Week 7 Flashcards
Why might sensory perception be considered an active process?
Sensory information are used to generate or update motor commands. Thus sensory perception takes place in the context of an active sensorimotor loop.
How can we map presynaptic neurons (e.g. premotor neurons)?
Rabies virus can be engineered to express fluorescent proteins and can be injected into muscle, being taken up by presynaptic terminals and retrogradely transported to the cell bodies of the motor neurons. The rabies virus can be further utilized to jump one synapse back by complementing them with a missing factor
What data suggest that primary somatosensory cortex participates in the conversion of a whisker sensory stimulus into licking motor output in the whisker detection task of Sachidhanandam et al., 2013?
How does reward-based learning occur in the brain?
Sensory input => (performing motor output => reward)
It works by increasing the connection of sensory input to motor output through long-term potentiation and synaptic plasticity.
When do dopamine neurons fire action potentials?
PHASIC dopamine signals seem to be the earliest indication of reward
When there is ‘unexpected’ reward, dopaminergic neurons fire. Over time, we instead see sensory neurons to motor neurons pathway fire.
Where/What are dopaminergic neurons? What are the two types and the differences between?
Most prominently innervate the striatum. They couple through G proteins. They have no obvious post-synaptic site => dopamine comes from diffusion.
one type has TYPE I receptors:
- cortex -> direct striatal projection neurons
- inhibit the SNr (substantia nigra pars reticulate)
- strengthens the inhibitory “direct striatonigral pathway”
- signal G(s) and G(off)
- signal through a variety of pathways (eg. adenylate cyclase -> cAMP)
other has TYPE II:
- cortex -> indirect striatal projection neurons
- innervate globus pallidus
- weakens the inhibitory “indirect striatopallidal pathway”
- signal through G(i) and G(o),
- INHIBITION of adenylate cyclase => less cAMP
What causes Parkinson’s disease? What treatments currently exist?
The degeneration of the dopaminergic neurons in the SNc (Substantia bigra pars compacta).
Result of drugs which damage SNc (eg MPTP which is metabolised to MPP+), or genetics:
- alpha-synuclein
- LARK2 gene variants causing increased kinase activity
Treatments:
L-DOPA can cross blood-brain barrier and become Dopamine via DOPA decarboxylase
DBS: electrical stimulation in STN (subthalamic nucleus)
In EU how many people suffer from Parkinsons, what is cost?
1mil, €14bn
How might DBS work?
- Weakens STN (which fires the SNr through glutamate, which in turn normally inhibits brain stem)
- Stimulates cortex axons which reach STN
- Maybe the 100Hz frequency disrupts the low frequency beta oscillations of Parkinsons patients.
What is the psychophysical psychometric function?
False alarms vs hits on the plot of stimulus strength (x) vs Prob(response) (y). We want hits to be well above false alarms!
Diagrammate the two pathways of dopaminergic neurons
