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Questions for Journal Club Participants (SPRING 2014)

Feb. 3, 2014. Kirsch et al. (2006) Oxytocin modulates neural circuitry ....

  1. 1. Describe the chemical properties of oxytocin. What other molecules share similar characteristics? 
  2. 2. What kinds of behaviors do increases/decreases in oxytocin levels produce, based on previous animal studies? How valid is it to assume oxytocin directly causes these behaviors?
  3. 3. What concerns do you have about the procedure (subjects, measuring methods, etc...): Is an fMRI a good enough technique for this study? Should women have been used too?
  4. 4. Based on this and previous studies mentioned, what role does the amygdala AND oxytocin play in fear and prosocial behavior?
  5. 5. What are some implications of the knowledge gained from this study? What sort of future directions could we go?

Feb. 8, 2014. Creating False Memories

  1. 1. Describe the anatomy of the hippocampus proper. What are the features of the areas of interest for this paper, the DG and CA1?
  2. 2. What are the advantages of using optogenetic stimulation in experiments compared to traditional methods of electrical stimulation. ?
  3. 3. How do stored and newly formed memories compete and interfere with each other? What problems does this cause? Are there any advantages to the interplay between memories?
  4. 4. The authors mention a potential application for these findings to subconscious and internal false memory formation and expression in humans.  Do you think there is a clinical application for what they have discovered?

Feb 24, 2014. Normal Gut Microbiota Modulates Brain Development.

  1. Describe the differences between synaptophysin and PSD-95 protein.
  2. How convincing are the results? Can you think of additional biochemical methods and/or experiments that could be factored into this study to produce more informative conclusions?
  3. Can you think of at least FIVE factors that can produced variation in a core human microbiome?
  4. Do you think the overuse of antibiotics could affect the brain development of human infants? Explain your reasoning..
  5. What is the significance of the data and results gained from this study? What future directions or experiments could be done?be done?

    -- Christopher Hwu Cornell University Class of 2014 College of Arts and Sciences

    -- Nischay Shah - Cornell University Class of 2014 College of Arts and Sciences

March 3, 2014. Dopaminergic modulationofmemoryandaffectiveprocessingin Parkinsondepression

  1. What effects does Parkinson’s disease have on a healthy working brain in regards to dopamine levels and general cognitive ability?
  2. The study found that depressed Parkinson’s disease patients were significantly younger and scored significantly lower in tests when compared to non-depressed patients. How might the age of patients impact their level of depression and does this effect the credibility of the results?
  3. What kinds of responsibilities do doctors have in regards to administering future Parkinson’s patients with particular medical regimens?
  4. What kinds of responsibilities do pharmaceutical companies have in making new Parkinson’s medication available to the public before all possible side effects are tested for and analyzed? For instance, should pharmaceutical companies hold off on releasing a potentially effective drug if they are not sure about how or for whom it will work best or should they release such drugs with a disclosure regarding potential effects on patients with depression?

March 10, 2014. Chen et al. (2013) Rescuing cocaine-induced prefrontal cortex hypoactivity prevents compulsive cocaine seeking. Nature 496:359-362.

1. How does cocaine affect the brain initially, and what brain regions are most affected?

2. Why did the authors chose the prelimbic cortex as the region of interest, and what are the main roles of the prelimbic cortex? What brain areas in humans did they say it might be similar to?

3. What promoter region did the authors use for their optogenetic experiments, and why was this promoter region chosen

4. What is the difference between ChR2 and eNpHR3.0? Why did the authors choose these two?

March 16, 2014. Mesgarani et al. (2014) Phonetic feature encoding in the humn brain. Science. 343, 1006 DOI:10.1126/science.1245994

1. Describe the superior temporal gyrus. Why did the researchers choose to focus on this area?

2. What is a phoneme? Define voice-onset time (VOT), spectral peak, and formants (F0, F1-F4).

3. Why did the authors choose to analyze high-gamma cortical surface field potentials? How do their measurements differ from single-unit recordings?

4. What are the implications of this study? Consider the fact that Edward Chang is interested in epilepsy and neuroprosthetics.

( From: Isabelle and Erika)

March 24, 2014. Soria-Gomez, Edgar et al., (2014) The endocannabinoid system controls food intake

1. How are the various cells referred to in the paper arrange into a neural circuit in the olfactory bulb? For example, how are the olfactory receptors, the mitral cells, the granule cells, the periglomerular cells connected, and where are the excitatory and inhibitory synapses? What are the input cells and the output cells in this circuit and how is this circuitry positioned relative to the olfactory epithelium and the glomeruli?

2. What are CB1 receptors and how do they affect glutamate transmission?

3. What is the effect of THC on the activation of the granule cell layer of the olfactory bulb and how does this affects food intake. (Hint: look at “CB1 signalling in the MOB couples olfaction to feeding”)

4. How did the authors make a direct test the effect of cannabinoid signaling on glutamatergic transmission from the Anterior Olfactory Nucleus /Anterior Piriform Cortex to the Main Olfactory Bulb? What about this method made it a direct test?

5. In the discussion, the authors mention the possible effect that THC has on memory processes, and how this might alter odour detection. Do you think THC’s effect on memory affected the results? Why or why not?

(- Iha and Rachel)

Zhang et al (2013) Regulation of AMPA receptor surface a cognitive enhancer..

1.) What type of cells are used in the study? Why are these type of cells used to study antidepressant drug effects? How do they relate to affective function?

2.) Briefly, how does AMPA receptor regulation contribute to “stronger” or “weaker” synapses? What kind of receptor is an AMPA receptor?

3.) Elements of a possible mechanism identified in the study include CaMKII, Stargazin, and PSD-95. Briefly, what is the role of each of these in the context of this study.

4.) How might chronic stress and acute stress affect the quantity and type of glutamate receptors at a synapse, and corresponding glutamatergic transmission?

5.) From the results on the effect of tianeptine on stress-induced changes in glutamatergic transmission, would it be advisable to administer the drug to chronically stressed individuals that do not yet present a DSM-criteria-satisfying disorder? How might mood/behavioral changes in response to stressful environments be advantageous?

Henderson et al (2013) Hippocampal neurons inhibit meal onset. Hippocampus 23:100.

1. Why did the authors target hippocampal neurons to study post-prandial intermeal interval (ppIMI) time variance? 
2. What functional distinction exists between the dorsal and ventral hippocampus, and why did the authors choose the dorsal region for muscimol infusion?
3. Why was only one side of the hippocampus infused with muscimol/PBS as opposed to bilateral infusion?
4. What factors might account for the differential effects of hippocampal lesions and muscimol-induced inhibition on meal onset?
5. How could the hippocampus be involved in a "vicious cycle" of overeating as supported by the results of the study?

Ziv, Y. et al. (2013) Long-term dynamics of CA1 hippocampal place codes. Nature Neurosci. 10 Feb., 2013.

    1. What are place cells and how would you characterize them? Where, eactly, are they found in the brain, and what kind of cell are they?
    2. What is the optical imaging method used in this study? Briefly describe how it works.
    3. What is the overall objective, question, or hypothesis of this study?
    4. How did the authors test whether the 15-25% place cell recurrence was sufficient to determine the mouse’s location?
    5. Why is this paper so progressive, what does this contribute/mean to future neuroscience research?
    6. What are some potential flaws or weaknesses in this paper? What future experiments could these neurobiologists do to improve their results?

    Suzy Xu and Emika Lisberger

Charlesworth, JD et al (2012) Covert skill learning in a cortical-basal ganglia circuit. Nature 486:251.

    1. In the "actor-critic" models of reinforcement learning three events must occur for learning to occur. What are these three events and how do they influence learning?
    2. The authors refer to "covert skill learning" in their paper. Why exactly do they say the learning is covert?
    3. The authors use birdsong as an example of learned behavior. What is the evidence that birds actually learn their songs?
    4. The authors claim that birds will learn how to change their songs without having the basal ganglia or anterior forebrain pathways contribute to skill practice. Does this violate the actor critic model of learning?
    5. Suppose that APV does not eliminate all connections between the anterior forebrain pathway and nucleus RA (primary motor cortex),. but merely reduces or blocks some of the connections? What could you conclude about covert learning if this were the case?

Ann Kennedy, Greg Wayne, Patrick Kaifosh, Karina Alviña, Larry F Abbott & Nathaniel B Sawtell (2014) A temporal basis for predicting the sensory consequences of motor commands in an electric fish. Nat. Neurosci. 19 (3): 416-22.
May 5, 2014

1)  We usually associate feed-forward control in our nervous system with motor systems and with the cerebellum.  For example, motor control systems often have a direct pathway to the muscles and an indirect pathway to the muscles via the cerebellum.  The indirect pathway is continuously adjusted and refined based upon errors in the movement outcome.  What about sensory systems? Could a sensory system be made better if the brain were able to make predictions about the sensory consequences of our actions and use them to anticipate and perhaps subtract expected sensations that are simply a consequence of our motor acts?  Give an example where a human sensory system could be improved by feed-forward (predictive) control.

2) The electric fish electro sensory lateral line lobe (ELL) is a cerebellum-like structure.   Which of the structures mentioned in Fig. 1b or in the associated text are found in both the ELL and cerebellum, and what are the names typically used in cerebellum?



    Medium ganglion cells  


    Granule cells


    Golgi cells


    Unipolar brush cells


    Sensory afferents


    Mossy fibers     


    Parallel fibers


    Molecular layer


3) The paper talks about a corollary discharge of the electric organ discharge signal.  What exactly is a corollary discharge?  Can you site an example of a corollary discharge in a mammalian or avian nervous system?

4) What is a the benefit of being able to form a negative image of an expected sensory response locked to a motor act?

5) The authors of this paper were attempting to explain how spike inputs from parallel fibers onto the dendrites of medium ganglion cells might persist for more than 200 milliseconds following the EOD command – the typical time that negative images are formed.  What is their conclusion for how this long, persistent discharge is sustained?




BioNB 4110


© Carl D. Hopkins | e-mail
Department of Neurobiology and Behavior
Ithaca, New York