SFS - Motor Learning / Ataxia

Start Studying!

Terms

undefined, object

copy deck

Outer region of the cerebellar cortex: Molecular layer
In the molecular layer, parallel fibers synapse with the __________.: dendrites of the Purkinje cells. Inhibitory neurons, such as the stellate and basket cells are here as well.
Site of the cell bodies for the granule cells. (take a wild guess): granular cell layer
Excitatory inputs into the cerebellum: Climbing fibers (olivary nucleus) and mossy fibers (series of diff. tracts)
Information from cortex through Purkinje cell and input to the deep cerebellar nuclei is inhibitory or excitatory?: inhibitory
Only cells that use glutamate in the cerebellar cortex: granule cells
When does the peak amplitude of the conditioned response occur in rabbits?: at about the time of the unconditional stimulus onset
The peak amplitude of the response in the motor nuclei occurs when?: When the US takes place
What was the logic that learning does not occur at the motor nuclei (in the eyeblink response)?: It would be difficult to coordinate them all at once. Therefore the neuronal model must occur upstream to allow for synchronous activation of the motor nuclei.
Nucleus with the most robust response during the eyeblink learning experiment...: Interpositus nucleus
What sends mossy fibers to the cerebellum?: pontine nucleus
The Golgi cell synapses on which cell modulating input from the mossy fiber?: granule cell
The granule cells send axons that form what fibers?: parallel, which form synapses in the molecular cell layer
Which fibers bifurcate and form excitatory synapses on the Purkinje cells and the other interneurons?: parallel
The excitatory signal onto the Purkinje cell causes it to release _______ onto its target, the ___________ nucleus.: GABA; interpositus
If you lesion the mossy fibers coming from the pontine nucleus, you eliminate the _________ response.: conditioned
The inferior olivary nucleus sends info to the Purkinje cell through what fiber?: climbing, also sends collaterals to the interpositus
Direct stimulation of what can substitute for the conditioned stimulus?: mossy fibers or the pontine nucleus
Direct stimulation of what can serve to replace the puff or schock to the eye?: the olive
Lesions to the climbing fibers will block the __________ response.: conditioned
As animal begins to learn and remember eyepuff, there is less activation of what?: inferior olive
Over training the interpositus n. will tone down input from what?: climbing fibers
What is blocking?: Pairing of the 1st CS, with a 2nd CS. Referred to as blocking becuase the 1st CS will activate the inhibitory projections of the interpositus n. back to the inferior olive. 2nd CS cannot be learned. To the animal, the airpuff is still occuring in response to the tone. The 2nd CS (light) is blocked.
What has direct input to the facial nucleus and indirect input to the facial n. through the reticular formation?: trigeminal n.
If you lesion the climbing fibers and mossy fibers, will it affect the UR?: no
What is the key structure for the CR?: interpositus nucleus
Will lesions in the interpositus nucleus block: a. the CR? b. the UR?: a. yes
b. no
Can lesion studies distinguish between the sites important for induction of memory and sites of storage of memory?: No, if you prevent info from entering in the first place, it can't be stored. DUH.
Studies that infuse an inactivator which exerts its inactivation effets for 1 or 2 hours and determine where along pathway that memory is stored.: Reversible inactivation studies.
Do you prevent learning if you inactivate the red n. and the cranial nerve motor nuclei?: NO. You can still train the animal and it will still express the CR after recovery.
When the interpositus nucleus was reversibly inhibited, what was observed?: No learning and memory
When the cerebellar cortex was reversibly inhibited, what was observed?: No learning and memory
Location of sites of memory storage for the eyeblink response?: interpositus nucleus and the cerebellar cortex
What encodes contextual into about the CS?: Parallel fibers
Learning, teaching, reinforcement, and error correction system sending info into the deep cerebellar nuclei: Climbing fibers
What receives excitatory input from CN V and inhibitory input from IPN?: Inf. olivary nucleus
Receptors in excitatory synapses between purkinje cells and climbing or parallel fibers.: AMPA
Also have metabotropic glutamate receptors coupled to PLC: parallel fiber synapses
Co-activation of what fibers will lead to a robust response of the Purkinje cell: mossy and parallel
Important in reinforcement and error correction: climbing fibers
Depression in the purkinje cell response is dependent on...: Ca++ transience
Phosphorylation of AMPA receptors results in...: internalization of receptors and, thus, a decreased response to future stimulation
Knockout of mGluR1 will result in a defective ____________: eyeblink response
Inability to coordinate muscles. Irregular muscle movements that can be seen in distal limbs. Could be present as dysmetria in the arms: Ataxia
Causes of cerebellar acute ataxia: toxic ingestions, ischemia or hemorrhagic stroke
Causes of chronic ataxia: alcoholism, MS, inherited cerebellar degenerative disorders
Medial cerebellar lesions can result in _______ ataxia, while lateral cerebellar lestions can result in _________.: truncal; dysmetria
T or F. Ataxia is IPSI.: True, due to double crossover
Flocculonodular lobe lesions cause...: oculomotor disturbances, balance, and eye movement
Medial/vermal cerebellar lesions result in....: dysarthria, changes in face muslces, inability to chew, problems with gait, respiration, and stance.
Zones of cerebellum thought of as being smarter and used in more complex functions.: intermediate and lateral zones
Tremor induced by movement: intension tremor
What is anticipation?: Offspring of patients get worse with subseuent generations. Phenotype gets worse. Ex. trinucleotide repeat expansion disorders
Hypothesized to mediate protein-protein aggregates.: PolyQ (glutamine) stretches (CAG codons)
Examination of SCA1 demonstrated that _______ _______ of the mutant proten was more important than its ability to form an aggregate: nuclear localization
Possible explanation for CAG expansion: DNA slips and adds extra repeats, post DNA replication change causing through phenomenon such as DNA breaks. Extra copies added in attempt to fix break.
If chaperones can't keeep CAG expanded proteins folded, what might be activated in the cell?: caspases and ubiquitinases.
Does the ubiquitin/proteosome pathway seem to celar the abnormal proteins?: No, which leads to aggregations in the cells...and cause the problem. Aggregates could activate the mitochondial apoptotic pathways as well.
Inherited ataxia characterized by lesions within the cerebellum. Can also affect things outside the cerebellum.: SCA - spino-cerebellar ataxia

Start Studying!

Deck Info

Number of cards 59