Neuro 26 name: Introduction to Neuroscience Test #2, Spring 2011 Prof. Baird’s Part 72 points Suggested time: 1 hour 25 minutes. Answer question 1 on this sheet. Put all other answers to Prof. Baird’s part in one blue book



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Neuro 26 NAME: _____________

Introduction to Neuroscience

Test #2, Spring 2011

Prof. Baird’s Part - 72 points Suggested time: 1 hour 25 minutes.

Answer question 1 on this sheet. Put all other answers to Prof. Baird’s part in one blue book. Put your name on the front and label it “Prof. Baird”
1. [30 points] Link the neurotransmitter to its receptor(s) and associated synthesis precursors and enzymes, metabolites, receptors, and postsynaptic signaling pathways. Also provide the name of either a direct or indirect agonist or antagonist of the neurotransmitter listed or that you have chosen. Fill in all of the empty boxes. Note that more than one answer is possible in some cases (e.g., synthesis enzymes or receptors –choose any), and the same answer must be repeated in some cases. The first answer is completed as an example. A filled box means that you are not expected to know that answer. Note: if the receptor is ionotropic, enter “n/a” for the second messenger enzyme. I have inserted this for the nicotine receptor…


Precursor molecule

NT Synthesis enzyme

Neuro-transmitter

Receptor

Gprotein / channel type

Second messenger enzyme

Agonist / antagonist

Metabo-lite

Acetyl CoA

Choline acetyltransferase

Acetylcholine

Muscarine M2

Gi

Adenylate cyclase

Botox

Choline

Choline/a-coa

Choline acetyltransferase

Ach

Nicotine

Na+ channel

n/a

Curare/etc…

Acetic acid/choline

DA

DBH

NE

Alpha 1

Gi

AC

EPI

O-methyl/EPI

DA

DBH

Norepinephrine

Beta 2

Gs

AC




O-methyl/EPI

NE

PNMT

EPI

Alpha/beta 1/2

Gi/Gs

AC







Tyrosine/L-dopa

TH/DD

DA

D1

Gs

AC

cocaine

DOPAC/HVA

Tyrosine/L-dopa

TH/DD

DA

D4

Gi

AC




DOPAC/HVA

Tryptophan

tryH/5HTP-D

5HT

5HT1a







Fluoxetine/LSD, etc

5HIAA

Phenylalanine

PAH/TH/DD

DA

D2

Gi

AC




DOPAC/HVA

Glutamate

GAD

GABA

GABAa

Cl-

n/a

ethanol




Glutamate

GAD

GABA

GABAb

Gi

AC













Glutamate

AMPA

NA+

n/a

AMPA










Glutamate

NMDA

NA+/K+/Ca++

n/a

NMDA










glutamate

mGluR1

Gq

PLC






2. [8 points: 2 pts each] Contrast any 4 of the 5 pairs below in a sentence or two each (i.e. state an important difference between the two):


A. Globus Pallidus, internal segment vs. Globus Pallidus, external segment

B. Golgi tendon organ vs. spindle

C. tip links vs. bitter taste transduction

D. echo delay versus Doppler shift

E. CF vs. FM calls
>> Many answers possible, just be correct.
3. [2 points] Describe two differences between pyramidal and extrapyramidal tracts.
>> pyramidal emanate from cortex, extrapyramidal do not

>> pyramidal necessary for distal limb / digit control

>> other answers possible
-- question was graded out of 4 instead so two extra points possible.
4. [4 points] Describe how pacemaker neurons generate their intrinsic rhythm. How would insertion of a D5 receptor affect the response of the pacemaker neuron to dopamine ?
>> describe the pattern of Na+, Ca++, and K+ ions fluxes as noted in lecture.

>> normally NE increase duration of K+ and ca++ opening via PKA through effects on Gs. D5 also increases Gs so we might speculate the same mechanisms would allow DA to increase heart rate the same way that NE does

5. [4 points] Discuss the differences between T1 and T2 type taste receptors.
- T1 code for Umami (T1r1+t1r3) and sweet (T1r2+t1r3)

- T2 code for bitter

- T1 are heterodimers, T2 are not

- T2 activate PLC pathways, can also open TRP channels

6. [6 points] The following data were obtained (on 2 separate days) from an animal with a unilateral 6-OHDA lesion of the nigrostriatal pathway. The animal was injected with apomorphine on one day and amphetamine on another and turning behavior was monitored for 30 minutes post injection.

Turns left Turns right

apomorphine 23 300

amphetamine 110 15


a) Which side of the brain was lesioned? How do these data allow you to come to your conclusion?

- Lesion is left side. AMPH increase release and blocks reuptake of DA from presyn terminal. The presyn terminals have been lost after lesion on left side, thus AMPH increases DA present in right hemisphere. Right hemisphere increases activation of the left limb and increases attention to left side, resulting in rotation to the left. When denervated, the postsynaptic DA receptors become supersensitive, thus systemic administration of APO a direct DA agonist will produce more postsynaptic activation on the dervated side, causing the right limb to increase activity and more attention to the right, resulting in rightward rotation.



b) Explain one method you could use to confirm your hypothesis regarding the side of the lesion by looking at neurochemical changes in the brain?
>> You could use microdialysis to measures levels of DA and DOPAC/HVA in each hemisphere. The lesioned side should show less DA and metabolites in the extracellular fluid. Other answers possible.
7. [6 points] A study by Champagne et al. (2008) describes the effect of a rat mother’s licking and grooming (LG) of her pups on the binding of cortisol (CORT) to glucocorticoid (GR) and mineralocorticoid (GR) receptors in later life.
A) Based on the description below, describe the probable relative Kd and Bmax values for CORT binding to MR versus GR. I.e., would we expect a difference in Kd and/or Bmax values across receptors, and if so, why ?

>> CORT binds preferentially binds to MR receptors at lower concentrations, thus less CORT would be needed be added to bind the 50% of the MR receptor, indicating a lower Kd for the MR receptors relative to the GR receptors.


B) Based on the description below, describe the probable relative Kd and Bmax values for CORT binding to MR versus GR in low LG and high LG pups. Would we expect a difference in Kd and/or Bmax values across conditions, and if so, why ?



>> Kd cannot be assessed since ligand binding was not measured. With low LG there are fewer overall receptors, both MR and GR are reduced to the same amount. Since Bmax corresponds to the maximum number of receptors (binding sites) we can infer that Bmax would be lower in low LG pups.

8. [4 points] What pathway is the globus pallidus external segment (GPe) a part of and how does it contribute to motor function ? What would happen to motor function if we inserted alpha2 receptors into the GPe neurons and the medium spiny neurons of the striatum released epinephrine onto these GPe neurons ?


>> GPe is part of indirect pathway. GPe will cause movement when stimulated because it inhibits the STN which normally depolarizes and drive the GPi, which is tonically inhibiting the VA/VL thalamus, preventing it from depolarizing motor cortex to intiate movement.
>> MSN neurons in the striatum inhibit the GPe via GABA, resulting in inhibition of movement because they prevent the GPe from inhibiting the STN. If you insert alpha receptors, they couple to Gi and will yield more relative hyperpolarization, inhibiting the GPe neurons. Thus the results would be same as the MSN GABA effect on GPe neurons: inhibition of movement in response to EPI.
9. [8 points] Compose a cogent paragraph using all the terms listed below. UNDERLINE the target words, or your answers may be overlooked ! Your paragraph must be correct and coherent.
Terms: Insertional plaque, phase locked, stereocilium, apex, basilar membrane, inferior colliculus, coincidence detector, calcium.
>> many answers possible, just make the paragraph correct and coherent. You do not need to use the terms in the order they are listed. You should form a true paragraph.

BONUS:
A. [1 point]: Why might enforced exercised of the weakened limb prevent 6OHDA induced paralysis ?
>> Mention GDNF from our reading at some point. Other answers possible.
B. [1 point]: Describe one difference and one similarity between the epinephrine and norepinephrine.
>> both are synthesized from DA, but they have different affinitied for alpha and beta receptors. Other answers possible.
C. [1 point]: Where in the brain would you find the subthalamic nucleus ?

ventral to the thalamus.


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