tonotopically organized - bundles
Receives information from both ears
What structure within the inner ear contains the auditory receptors? What membrane does it sit on
Organ of Corti, sits on the basilar membrane and covered by tectorial membrane.
