Conte-Exam MBV4340 / 9340 – June 2012 Page 1 UNIVERSITY OF

Conte-Exam MBV4340 / 9340 – June 2012
Page 1
UNIVERSITY OF OSLO
Faculty of Mathematics and Natural Sciences
New exam in MBV4340/ MBV9340 Advanced Neurobiology
Day of exam: Tuesday June 18
Exam hours: 09.00 – 12.00
This examination paper consists of 3 pages.
Appendices: None
Permitted materials: None
Make sure that your copy of this examination paperis complete before answering.
Part A: Please answer 5 of the following 6 questions (short answers):
A1: Make a sketch of a synapse and briefly explain the term "tripartite synapse". What is the
main functions of glia cells in the brain ?
A2: Why is impaired function of K+ channels often associated with epilepsy ?
A3: What is a critical period for plasticity ? Please give one example or describe an
experiment demonstrating the critical period.
A4: Does all people have the same amount and the same ratio of M & L cones ?
How can you “see” yellow light when you don’t have any cones specialized for the
wavelength of yellow light ?
A5: A topographic map is the ordered projection of a sensory surface, like the retina or the
skin, to one or more structures in the central nervous system. E.g. adjacent spots on the
retina are represented by adjacent neurons in the primary visual cortex. Are hippocampal
place cells organized in the same manner? (Don’t forget to explain what a place cell is.)
A6: You are recording extracellular currents from five neurons and from the recording you see
the spikes when a neuron is firing an action potential. Draw a “recording-trace” for each
neuron during awake and slow-wave sleep and underneath draw a trace with the “sum” of
the activity. How does this sum relate to what you record with a scalp electrode ?
Part B: Please answer all questions below (more comprehensive answers compared to part A):
B1: You are conducting a patch-clamp experiment with frog oocytes that express voltagegated Na+ channels. You start out in cell-attached mode and record current through a
single voltage-gated Na+ channel. You have a separate stimulation electrode inside the
cell and use that to make a long-lasting depolarising square pulse. (a) Draw 4-5 lines
of the current you measure, and draw a trace of the sum of the currents. (b) Next, you
make a hole in the cell and record the macroscopic current in the whole-cell mode.
Explain the similarity between the current response seen here and the summed current
in (a).
B2: What is LTP? Describe a classical experiment demonstrating LTP. What are the main
molecular mechanisms underlying early-phase and late phase LTP.
B3: Cortical gamma oscillations (20-120 Hz) increase during attention and memory-tasks.
Failure in gamma oscillations is a hallmark of neurological and psychiatric diseases.
B 3.1 Based on these observations, can we conclude that it is a correlational or causal link
between gamma oscillations and cognitive function? What is the best scientific prove
(correlational or causal) ?
B 3.2 Current theory predicts that gamma oscillations are generated by synchronous activity
of fast-spiking inhibitory interneurons. Cardin et al. (2009) managed to get Channel
Rhodopsin expressed selectively in fast-spiking PV interneurons. What happened
when they stimulated these cells by light? Explain figure 2d where you see the effect
of light flash on one such interneuron (FS) and the effect of whisker stimulation on a
nearby pyramidal cell (RS) (figure 2d).
B 3.3 Furthermore, when the blue light was flashing every 25th ms (40Hz) they also
observed an effect on the oscillations seen in the local field potential (LFP).
Explain figure 3 a and c. Explain how this experiment supports their conclusion: “Our
results provide the first causal demonstration of cortical oscillations induced by celltype-specific
activation.”
Figure 2d: Light-evoked
activity in FS-PV1 inhibitory
interneurons suppresses
sensory processing in nearby
excitatory neurons.
Figure 3 a&c: FS
inhibitory interneurons
generate gamma
oscillations in the local
cortical network.