Tuesday 23 February 2016

Biosciences Seminar Speaker 25 February 2016

Biosciences Seminar Series - Winter 2016
25 February 2016 - 1pm - Zoology Museum

          Diel colour changes in male Sapphirina 

nigromaculata (Cyclopoida, Copepoda)

Prof Kazutaka Takahashi

We are delighted to welcome to our Biosciences seminar series a visitor from The University of Tokyo, Prof Kazutaka Takahashi. Kazutaka is based at the Department of Aquatic Bioscience at the Graduate School of Agricultural and Life Sciences. Kazutaka has a keen interest in zooplankton dynamics, especially the ecology, behaviour and physiology of copepods.

Males of the pelagic copepod genus Sapphirina are known to exhibit brilliant iridescence, presumably to attract mates. However, the males of some species have been described as not being able to produce iridescence. To resolve this 
apparent contradiction, we conducted detailed observations of colouration patterns in Sapphirina nigromaculata, which has been previously described as both iridescent and non-iridescent. 

from: www.whoi.edu
The colouration of male S. nigromaculata ranges from intensely iridescent to transparent with pigmented spots. These two phases appear to have a circadian rhythm, with males turning iridescent at midnight and remaining in that state until several hours after sunrise, then becoming transparent again towards the afternoon. Adult S. nigromaculata occurrence in surface waters shows temporal changes, in that they occasionally occur in higher densities than their average in the water column, particularly from midnight to around noon. 

The synchronization of iridescence in concert with upward migration is considered to be an adaptation for increasing the likelihood of encountering a mate. Observations using a video plankton recorder revealed that the transparent phase is an adaptation for decreasing predation risk by making the copepods more difficult to distinguish while they are associated with doliolids.

Hope to see many of you - everyone most welcome to attend!

Tuesday 16 February 2016

Biosciences Seminar Speaker 18 February 2016

Biosciences Seminar Series - Winter 2016
18 February 2016 - 1pm - Wallace Lecture Theatre

Note Change of Room!

          Spatial cognition in wide-ranging birds

Prof Tim Guilford

Our Biosciences seminar series continues with an exciting talk by Prof Tim Guilford, from the Department of Zoology at the University of Oxford (UK) and member of the Oxford Navigation Group. Tim is fascinated about animal behaviour and understanding what drives their decisions. Initially Tim focussed his research on understanding the evolution of animal signals, such as warning signals. More recently Tim has been working hard on unravelling the mysteries of how animals map the environments and find their ways, from more localised movement of pigeons to long-distance travels of seabirds. To achieve these goals Tim uses a wide combination of new technological developments, such as on-board cameras and miniatures GPS loggers, experiments and new analytical approaches borrowed from other fields, such as computational engineering. In short - expect a fascinating talk!

Birds are amongst the greatest long-distance navigators on earth, but what do we know about the spatial cognition that underlies their wide-ranging movements? Using miniature tracking technology to follow movements in a variety of field-experimental and naturally free-ranging paradigms, I will explore what we have learnt about the nature of the bird’s large-scale familiar area map. From route-following behaviour in homing pigeons to migratory navigation in pelagic seabirds, I will concentrate especially on the perhaps neglected role of individual learning and memory in the control of long-distance movements in birds.

Hope to see many of you - everyone most welcome to attend!

Monday 1 February 2016

BioMaths Colloquium - -05/02/2016

BioMaths Colloquium Series - 2015/16

05 February 2016 - 3pm Maths Seminar Room 

(room 224 Talbot Building 2nd floor)

Mathematical modelling of Ca2+ influx and calmodulin activation in dendritic spines: implications for synaptic plasticity

Prof Krasimira Tsaneva-Atanasova

from: www.wun.ac.uk

Our BioMaths Colloquium seminars resume for the winter term, with a great programme! We kick it off with a talk by Prof Krasimira Tsaneva-Atanasova from the College of Engineering, Mathematics and Physical Sciences at the University of Exeter. Krasimira is a Professor of Mathematics for Healthcare and her research is focussed on biomathematics. Her ultimate goals are to develop novel applications of mathematics for improved quantitative healthcare methods. 

The rise of intracellular calcium concentration [Ca2+] is believed to play a critical role in triggering synaptic plasticity. This is supported by experimental evidence demonstrating that both, synaptic long-term potentiation (LTP) and depression (LTD), are blocked by pharmacological buffering of Ca2+. The importance of intracellular Ca2+ is reflected in the fact that the dynamics of [Ca2+], acting as intermediate signals for induction of plasticity, are a common feature of most biophysical models of STDP.

Calcium-based biophysical models of STDP include a description of the changes in [Ca2+] due to pre- and post-synaptic spiking. Ca2+ sources may depend on the particular synapse to be modelled, but most frequently include: influx via NMDA receptors (NMDARs); influx via Ca2+-permeable AMPA receptors (AMPARs); influx via voltage-gated Ca2+ channels, or Ca2+ release from intracellular stores. Entry of extracellular Ca2+ via postsynaptic membrane ion channels can be dependent on both the postsynaptic membrane-potential and the action of neurotransmitters in the synaptic cleft, therefore biophysical models of STDP often contain descriptions of electrophysiological cell membrane phenomena and AMPAR/NMDAR ligand-gating in response to neuron pair-spiking.

It is an open question how the multiple special and temporal scales involved in intracellular Ca2+ handling within the STDP models affect the plasticity outcomes predicted by these models. Hebbian or associative plasticity is triggered by postsynaptic Ca2+ influx which activates calmodulin and CaMKII. The influx of Ca2+ through voltage-dependent NMDA receptors and Ca2+ channels is regulated by Ca2+ -activated K+ channels (SK-channels) providing negative feedback regulation of postsynaptic [Ca2+]. Using 3-dimensional modelling of Ca2+ and calmodulin dynamics within dendritic spines we show that the non-linear relationship between Ca2+ influx and calmodulin activation endows SK-channels with the ability to “gate” calmodulin activation and therefore the induction of Hebbian synaptic plasticity. Since SK-channels are inhibited by several neuro-modulator receptors including acetylcholine and noradrenaline, the gating of synaptic plasticity by SK-channels could represent a common mechanism by which neuro-modulators control the induction of synaptic plasticity.  

The discussions will continue over biscuits and tea/coffee after the seminar. 
Hope to see many of you!