HONOURS DEGREE OF BSc IN PHARMACOLOGY 1997
LEVEL THREE EXAMINATION
PCL 301: MOLECULAR PHARMACOLOGY
Friday May 23rd, 1997 9.30am -12.30pm
Attempt ONE QUESTION from each Section
Section A
1. (a) Review the experimental evidence which has led to gamma-aminobutyric acid (GABA) being accepted as a neurotransmitter in the mammalian central nervous system.
(b) GABAA and GABAC receptors are both ligand-gated chloride channels. Distinguish between these receptors with particular reference to their molecular structure and pharmacology.
(c) Giving examples, define use-dependent and voltage-dependent block of named ligand-gated ion channels.
2. Compare and contrast the physiology, pharmacology and molecular biology of the GABAA and NMDA receptor.
Section B
3. Briefly describe the general properties of ion channels. Discuss, with specific examples, the functional roles of voltage-gated Na+, K+ and Ca2+ channels in excitable cells and indicate how their activity may be pharmacologically modulated for therapeutic benefit.
4. "Maintenance of intracellular Ca++ homeostasis is a typical case of cells investing so much of their energy and resources in a pointless, useless and totally unnecessary venture - truly a 'much ado about nothing', if ever there was one". Discuss this statement.
Section C
5. Using named examples, give an account of how variations in the actions of G-protein subunits may give rise to a wide range of biochemical events resulting from stimulation of receptors with seven transmembrane domains.
6. Describe the classification of metabotropic glutamate receptors in the mammalian central nervous system. Comment briefly on the signal transduction mechanisms and the physiological relevance of these receptors.
HONOURS DEGREE OF BSc IN PHARMACOLOGY 1997
LEVEL THREE RESIT EXAMINATION
PCL 301: MOLECULAR PHARMACOLOGY
Wednesday 3rd. September 1997 9.30am -12.30pm
Attempt ONE QUESTION from each Section
Section A
1. (a) Distinguish between the strichnine-sensitive glycine receptor and the glycine binding site of the NMDA receptor?
(b) Bicuculline and picrotoxin are GABAA receptor antagonists with different mechanisms of action. Discuss.
(c) Discuss, with specific examples, how drugs (both establised and investigational) which modulate NMDA receptor-mediated (excitatory) and GABAA receptor-mediated (inhibitory) neurotransmission can be used in the treatment of epilepsy.
2. 'Many chemically-diverse drugs act as allosteric modulators at the GABAA receptor'. Discuss.
Section B
3. Briefly describe the general properties of ion channels. Discuss, with specific examples, the functional roles of voltage-gated Na, K and Ca channels in excitable cells and indicate how their activity may be pharmacologically modulated for therapeutic benefit.
4. 'Intracellular Ca++ homeostasis is orchestrated by the concerted operation of plasma membrane ion channels and translocases and intracellular compartmentalisation systems'. Discuss this statement, highlighting the systems and mechanisms involved, how they operate and why cells need to tightly control changes in their intracellular levels of free, ionised calcium.
Section C
5. Using a named example of a G-protein coupled receptor system, give a detailed account of the sequence of events which couples receptor activation to biochemical effects within the cell. Indicate in your answer the points at which amplification of the signal may occur and highlight possible sites of 'crosstalk' between coupling systems occurring in the same cell.
6. Write an essay on 'The metabotropic glutamate receptor, its classification and physiological role in the mammalian central nervous system'.
HONOURS DEGREE OF B.Sc. IN PHARMACOLOGY 1996
THIRD YEAR EXAMINATIONS
SEMESTER TWO
PCL301 : MOLECULAR PHARMACOLOGY
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Friday 24th. May 1996 9.30am - 12.30pm
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Attempt ONE QUESTION FROM EACH SECTION
Section A
1. Discuss the physiological, pharmacological and molecular biological evidence that the GABAA receptor is a multi-subunit protein complex.
2. What is 'long term potentiation'? What mechanisms are thought to underlie its induction?
Section B
3. 'It is difficult to understand the current fascination and pre-occupation of biophysicists and electrophysiologists with ion channels. After all they are nothing more than vestiges of our evolutionary past, mere unguarded aqueous pores in cell membranes which allow the unregulated flux of ions. They have no physiological or therapeutic significance and they would not be missed by most cells'. Discuss this statement with particular reference to voltage-gated ion channels.
4. 'Intracellular Ca++ homeostasis is orchestrated by the concerted operation of plasma membrane ion channels and translocases and intracellular compartmentalisation systems'. Discuss this statement, highlighting the systems involved, how they operate and why cells need to exert tight control over changes in their intracellular levels of free, ionised calcium.
Section C
5. 'The stimulation of some cell membrane receptors results in changes in the levels of intracellular free calcium'. Using a named example of such a receptor, give a detailed account of the mechanism by which such receptor activation results in changes in calcium ion levels within the cell..
6. Outline the classification and pharmacology of metabotropic glutamate receptors. Discuss the role of these receptors in normal and abnormal physiological states.
HONOURS DEGREE OF B.Sc. IN PHARMACOLOGY 1996
THIRD YEAR EXAMINATIONS
SEMESTER TWO REFERRED EXAMINATION
PCL301 : MOLECULAR PHARMACOLOGY
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Wednesday 4th September 1996 9.30am - 12.30pm
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Attempt ONE QUESTION FROM EACH SECTION
Section A
1. The NMDA receptor requires two (different) agonists for activation. Outline the evidence for this. What special role might this receptor have in synaptic signalling?
2. Agonists at benzodiazepine receptors are sedative-hypnotic drugs. Describe the pharmacological mechanisms thought to underlie this property, with particular reference to their molecular site of action.
Section B
3. Briefly describe the general properties of ion channels. Discuss, with specific examples, the functional roles of voltage-gated Na, K and Ca channels in excitable cells and indicate how their activity may be pharmacologically modulated for therapeutic benefit.
4. Discuss, with specific examples and with the aid of clearly labelled diagrams, where appropriate, the role of calcium as an intracellular second messenger.
Section C
5. Using a named example, give an account of the mechanism by which activation of a receptors containing seven transmembrane-spanning regions may result in biochemical changes within a cell.
6. Discuss our current understanding of the classification, pharmacology and signal transduction mechanisms of metabotropic glutamate receptors (mGluRs) in the mammalian central nervous system. Outline the involvement of mGluRs in normal and abnormal physiological states.
HONOURS DEGREE OF B.Sc. IN PHARMACOLOGY 1995
THIRD YEAR EXAMINATIONS
SEMESTER ONE
PCL301 : MOLECULAR PHARMACOLOGY
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Monday 16th. January 1995 9.30am - 12.30pm
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Attempt ONE QUESTION FROM EACH SECTION
Section A
1. Give an account of the evidence which supports the concept that the GABAA receptor is a macromolecular ion channel complex.
2. Describe the role of glutamate receptors and ion channels in long term potentiation.
Section B
3. Describe the general properties of ion channels. Discuss, with specific examples, the functional roles of voltage-gated Na+, K+ and Ca2+ channels in excitable cells. How can their activity be pharmacologically modulated for therapeutic benefit?
4. Give a critical account of the mechanisms and processes involved in intracellular Ca2+ homeostasis. Why is it important to maintain intracellular free Ca2+ at low levels?
Section C
5. Give an account of the major physiological and pathophysiological roles played by nitric oxide.
6. Discuss our current understanding of the classification and functions of metabotropic glutamate receptors.
HONOURS DEGREE OF B.Sc. IN PHARMACOLOGY 1995
THIRD YEAR EXAMINATIONS
SEMESTER ONE REFERRED EXAMINATION
PCL301 : MOLECULAR PHARMACOLOGY
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Thursday 1st. June 1995 2.00 - 5.00pm
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Attempt ONE QUESTION FROM EACH SECTION
Section A
1. Outline the clinical features of unipolar (major) depression. With reference to the amine hypothesis of affective disorders, give an account of the mechanisms of action of drugs with antidepressant actions.
2. With reference to the GABAA receptor, describe the pharmacological means by which inhibitory synaptic transmission could/can be modulated, by drugs, to therapeutic effect.
Section B
3. Describe, with named examples, the various ways by which drugs may interact with ion channels. Give a brief account of how Na+ channel blocking drugs produce their cardiac antiarrhythmic actions and why they are most effective against tachyarrhythmias and in depolarised tissue.
4. Discuss, with particular reference to muscle contraction and neurotransmitter release, the second messenger or transductional role of Ca2+ in excitable cells. What are the main portals for entry of Ca2+ into excitable and non-excitable cells?
Section C
5. Discuss the interactions between local hormones and neuronal activity in the control of peripheral blood flow.
6. Write an essay entitled "Our current understanding of the pharmacology and physiology of the metabotropic glutamate receptor".