Seminars | This Week

Centre for Advanced Imaging

Date/Time: Tuesday 23rd January 2018 09:30

Location: Seminar Room Centre for Advanced Imaging Bldg 57

Title of talk: Clinical translation of hyperpolarized Metabolic MR
Speaker's name: Professor Jan Henrik Ardenkjær-Larsen
Speaker's organisation: Centre for Hyperpolarsisation in Magnetic Resonance Technical University of Denmark
Talk abstract: Hyperpolarization by dissolution Dynamic Nuclear Polarization (dDNP) is a versatile method for making solutions of strongly polarized nuclear spins in small molecules. The method has enabled a range of in vivo and in vitro applications that otherwise would not be possible. In particular, clinical imaging is now a reality with hyperpolarized 13C-pyruvate. In this talk I will give an introduction to the method and the applications.

Other Details: If you would be interested in meeting with this speaker please email Lorine Wilkinson l.wilkinson@uq.edu.au

Host name: Lorine Wilkinson
Host phone number: 3346 0364
Host email: l.wilkinson@uq.edu.au

Seminars | This Week

QBI Neuroscience Seminar

Date/Time: Tuesday 23rd January 2018 11:00

Location: QBI, Level 7 Auditorium

Title of talk: Activity-dependent bulk endocytosis: presynaptic function and dysfunction in Huntington's Disease
Speaker's name: Professor Mike Cousin
Speaker's organisation: Chair of Neuronal Cell Biology, Centre for Integrative Physiology, University of Edinburgh
Talk abstract: The coordinated recruitment and integration of presynaptic synaptic vesicle (SV) recycling modes is a key factor in maintaining synaptic transmission during elevated neuronal activity. During periods of high neuronal activity, activity-dependent bulk endocytosis (ADBE) is the dominant mode, which retrieves large areas of membrane directly forming bulk endosomes from which SVs can bud. We have identified the first ADBE-specific SV cargo, called VAMP4, and have shown that it is essential for ADBE to proceed. In addition to a key role in neuronal physiology ADBE dysfunction may precipitate a series of neuronal disorders that rely on high frequency neurotransmission. One such disorder is Huntington's disease (HD), which is caused by mutation of the HTT gene, with synaptic atrophy prevalent in striatal medium spiny neurons. We tested whether this vulnerability originates from an inability to sustain presynaptic performance during intense neuronal activity. Two distinct activity-dependent signatures of presynaptic dysfunction were revealed in neurons derived from a HD mouse model. First, ADBE was increased in neurons derived from different brain regions. Second, clathrin-mediated endocytosis was disrupted specifically in striatal neurons and only during elevated activity. Loss of wild-type huntingtin function precipitated these disease signatures, since both were recapitulated by depletion of endogenous huntingtin from wild-type neurons. Importantly both disease signatures were eliminated by overexpression of wild-type huntingtin in HD neurons. Intrinsic susceptibility of specific HD neurons to elevated neuronal activity via ADBE dysfunction may therefore render them vulnerable to ongoing physiological firing patterns, potentially explaining synapse failure and degeneration in later life.

Host name: Deirdre Wilson
Host email: d.wilson5@uq.edu.au