We strive to understand the central nervous system at multiple levels of function, from cells to cognition to social interactions. Our approaches range from molecular, cellular and experimental systems to the brain imaging of human behaviour and cognition as well as social level investigations.
Neurobiology of multisensory decision making in humans
Supervisor: Prof. Christoph Kayser
Project outline: Imagine trying to communicate with a friend in a noisy place, such as a noisy bar. You hear their voice only in between background music and people chatting, making it difficult to decipher what is being said. In this situation your ability to communicate is significantly enhanced if your eyes are directed towards your friend’s mouth, allowing you to combine visual information with the acoustic speech. Perceptual decision making is the act of choosing one action on the basis of the available sensory evidence.
To date, research on the neurobiological mechanisms underlying decisions has focused primarily on those processes associated with individual sensory modalities, hence falling short of the complexity of daily requirements. Little is known about how multisensory evidence is combined for decision making. Our main objective is to study the neurobiological underpinnings of perceptual decision making when they rely on multiple sensory modalities (e.g. sight and hearing). We use a combination of neuroimaging (M/EEG and/or fMRI) in human participants to map out the neural components associated with different unisenory and multisensory decision processes in order to disentangle the different neurobiological mechanisms linking multiple sensory inputs to a single behavioural output. To this end we use theoretical frameworks and advanced statistical data analysis applied to neuroimaging data obtained from human subjects.
The ultimate aims of this work are to link conceptual and computational models of optimal decision making and sensory integration with localized neural processes and to derive markers of neural activity that are linked to identified neural processes. Such markers could then be used in subsequent basic or clinical work to understand why and in which disease conditions specific decision processes fail.
Summary aim: Projects are available to investigate the neurobiological basis of multisensory decision making in humans using neuroimaging (MEG/EEG); these projects characterize the patterns of brain activity underlying multisensory decisions, how they relate to computational models and how they can be used to identify biomarkers for specific aspects of cognition to be used in future neurobiological or clinical research.
Techniques to be used
- high-density neuroimaging based on EEG or MEG
- analysis of MEG/EEG data based on multivariate statistics or biological response models in Matlab
- computer models of decision making
- Matlab programming
- Rohe, T., and Noppeney, U. (2016). Distinct Computational Principles Govern Multisensory Integration in Primary Sensory and Association Cortices. Curr Biol 26, 509-514.
- Philiastides, M.G., Heekeren, H.R., and Sajda, P. (2014). Human scalp potentials reflect a mixture of decision-related signals during perceptual choices. J Neurosci 34, 16877-16889.
- Kayser, S.J., McNair, S.W., and Kayser, C. (2016). Prestimulus influences on auditory perception from sensory representations and decision processes. Proc Natl Acad Sci U S A 113, 4842-4847.
- Christoph Kayser, Institute of Neuroscience and Psychology, Centre for Cognitive Neuroimaging (CCNi), University of Glasgow, 58 Hillhead Street, Glasgow G12 8QB, UK. Christoph.Kayser@glasgow.ac.uk Ph: +44 (0) 141 330 6847
Age-related changes in the content and temporal dynamics of visual information processing
Supervisor: Dr. Guillaume Rousselet
Project outline: Understanding how visual perception changes with age is vital, as changes in perception affect cognitive tasks reliant on visual inputs. Whereas most cognitive aging research focuses on where and when age-related changes occur, little is known about how aging affects what the brain is processing (i.e. differences in the information content of brain activity). This project will address this gap by examining age related changes in human visual information processing across the adult lifespan. Concretely, we will isolate trial-by-trial the face information (e.g. specific facial features) and the information processing function (e.g. integration of facial features) associated with brain activity. By using EEG recordings, we will be able to assign specific information processing content to brain signals evolving from stimulus onset to the subject’s response.
The project will examine when, where and what information is processed as a function of task. By using a range of tasks we can reveal how visual information processing changes over the lifespan, and identify aging effects common across tasks, and those that are task specific. For the first time we will address what changes occur in the information content of brain activity with age. We anticipate that with age, information processing will be delayed and less task specific.
Summary aim: To quantify age-related changes in human visual information processing across the adult lifespan.
Techniques to be used
- Visual psychophysics
- reverse correlation
- information theory
- Matlab programming
- Schyns et al. (2011). Cracking the code of oscillatory activity. PLoS Biology
- Rousselet et al. (2010). Healthy aging delays scalp EEG sensitivity to noise in a face discrimination task. Frontiers in Psychology
- Rousselet et al. (2014). Eye coding mechanisms in early human face ERPs. Journal of Vision
Synaptic circuitry of the spinal dorsal horn: unmasking the anatomical basis of chronic pain
Supervisor: Dr. David I Hughes
Project outline: Chronic (persistent) pain affects 7.8 million people in the UK, however, only 66% of these patients respond to treatments that are currently available. Our failure to offer effective pain relief for a significant proportion of the population not only presents serious welfare problems, but also serves to highlight how little is known about the anatomical, physiological and pharmacological basis of sensory systems in health and disease. One of the defining characteristics of chronic pain is the development of tactile allodynia, in which previously innocuous mechanical stimuli are perceived as being painful.
This project aims to further our understanding of neuronal circuitry in the spinal dorsal horn by identifying populations of interneurons that receive direct inputs from tactile afferents and have the capacity to activate pain pathways following the development of neuropathic pain.
Summary aim: To identify dorsal horn interneurons implicated in the development of tactile allodynia after peripheral nerve injury.
Techniques to be used: A variety of molecular, cellular and systems level techniques will be used, including
- Recovery surgical techniques
- behavioural testing
- general histological techniques and immunocytochemistry
- confocal microscopy
- transmission electron microscopy
- image analysis using dedicated software (e.g. Neurolucida for confocal, Neurolucida Explorer, Meta Morph and Image J)
- Todd AJ (2010). Neuronal circuitry for pain processing in the dorsal horn. Nature Reviews Neuroscience 11:823-836 (doi:10.1038/nrn2947)
- Yasaka T, Tiong SY, Hughes DI, Riddell JS, Todd AJ (2010). Populations of inhibitory and excitatory interneurons in lamina II of the adult rat spinal dorsal horn revealed by a combined electrophysiological and anatomical approach. Pain 151: 475-488 (doi:10.1016/j.pain.2010.08.008)
- Hughes DI, Scott DG, Riddell JS, Todd AJ (2007). Upregulation of substance P in low-threshold myelinated afferents is not required for tactile allodynia in the chronic constriction injury and spinal nerve ligation models. Journal of Neuroscience 27: 2025-2034 (doi:10.1523/JNEUROSCI.5401-06.2007)
- Hughes DI, Sikander S, Kinnon CM, Boyle KA, Watanabe M, Callister RJ, Graham BA (2012). Morphological, neurochemical and electrophysiological features of parvalbumin-expressing cells: a likely source of axo-axonic inputs in the mouse spinal dorsal horn. Journal of Physiology 590: 3927-3951 (doi:10.1113/jphysiol.2012.235655)
- Smith KM, Boyle KA, Madden JF, Dickinson SA, Jobling P, Callister RJ, Hughes DI, Graham BA (2015) Functional heterogeneity of calretinin-expressing neurons in the mouse superficial dorsal horn: implications for spinal pain processing. J Physiol 593: 4319-4339 (doi:10.1113/JP270855)
- Abraira VE, Kuehn ED, Chirila AM, Springel MW, Toliver AA, Zimmerman AL, Orefice LL, Boyle KA, Bai L, Song BJ, Bashista KA, O?Neill TG, Zhuo J, Tsan C, Hoynoski J, Rutlin M, Kus L, Niederkofler V, Watanabe M, Dymecki SM, Nelson SB, Heintz N, Hughes DI, Ginty DD (2017) The cellular and synaptic architecture of the mechanosensory dorsal horn Cell 168: 295-310 (doi:10.1016/j.cell.2016.12.010)
Dr David I Hughes (David.I.Hughes@glasgow.ac.uk), Senior Lecturer, Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ
Synaptic plasticity deficits in schizophrenia
Supervisor: Prof. Brian Morris
Project outline: Schizophrenia is a common disease with a strong genetic influence. A number of functionally-related genes are believed to interact with environmental factors, such as stress or infection during early development, to cause the disease. We have recently found a gene involved in glutamatergic signalling that shows strong genetic association with schizophrenia. This gene is also linked to immune signalling and stress responses. This project aims to test the hypothesis that dysfunction in this gene mediates stress and immune influences on disease risk, and contributes to the neurochemical and cognitive impairments of the disease.
Summary aim: To determine whether gene deficiency produces cortical GABAergic deficits, impairs glutamatergic signalling or produces behavioural changes characteristic of schizophrenia (deficits in working memory and attentional processing).
Techniques to be used: A variety of molecular, cellular and systems level techniques will be used, including
- neural cell cultures
- gene transfection
- western blotting
- mouse behavioural analysis.
- Morris, B. J. and J. A. Pratt (2014). "Novel treatment strategies for schizophrenia from improved understanding of genetic risk." Clinical Genetics. (DOI 10.1111/cge.12485)
- Winchester, C. L., H. Ohzeki, et al. (2012). "Converging evidence that sequence variations in the novel candidate gene MAP2K7 (MKK7) are functionally associated with schizophrenia." Human Molecular Genetics 21: 4910-21.
- Coffey, E. T. (2014). "Nuclear and cytosolic JNK signalling in neurons." Nature Reviews Neuroscience 15: 285-99
- Prof Brian Morris (Brian.Morris@glasgow.ac.uk), Professor of Molecular Neurobiology, Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ
Developing genetic therapy approaches for CNS disorders
Supervisor: Dr Stuart Cobb
Project outline: The aim of this project is to develop gene therapy and genome editing approaches that can be applied to disorders of the nervous system. The primary focus of the project is on Rett Syndrome, a single gene disorder that affects girls. Mutations in this gene cause severe intellectual disabilities as well as a range of other neurological features. Furthermore, deletion of this gene in mice recapitulates the same pattern of neurological signs and thus represents an accurate genetic model of the disorder. At present Rett patients require intensive lifelong support as there is no cure. We know that the disorder is potentially reversible when modelled in mice.
The challenge of this project is to learn more about the role of the gene (MECP2) in the brain and to develop therapeutic strategies that have the potential to ultimately be translated to the clinic.
- assess the consequences of MeCP2 deficiency in the brain
- identify how the gene is regulated and how protein levels differ between cell types in the brain
- develop gene replacement therapies using viral delivery vectors that are amenable to brain delivery/cross the blood brain barrier
- develop genome repair strategies to repair Rett Syndrome-causing mutations in neurons in situ
Techniques to be used
- cell culture
- fluorescence and light microscopy
- genome sequencing
- genetic manipulation
- in vivo models of Rett Syndrome
- Gadalla, K.K.E. et al. (2013) Improved survival and reduced phenotypic severity following AAV9/MECP2 gene transfer to neonatal and juvenile male Mecp2 knockout mice. Molecular Therapy, 21 (1). pp. 18-30.
- Gadalla, K.K.E., Bailey, M.E.S., and Cobb, S.R. (2011) MeCP2 and Rett syndrome: reversibility and potential avenues for therapy. Biochemical Journal, 439 (1). pp. 1-14.
- Guy, J., Gan, J., Selfridge, J., Cobb, S., and Bird, A. (2007) Reversal of neurological defects in a mouse model of Rett syndrome. Science, 315 . pp. 1143-1147.
- Dr Stuart Cobb (firstname.lastname@example.org), Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow
Hormonal regulation of social perception and physical appearance
Supervisor: Prof. Benedict Jones
Project outline: Recent work suggests that mate preferences and aspects of physical appearance are influenced by changes in hormone levels in many primate species, including humans. The proposed research will explore these issues further, focusing on how aspects of social appearance, such as judgments of adults’ attractiveness and infants’ cuteness, and aspects of appearance, such as facial colouration and shape, change as a function of men’s and women’s hormone levels.
Summary aim: To investigate links among aspects of social perception, physical appearance and men’s and women’s hormone level
Techniques to be used: Computer graphic techniques, such as Psychomorph, will be used to experimentally manipulate cues in digital face images. Other techniques from computer and vision science will also be used to objectively measure aspects of appearance. Hormone levels will be assessed from saliva samples.
- Higham JP et al. (2011) Familiarity affects the assessment of female facial signals of fertility by free-ranging male rhesus macaques. Proceedings of the Royal Society of London B, 278, 3452–3458.
- Setchell JM et al. (2006) Signal content of red facial colouration in female mandrills (Mandrillus sphinx). Proceedings of the Royal Society of London B 273, 2395–2400.
- Welling LLM et al. (2008). Men report stronger attraction to femininity in women’s faces when their testosterone levels are high. Hormones and Behavior, 54, 703-708.
- Welling LLM et al. (2007). Raised salivary testosterone in women is associated with increased attraction to masculine faces. Hormones and Behavior, 52, 156-161
- Prof Benedict Jones (email@example.com), Institute of Neuroscience & Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow.
The role of family and visual experience in mate choice
Supervisor: Dr. Lisa DeBruine
Project outline: Humans exhibit homogamy in mate choice and preferences across a range of characteristics, including facial appearance, hair colour and eye colour [1,2]. Explanations for this phenomenon fall into three main categories: those that emphasize matching to own characteristics , those that emphasize learning from parental models [4-6], and those that emphasize the transmission of preferences from parents [7,8].
This project will test predictions from these three hypotheses using both actual partner characteristics and data from visual preference studies. We will aim to test these hypotheses in various populations, such as same-sex versus different-sex couples, adoptees versus non-adoptees, in large population-level datasets, and in twin populations.
Summary aim: This project will aim to test hypotheses for the relationship between own, parental, and partner phenotypic characteristics.
Techniques to be used:
- Face morphing and transformation software (PsychoMorph)
- multilevel regression analyses (using R)
- database management (MySQL)
While statistical and coding experience are helpful, training will be provided in all techniques.
- Little, A. C., Penton-Voak, I. S., Burt, D. M., Perrett, D. I. (2003). Investigating an imprinting-like phenomenon in humans: partners and opposite-sex parents have similar hair and eye color. Evolution and Human Behavior, 24:43–51.
- Bereczkei, T., Gyuris, P., Weisfeld, G.E. (2004). Sexual imprinting in human mate choice. Proceedings of the Royal Society B, 271:1129–1134. doi:10.1098/rspb.2003.2672.
- Keller, M. C., Thiessen, D., Young, R. K. (1996). Mate assortment in dating and married couples. Personality and Individual Differences, 21: 217–221.
- Bateson, P. P. G. (1966). The characteristics and context of imprinting. Biological Review, 41:177–220.
- Ten Cate, C., Verzijden, M. N., Etman, E. (2006). Sexual imprinting can induce sexual preferences for exaggerated parental traits. Current Biology, 16:1128–1132. doi:10.1016/j.cub.2006.03.068.
- Little, A. C., DeBruine, L. M., & Jones, B. C. (2005). Sex-contingent face aftereffects suggest distinct neural populations code male and female faces. Proceedings of the Royal Society of London B, 272, 2283–2287.
- Rantala, M. J., & Marcinkowska, U. M. (2011). The role of sexual imprinting and the Westermarck effect in mate choice in humans. Behavioral Ecology and Sociobiology, 65(5): 859–873. doi:10.1007/s00265-011-1145-y
- Verweij, K. J. H., Burri, A. V, Zietsch, B. P. (2012). Evidence for genetic variation in human mate preferences for sexually dimorphic physical traits. PloS One, 7(11): e49294. doi:10.1371/journal.pone.0049294
- Lisa DeBruine (firstname.lastname@example.org), Reader, Instiute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, 58 Hillhead Street, Glasgow. G12 8QB
Inhaled Nitric Oxide for treatment of stroke
Supervisor: Dr. Chris McCabe
Project outline: Stroke, the 3rd leading cause of death in the UK, affects ~150,000 individual’s p.a., 20-30% of whom die within a month. Equally important, it is the major cause of significant disability with a high proportion of survivors left moderately to severely disabled. Stroke patients occupy 2.6 million acute hospital bed days p.a., stroke care consumes 4-6% of total NHS expenditure (www.stroke.org.uk) and at any one time, 1 in 5 acute hospital beds and 1 in 4 long term beds are occupied by stroke patients.
Currently the only licensed acute stroke therapy is thrombolysis using recombinant tissue plasminogen activator (rt-PA), which increases the probability of recanalisation of the occluded blood vessel and restoration of flow. rt-PA is currently licensed for use within 4.5 hours of stroke onset, resulting in only 2-5% of ischaemic strokes being treated with rt-PA globally. In those patients that receive rt-PA the recanalisation rate can be less than 50% highlighting the desperate need for alternative and/or adjunctive therapies for acute stroke. Nitric Oxide (NO) is a potent endogenous vasodilator that plays a role in the maintenance of cerebral blood flow and neuronal activity. Inhaled NO is FDA approved and has been used in the treatment of pulmonary hypertension in newborns. Recently there has been increasing interest in the role of inhaled NO in animal models of focal cerebral ischaemia and brain injury where a number of studies have demonstrated protective effects.
Terpolilli and colleagues have recently demonstrated that inhaled NO can selectively dilate arterioles and increase collateral blood flow to the ischaemic penumbra (without effecting CBF in the normal cortex) following transient MCAO in the mouse resulting in a reduction in ischaemic damage. The available experimental studies from the literature provide convincing evidence that inhaled NO can improve collateral CBF and outcome following stroke. This form of therapy could be particularly important in animal models that have stroke co-morbidities (i.e hypertension, age) where vascular changes occur in cerebral vessels resulting in impaired flow and vascular reactivity.
Summary aim: This project will investigate the effect of inhalation of NO on ischaemic brain damage following stroke. The effects on cerebral blood flow, infarct volume and functional recovery will be assessed as well as the mechanisms behind these observed effects.
Techniques to be used:
- In vivo models of experimental stroke
- Cerebral Blood Flow measurement
- Behavioural testing
- Western Blotting
- Terpolilli NA, Kim SW, Thal SC, Kataoka H, Zeisig V, Nitzsche B, Klaesner B, Zhu C, Schwarzmaier S, Meissner L, Mamrak U, Engel DC, Drzezga A, Patel RP, Blomgren K, Barthel H, Boltze J, Kuebler WM, Plesnila N (2012) Inhalation of nitric oxide prevents ischemic brain damage in experimental stroke by selective dilatation of collateral arterioles. Circ Res 110: 727-738.
- McCabe C, Gallagher L, Gsell W, Graham D, Dominiczak AF, Macrae IM (2009) Differences in the evolution of the ischemic penumbra in stroke-prone spontaneously hypertensive and Wistar-Kyoto rats. Stroke 40: 3864-3868.
- Reid E, Graham D, Lopez-Gonzalez MR, Holmes WM, Macrae IM & McCabe C (2012). Penumbra detection using PWI/DWI mismatch MRI in a rat stroke model with and without co-morbidity: comparison of methods. J Cereb Blood Flow Metab 32 (9): 1765-1777.
- Dr Chris McCabe (Chris.McCabe@glasgow.ac.uk), Research Fellow, Institute of Neuroscience & Psychology, College of MVLS, University of Glasgow, +44 141 330 5822.
Circadian desynchrony and experimental stroke
Supervisor: Dr. Deborah Dewar
Project outline: Disruption of circadian rhythms (circadian desynchrony) by exposure to erratic light dark cycles, is one factor that contributes to diseases associated with urbanisation. In humans and animals, circadian desynchrony is associated with obesity, diabetes, hypertension - factors that predispose to stroke. Stroke is the leading cause of neurological disability in adults and the third major cause of death in the UK. Given the economic and societal burdens stroke imposes there is a need not only to reduce the risk of stroke but also to reduce the impact of ischaemia on the brain when stroke occurs.
The risk of stroke onset is increased by co-morbidities including hypertension, diabetes and obesity, the diseases associated with urbanisation. These same co-morbidities influence the severity of stroke outcome: hypertension, hyperglycemia and obesity (features of “metabolic syndrome”) at stroke onset lead to more severe brain damage.
The Stroke and Brain Imaging group at the University of Glasgow comprises both stroke clinicians and experimental scientists. A study of hyperglycemia in stroke patients (1) led us to investigate the detrimental effects of hyperglycemia in experimental models of stroke. Hyperglycemia, at levels observed in patients, rapidly exacerbated the growth of ischaemic lesions, as determined by MRI imaging as did features of metabolic syndrome or hypertension (2). Thus, the types of physiologic and metabolic changes that exacerbate the severity of ischaemic brain damage are associated with circadian desynchrony. This has led to a new collaboration between stroke and circadian rhythm researchers at the University of Glasgow.
Summary aim: To investigate how circadian desynchrony affects the amount of brain damage after stroke.
Techniques to be used:
- experimental models of stroke
- behavioural analyses
- physiological measurements
- histology and immunohistochemistry
- analysis of oxidative stress markers.
- McCormick et al, Ann.Neurol;2010 570-8
- Tarr et al, J.Cereb.Blood.Flow Metab. 2013 33:1556-63
- McCabe et al., Stroke. 2009 40:3864-8
Spinal cord neuronal pathways for pain and itch
Supervisor: Prof. Andrew Todd
Project outline: The dorsal horn of the spinal cord plays an important role in processing sensory information that is perceived as pain and itch, but despite its importance we know little about the organisation of neural circuits in this region. Sensory information is conveyed to the brain via projection neurons, which are concentrated in lamina I and scattered through the deeper dorsal horn laminae. However, the vast majority of neurons in laminae I-III are interneurons, with axons that arborise locally. Around two-thirds of these are glutamatergic (excitatory), while the remainder are inhibitory and use GABA and/or glycine.
Recent studies have demonstrated that the inhibitory interneurons can be divided into a number of distinct neurochemical populations that differ in their synaptic inputs and outputs, and this has begun to shed light on how the inhibitory circuits are organised. We offer a variety of projects that will explore the neuronal organisation and synaptic circuitry of the dorsal horn, and how these circuits contribute to the transmission and modulation of sensory information at the spinal level.
Summary aim: To identify distinct functional populations among dorsal horn neurons and to define their roles in synaptic circuits that are responsible for the perception of pain and itch.
Techniques to be used:
- confocal and electron microscopy
- neuronal reconstruction
- retrograde neuronal tracing
- PCR (for genotyping).
- Todd AJ (2010) Neuronal circuitry for pain processing in the dorsal horn. Nature Reviews of Neuroscience 11:823-836.
- Polgár E, Sardella TCP, Tiong SYX, Locke S, Watanabe M, Todd AJ (2013) Functional differences between neurochemically-defined populations of inhibitory interneurons in the rat spinal cord. Pain 154:2606-2615.
- Kardon AP, Polgár E, Hachisuka J, Snyder LM, Cameron D, Savage S , Cai X, Karnup S, Fan CR,. Hemenway GM, Bernard CS, Schwartz ES, Nagase H, Schwarzer C, Watanabe M, Furuta T, Kaneko T, Koerber HR, Todd AJ, Ross SE (2014) Dynorphin acts as a neuromodulator to inhibit itch in the dorsal horn of the spinal cord. Neuron 82:573-586.
- Prof Andrew J Todd (email@example.com) MBBS, PhD, FSB, Professor of Neuroscience, Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ;
- Dr John S Riddell (firstname.lastname@example.org) PhD, Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ
Neurobiology of reward learning and decision making in humans
Supervisor: Dr. Marios Philiastides
Project outline: Imagine picking wild berries in a forest when suddenly a swarm of bees flies out from behind a bush. In a split second, your motor system has already reacted to flee the swarm. This automatic response constitutes a powerful survival mechanism that allows efficient behaviour switching to escape from a potential hazard in the environment. In turn, a separate and more deliberate process of learning to avoid similar situations will also occur, rendering future berry picking attempts less appealing.
Our lab is interested in understanding the neural pathways and mechanistic principles guiding these processes. To this end we use a multimodal neuroimaging approach in combination with computational modelling and advanced statistical data analysis techniques to closely scrutinise the data collected from human participants.
Our ultimate goal in characterising these neural processes is to further improve our understanding of how everyday responses to rewarding or stressful events can affect our capacity to make optimal decisions, as well as facilitate the study of how mental disorders—such as chronic stress, obsessive-compulsive-disorder, post-traumatic disorder and depression—affect learning and strategic planning.
Summary aim: Projects are available to investigate the neurobiological basis of reward learning and decision making in humans using multimodal neuroimaging (e.g. MEG/EEG, fMRI, simultaneous EEG/fMRI) and computational modelling. These projects are designed to characterize the patterns of brain activity underlying reward and value-based decisions, the computational principles underlying such decisions, and how these can be used to identify biomarkers for disorders known to compromise ones decision making faculties to be used in future neurobiological or clinical research.
Techniques to be used:
- ultra-high field (7T) fMRI
- simultaneous EEG/fMRI
- multivariate pattern analysis
- computational modelling
- Elsa Fouragnan, Chris Retzler, Karen Mullinger and Marios G. Philiastides (2015), Two spatiotemporally distinct value systems shape reward-based learning in the human brain, Nature Communications, 6: 8107.
- Marios G. Philiastides, Guido Biele, and Hauke R. Heekeren (2010), A mechanistic account of value computation in the human brain, PNAS, 107 (20): 9430-9435.
- Marios G. Philiastides, Guido Biele, Niki Vavatzanidis, Philipp Kazzer and Hauke R. Heekeren (2010), Temporal dynamics of prediction error processing during reward-based decision making, NeuroImage, 53 (1): 221-232.
- Marios Philiastides, Institute of Neuroscience and Psychology, Centre for Cognitive Neuroimaging (CCNi), University of Glasgow, 58 Hillhead Street, Glasgow G12 8QB, UK. Marios.Philiastides@glasgow.ac.uk Ph: +44 (0) 141 330 4774
Physiology of Cognitive Deficits in Schizophrenia
Supervisor: Dr. Peter Uhlhaas
Project outline: Converging evidence from electrophysiological, physiological and anatomical studies suggests that abnormalities in the synchronized oscillatory activity of neurons may have a central role in the pathophysiology of schizophrenia. In patients with schizophrenia, the synchronisation of beta- and gamma-band activity is abnormal, suggesting a crucial role for dysfunctional oscillations in the generation of the cognitive deficits and symptoms of the disorder. Dysfunctional oscillations may arise due to anomalies in the brain’s rhythm generating networks of GABA (γ-aminobutyric acid) interneurons and deficits in NMDA-receptor functioning.
In our current work, we employ magnetoencephalography (MEG) and Magentic Resonance Spectroscopy (MRS) in schizophrenia patients as well as in participant at ultra-high risk for psychosis to identify biomarkers for early detection and diagnosis that shall aid development of novel treatments.
Summary aim: To identify the role of rhythmic activity in cognitive and clinical symptoms of schizophrenia
Techniques to be used:
- Brain Stimulation
- Grent-'t-Jong, T., Rivolta, D., Sauer, A., Grube, M., Singer, W., Wibral, M., Uhlhaas, P.J. MEG-measured visually induced gamma-band oscillations in chronic schizophrenia: Evidence for impaired generation of rhythmic activity in ventral stream regions. Schizophr Res. doi: 10.1016/j.schres.2016.06.003
- Uhlhaas, P.J., Singer, W. Oscillations and neuronal dynamics in schizophrenia: The search for basic symptoms and translational opportunities. Biological Psychiatry 15;77(12):1001-1009. doi: 10.1016/j.biopsych.2014.11.019. (IF: 9.5)
The role of brain rhythms in human communication
Supervisor: Prof Joachim Gross
Project outline: Human brain activity is characterised by rhythmic fluctuations - so called brain rhythms. They are expressed in different aspects of action and perception. A notable example is continuous speech where syllables are typically produced at a rate of 3-6 per second. This rhythmicity likely facilitates human communication because it allows for temporal prediction.
This project will investigate the role of brain oscillations in communication between two people. It starts with a characterisation of auditory and visual signals (speech and mouth movements) and continuous to use MEG and EEG to record brain activity during natural conversations. Rhythmic components in neural activity will be related to turn-taking in conversations and to behavioural performance during communication.
Summary aim: To characterise rhythmic components in auditory and visual signals during continous speech. To relate brain rhythms to communication.
Techniques to be used:
- high-density neuroimaging based on MEG
- MEG analysis in time and frequency domain
- connectivity analysis
- preparation of scientific manuscripts for publication
- general presentation skills
- Lip movements entrain the observers’ low-frequency brain oscillations to facilitate speech intelligibility. H Park, C Kayser, G Thut, J Gross - eLife, 2016
- Speech rhythms and multiplexed oscillatory sensory coding in the human brain J Gross, N Hoogenboom, G Thut, P Schyns, S Panzeri… - PLoS Biol, 2013
- Prof Joachim Gross, Institute of Neuroscience and Psychology, Centre for Cognitive Neuroimaging (CCNi), University of Glasgow, 58 Hillhead Street, Glasgow G12 8QB, UK. Joachim.Gross@glasgow.ac.uk Ph: +44 (0) 141 330 3947