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BIOL-415 Nerve cell mechanisms in behavior

BIOL-615 Neural bases of behavior

First test - Tuesday, February 10, 2009 - Prof. Stark

All questions are short answer. 65 points total.

1. Medulla plus pons plus midbrain is called (what?).

brainstem

2. How could somebody in the mid 1800’s identify a specific area in the cerebral cortex as being critical for language and speech?

See the brain of a speech challenged patient upon autopsy

3. Occlusion of one internal carotid might not be fatal because of (what structural adaptation?).

circle of Willis

4. In a mid-sagittal brain section, the most conspicuous tract seen connects one side (hemisphere) of the brain with the other. What is that called?

Corpus callosum

5. Why was Ramon y Cajal’s body of work using Golgi’s technique a contribution worthy of the Nobel Prize?

He showed the complete anatomy of neurons in many systems and developed cell theory

6. Lashley, concluding that memories were stored all over the cerebral cortex, came up with the term “equipotentiality.” By contrast, textbooks colorize the cortex to present what alternative viewpoint on how the cortex represents specific sensory and motor systems?

Localization of function

7. Gray matter areas in the brain with cell bodies and synaptic connections (such as the so-called “basal ganglia”) are supposed to be called (what?).

nuclei

8. For the knee-jerk reflex, cells that connect (what?) to the spinal cord are found in the dorsal root ganglion.

Muscle spindle, stretch receptor

9. Why are there cervical and lumbar enlargements in the spinal cord?

More spinal motor neurons for the forelimbs and hindlimbs

10. In the 1960’s, scientists determined that the substantia nigra sends dopamine all over the brain. How did they do this?

Histochemical fluorescence

11. You buy some antibody linked to 10 nm colloidal gold from a company. To localize aardvarkia, the protein you are studying in the aardvark caudate, answer either (1) What other reagent do you need to make or buy? Or (2) What apparatus will you use to visualize the colloidal gold and the aardvarkia protein it labels?

Primary antibody against aardvarkia, transmission electron microscope

12. Where do you expect to find spines, those structures with tubulin and actin, in the nervous system?

Where the postsunaptic area is, cell body or dendrite

13. "Postsynaptic density" - what technique and "staining" affords us the resolution to see this as a "density?"

need to stain for transmission electron microscopy with heave metals

14. Relate the concept of the motor unit with Halstead’s theory of the cause of post-polio syndrome.

One spinal motor neuron innervates multiple muscle cells. Surviving ones sprout to innervate more during recovery. These sprouts are lost in post polio syndrome

15. How does the prefix “oligo” describe the function of the oligodendrocyte?

This cell myelinates multiple axons

16. “Myelin helps the action potential go faster.” For the peripheral nervous system, answer either (1) It keeps jumping past what kind of cell? Or (2) It jumps from one (name of gap) to the next.

Schwann cell, node of Ranvier

17. Membranes (and glass micropipettes) have resistance. But they also have (what else?) that causes the voltage change to be delayed.

capacitance

18. Permeability of a particular ion, say sodium, across the membrane is inversely related to the resistance across the membrane for that ion and directly related to (what electrical property?).

conductance

19. Explain why the electrical potential calculated with the Nernst equation is called the equilibrium potential.

The assumption is tantamount to equilibrium (electrical and chemical potentials equal and opposite

20. Answer one of these about Cole and Curtis’s AC Wheatstone bridge (1) What is meant by “voltage divider?” or (2) What did they conclude on the basis of their bridge going out of balance?

Two resistors in a row where the voltage acroee each is IR, resistance decreases (during the action potential

21. Describe or draw how Nobel prize winners Neher and Sackmann measured current through individual channels.

The patch clamp electrode nudges against the membrane where there is one channel

22. Why did the efflux of radioactive sodium from the squid giant axon eventually decrease when DNP inactivated the mitochondria in Hodgkin and Keynes classic experiment in the 1950s?

without ATP, the sodium pump stops

23. You are recording the membrane potential (resting potential). What happens to this potential if you replace the extracellular fluid with potassium chloride at the same concentration as the intracellular concentration?

It goes to zero (from, say, -70)

24. You remove both adrenal glands of a rat and let it recover. Answer either (1) What is different about the animal’s specific appetite? Or (2) This is explained by the absence of what hormone?

Craves salt (NaCl) b/c of loss of aldosterone

25. A certain voltage is applied at one place in an axon. On the basis of passive spread only (no action potentials) what would be the voltage (relative to the applied voltage) one space constant away? (Your answer can be very approximate.)

1/3 approximates 1/e

26. The voltage of an axon is clamped from the resting potential to 0 mV. At 0.7 ms (early), Answer either (1) What direction is the current? Or (2) How is this current changed if 460 mM sodium chloride is replaced by choline chloride?

In, there is no sodium current if there is no sodium

27. In terms of the protein, what would be the genetic explanation of permissive vs restrictive temperatures in a temperature sensitive conditional mutation?

A missense mutation might only disrupt function if temperature denatures the protein

28. For long Q-T syndrome, answer either (1) What cell type has a long action potential that should become shorter in strenuous exercise but does not? Or (2) The channel was first found because what conditional behavior was first noticed in Drosophila mutants?

Ventricular myocardial cell, shaking under ether anesthesia

29. Why do they distinguish Shaker vs Electrophorus channels as tetramer vs pseudotetramer?

It takes 4 shaker proteins, the electrophorus protein has all 4 domains in one big molecule

30. “Silencing of synaptotagmin in PC12 cells inhibits Ca²⁺-evoked catecholamine release.” Why does calcium elicit release if synaptotagmin is not inhibited?

Calcium, coming in through calcium channels, mediates vesicle release

31. Knowing about cystic fibrosis might help you to understand the channel for what neurotransmitter?

GABA’s channel passes chloride

32. Relative to a potassium channel, what would you guess the magnitude of the conductance of a channel made up of connexin-36 (Cx-36) molecules to be?

Gap junctions have huge conductance

33. “The spinal motor neuron is ‘the final common pathway in the integrative action of the nervous system.’” What distinguishes this cell from the striated muscle cell that gives the neuron (and not the muscle) this distinction?

Since muscle has only one junction, and this is excitatory only, no integration takes place on the muscle cell

34. Why would injection of Cl^- (through an ion-specific electrode) into the cell change the potential elicited by GABA (gamma amino butyric acid)?

Because it would make the chloride gradient, seen across the GABA channel, less steep

35. Consider the mepp (miniature end plate potential) and answer either (1) What cellular mechanism delimits it to be way smaller than the full end plate potential? Or (2) Suppose your preparation were giving you just a few mepps on the average – what would you do to the preparation to restore the full end plate potential?

Fewer vesicles are released with low extracellular calcium, add calcium

36. There are synaptic connections to the dendrites and cell bodies of vertebrates. How is the situation strikingly different for invertebrates?

Synapses are in a neuropil(e) and cell bodies are on the outside of ganglia

37. At first they were surprised that a mutation in dynamin (shibire) would exhibit paralysis when moved to the restrictive temperature. Rationalize why.

If vesicle membrane fails to recycle, eventually vesicles would not be released

38. “Botulism and tetanus toxins cleave synaptobrevin.” Precisely what membrane is synaptobrevin on?

vesicle

39. In what way is the expression “putative neurotransmitter” distinguished from the meaning of the word neurotransmitter?

Putative implies that they are not yet convinced it qualifies as a neurotransmitter

40. Say something about how vesicles or enzymes for transmitter synthesis get from the cell body to the synaptic terminal.

Axon transport along microtubules

41. Beta-endorphin is cleaved from what protein precursor?

POMC

42. “Nicotinic acetylcholine receptor.” Answer either (1) On precisely what membrane is it located at the neuromuscular junction? Or (2) What is the nature of its molecular configuration that leads its activation to generate a potential?

End plate (on muscle cell), it is a channel

43. Does Viagra function “upstream” or “downstream” of NO (nitric oxide) action? Explain your reasoning.

Since NO activates GC and Viagra inhibits cGMP PDE, downstream

44. Potentiating or inhibiting (which?) the action of a neurotransmitter (which one?) explains the action of Prozac.

An uptake inhibitor would potentiate seretonin

45. “Day length” (what fraction of a 24 hr period is illuminated) affects the size of the testes in a hamster by… Answer either (1) What hormone? Or (2) From what brain structure?

Melatonin, pineal

46. Why does the neighboring glial cell have special significance for glutaminergic transmission?

Reuptake and delivery back to the neuron

47. Atropine affects the enteric nervous system to achieve (what?)?

decrease GI motility

48. Out of the four CNS locations from which autonomic nerves originate, where is the origin of the nerves that mediate erection?

sacral

49. In the cases of both norepinephrine and serotonin, a decarboxylase turns an amino acid into (what chemical class of molecules?).

amine (monamine)

50. When more acetylcholine is needed, vesicles are released. How is the "transmitter" NO (nitric oxide) increased when it is needed?

Activation of enzyme (NO synthase)

51. "Acetylcholine is used in the sympathetic nervous system." Where?

At the ganglion

52. The discovery that MPTP was a contaminant in a bad batch of heroin helped to develop an animal model to study (what?).

Parkinson’s disease

53. l-DOPA… Answer either (1) Why do you need to give a lot of it? Or (2) Why do you give that instead of dopamine? (for Parkinson’s)

because it gets decarboxylated everywhere, dopamine does not cross the blood brain barrier

54. “Lesions of the lateral hypothalamus result in a thinner rat.” In what way does this story relate to Parkinson’s disease?

Loss of affect (motivation) results from disrupting dopaminergic tract

55. Explain why action potentials might be smaller if lithium were given?

Since lithium is not pumped but does go through channels, the gradient of sodium plus lithium is less steep

56. What is the general class of molecules that serve as the precursor of “endogenous tetrahydrocannabinol?”

membrane phospholipids

57. Torpedo was useful… Answer one (1) To do what? (2) Why was it particularly useful?

Clone the acetylcholine receptor, which is plentiful in T’s electric organ

58. What would you use radioactively labeled (¹²⁵I) alpha-bungarotoxin to do?

To isolate the acetylcholine receptor

59. Anesthetics, benzodiazepines and barbiturates affect the GABA-A receptor. Describe or draw what this receptor looks like.

channel

60. Describe or draw what a dopaminergic receptor looks like.

G protein coupled receptor crosses membrane 7 times

61. Related to adrenergic receptors, answer either (1) Why would an alpha agonist unstuff a stuffed nose? Or (2) Why would a beta antagonist help alleviate hypertension?

Stimulate arteriole (precapillary sphincter) smooth muscle, decrease rate and contractility of heart

62. Why would atropine save your life if you were dying of acetylcholinesterase inhibitor poisoning?

Block muscarinic receptors that are making the heart stop when there is too much acetylcholine

63. Tell me one of the things the alpha subunit of the G protein does when it is activated by binding GTP.

Dissociate from beta-gamma, activate the next molecule in the cascade, break down GTP

64. When a G protein signals to PLC (phospholipase C), answer either: (1) What is the next effect for one product of that enzyme (DAG=diacyl glycerol)? Or (2) What is the next effect after the production of the other (IP₃ = inositol trisphosphate)?

DAG activates protein kinase C, IP3 is the ligand for a calcium channel on an intracellular cistern (smooth ER) of calcium

65. For cAMP answer either: (1) How, molecularly, were 4 cAMP molecules used to achieve their effect? Or (2) What drug would keep cAMP present for a longer amount of time?

Two each bind to and remove 2 inhibitory subunits from two catalytic subunits, caffeine or theophyline