Undergraduate Course: Synaptic Function and Plasticity in Health and Disease (BIME10012)
|School||Deanery of Biomedical Sciences
||College||College of Medicine and Veterinary Medicine
|Credit level (Normal year taken)||SCQF Level 10 (Year 4 Undergraduate)
||Availability||Available to all students
|Summary||This course covers the physiological and molecular mechanisms underlying the function of synapses before showing how dysfunction of the mechanisms leads to disease.
Synapses are essential for brain function by allowing communication between neurons. The efficacy of this communication is adjusted by a complex series of processes collectively termed synaptic plasticity. Plasticity is both critically involved in normal brain development and underlies learning and memory throughout life. Alterations in normal synaptic function and plasticity have been implicated in a wide variety of neurological conditions.
This course will start with introductory lectures focussing on pre- and postsynaptic function and the molecular mechanisms involved in plasticity at both excitatory and inhibitory synapses. This will be followed by more detailed lectures including explanation of the latest experimental techniques being used to elucidate these mechanisms. These lectures will alternate with student presentations of recent research papers in the subject area. Finally we will use specific examples to explain how synaptic dysfunction can lead to neurological conditions, such as autism and schizophrenia, and study the experimental approaches and model systems currently being used to design clinical treatments.
Contributors: Mike Cousin, Peter Kind, Giles Hardingham
Entry Requirements (not applicable to Visiting Students)
||Other requirements|| None
|Additional Costs|| None
Information for Visiting Students
|High Demand Course?
Course Delivery Information
|Academic year 2015/16, Not available to visiting students (SS1)
|Learning and Teaching activities (Further Info)
Lecture Hours 24,
Seminar/Tutorial Hours 6,
Supervised Practical/Workshop/Studio Hours 8,
Feedback/Feedforward Hours 2,
Formative Assessment Hours 1,
Summative Assessment Hours 2,
Revision Session Hours 2,
Programme Level Learning and Teaching Hours 4,
Directed Learning and Independent Learning Hours
|Assessment (Further Info)
|Additional Information (Assessment)
||Feedback will be available throughout the course in many forms:
¿ Feedback from course organiser and peers on your presentations
¿ Mid-course feedback session: this will provide personal feedback on the in-course essay
¿ Feedback from the exam will be made available ¿ please contact Caroline Morris for more
information about how and when this will be done
||Hours & Minutes
|Main Exam Diet S1 (December)||Synaptic Function and Plasticity in Health and Disease||2:00|
On completion of this course, the student will be able to:
- Understand processes involved in neurotransmitter vesicle recycling, endo- and exocytosis and Understand the molecular mechanisms of regulation of synaptic efficacy
- Conceive an experimental program to investigate synaptic dysfunction in a neurological disorder
- Knowledge of the role of inhibitory synapses
- Ability to interpret, evaluate and present experimental findings
- Coherently and logically present (written and oral) an argument explaining how synaptic dysfunction leads to disease.
|Synaptic vesicle exocytosis |
Jahn R and Fasshauer D (2012) Molecular machines governing fusion of synaptic vesicles. Nature 490 : 201-7
Rizo J and Sudhof TC (2012) The membrane fusion enigma: SNAREs, Sec1/munc18 proteins, and their accomplices, guilty as charged? Ann. Rev. Cell Dev. Biol. 28: 279-308.
Synaptic vesicle endocytosis and recycling
Dittman J and Ryan TA (2009) Molecular circuitry of endocytosis at nerve terminals.
Ann. Rev. Cell Dev. Biol. 25: 113-160.
Clayton EL and Cousin MA (2009) The molecular physiology of activity-dependent bulk endocytosis of synaptic vesicles. J. Neurochem. 111:901-14
Rao Y et al (2012) The early steps of endocytosis: from cargo selection to membrane deformation. Eur. J. Cell Biol. 91: 226-233.
Function and Diversity of Inhibitory Neurons
Isaacson, J.S., and Scanziani, M. (2011). How inhibition shapes cortical activity. Neuron 72, 231-243.
Klausberger, T., and Somogyi, P. (2008). Neuronal diversity and temporal dynamics: the unity of hippocampal circuit operations. Science (New York, NY 321, 53-57.
Inhibition in Development and Disease
Ben-Ari, Y., Khalilov, I., Kahle, K.T., and Cherubini, E. (2012). The GABA excitatory/inhibitory shift in brain maturation and neurological disorders. Neuroscientist 18, 467-486.
Gonzalez-Burgos, G., Fish, K.N., and Lewis, D.A. (2011). GABA neuron alterations, cortical circuit dysfunction and cognitive deficits in schizophrenia. Neural Plast 2011, 723184.
Hensch, T.K. (2005). Critical period plasticity in local cortical circuits. Nat Rev Neurosci 6, 877-888.
Synapse to Nucleus Signalling
Pizzarelli, R., and Cherubini, E. (2011). Alterations of GABAergic signaling in autism spectrum disorders. Neural Plast 2011, 297153.
West AE, Greenberg ME. (2011) Neuronal activity-regulated gene transcription in synapse development and cognitive function. Cold Spring Harb Perspect Biol.3(6) pii: a00574
Hardingham GE, Bading H.(2010) Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders. Nat Rev Neurosci. (10):682-96
Bading H (2013). Nuclear calcium signalling in the regulation of brain function. Nat Rev Neurosci. 2013 Sep;14(9):593-608
Bell KF, Hardingham GE.(2011) The influence of synaptic activity on neuronal health
Curr Opin Neurobiol. 21(2):299-305
Hardingham GE. (2009) Coupling of the NMDA receptor to neuroprotective and neurodestructive events. Biochem Soc Trans. 37(Pt 6):1147-60.
|Graduate Attributes and Skills
|Course organiser||Dr Michael Daw
Tel: (0131 6)50 3722
|Course secretary||Mr Kevin Mcarthur
Tel: (0131 6)51 1824
© Copyright 2015 The University of Edinburgh - 18 January 2016 3:31 am