Postgraduate research 

Neuroscience & Psychology PhD/iPhD/MD

brain scan and patient

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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.

  • PhD: 3-4 years full-time; 5 years part-time;
  • MD (Doctor of Medicine): 2 years full-time; 4 years part-time;
  • IPhD: 5 years full-time;

Unfortunately our Application and Applicant Self Service systems are currently unavailable. We will post updates on the availability of these systems as soon as possible on our Enquiry and Programme pages. We can assure you that no applicant will be disadvantaged in respect to deadlines as a result of these systems issues.

Research projects

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Towards restoring memory dysfunction in prodromal Alzheimer’s Disease

Supervisor: michael.kohl@glasgow.ac.uk

Project outline: 

Brains contain billions of specialised cells, called neurons, which are the fundamental building blocks of every circuit in the nervous system. The principal purpose of a neuron is to transmit information: when they receive sufficient input from other neurons, they send brief electrical pulses, called action potentials, which allows them to communicate with other neurons. Broadly speaking, neurons exist as two types: excitatory neurons, which make other neurons more likely to fire action potentials, and inhibitory interneurons, which make other neurons less likely to fire action potentials. If one were to compare the brain's electrical activity to music, then excitatory neurons provide the notes for the brain's 'music', whilst inhibitory interneurons provide the pauses between notes. All computations in the brain require very precise synchrony between different neurons: without the notes, there would be only silence, and without the pauses, the music would become a cacophony.

Recent research has shown that dementias, such as Alzheimer's Disease, cause a dysfunction in inhibitory interneurons. The resulting effects on normal brain function are severe and thought to translate to the cognitive and memory impairments seen in Alzheimer's Disease. Data from our labs shows that selectively manipulating inhibitory interneuron activity can restore normal brain function in mouse models of Alzheimer's Disease. Intriguingly, a similar rescuing effect has recently been attributed to non-invasive light and acoustic stimulation at frequencies similar to the frame rate of video (40 Hz).

Ongoing work on this subject matter in the Kohl Group is addressing two aims. One is of a basic science nature: We would like to determine the mechanisms underlying the rescue effects following stimulation of inhibitory interneurons and delivery of light and acoustic stimuli in mouse models of Alzheimer's Disease. The other aim is of a translational nature: We would like to see whether stimulation of inhibitory interneurons and delivery of light and acoustic stimuli in mouse models of Alzheimer's Disease can restore memory function in the early stages of Alzheimer's Disease.

This PhD position would contribute to our ongoing work using a combination of state-of-the-art methods. The student would be supervised by the PI and a senior post-doc and receive training in all experimental methods as well as sophisticated analysis.

Summary aim: Characterise cellular/circuit level dysfunction of genetically identified inhibitory neurons in the retrosplenial cortex in mouse models of dementia; link cellular/circuit level dysfunction to dementia-related behavioural phenotypes; develop and test rescue strategies for dementia-related behavioural phenotypes. 

Techniques to be used: 

A variety of cellular, systems and behavioural level techniques will be used, including

  • Electrophysiology
  • Miniature microscope imaging
  • Multiphoton imaging
  • Optogenetic manipulations
  • Behavioural assays
  • Information theory
  • Artificial neural networks

References:

  1. Park, M. et al. Effects of transcranial ultrasound stimulation pulsed at 40 Hz on Aβ plaques and brain rhythms in 5×FAD mice. Transl Neurodegener 10, 48 (2021) | Barros, A. C. B. de et al. Retrosplenial cortex is necessary for spatial and non-spatial latent learning in mice. Biorxiv 2021.07.21.453258 (2021) doi:10.1101/2021.07.21.453258.

  2. Park, K. et al. Optogenetic activation of parvalbumin and somatostatin interneurons selectively restores theta-nested gamma oscillations and oscillation-induced spike timing-dependent long-term potentiation impaired by amyloid β oligomers. Bmc Biol 18, 7 (2020)

  3. Chung, H., Park, K., Jang, H. J., Kohl, M. M. & Kwag, J. Dissociation of somatostatin and parvalbumin interneurons circuit dysfunctions underlying hippocampal theta and gamma oscillations impaired by amyloid β oligomers in vivo. Brain Struct Funct 1–20 (2020) doi:10.1007/s00429-020-02044-3

  4. Iaccarino, H. F. et al. Gamma frequency entrainment attenuates amyloid load and modifies microglia. Nature 540, 230–235 (2016).

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Functional MRI of visual predictions in cortex

Supervisor: Prof Lars Muckli & Dr Bianca van Kemenade

Project outline: Perception is an active and dynamic process. Our senses are constantly bombarded by sensory input, and in order to make sense of this (sometimes noisy) information, it is thought that we generate predictions that enable us to either enhance the signal to allow for more veridical perception, or to suppress expected input to allow for more resources processing unexpected input. There are still many questions regarding how we generate such sensory predictions, where they are generated in the brain, and how they influence our perception. This project will combine psychophysics and fMRI to answer such questions.

Summary aim: To determine how sensory predictions are generated in the human brain, and how these predictions influence our perception.

Techniques to be used:

  • Brain imaging (fMRI)
  • Behavioural methods (psychophysics)
  • Python programming

References:

  • Petro et al., (2014), Contributions of cortical feedback to sensory processing in primary visual cortex. Frontiers in Psychology
  • Press et al., (2019), The perceptual prediction paradox. Trends in Cognitive Sciences.

Contact:

Prof Lars Muckli, School of Psychology and Neuroscience, Lars.Muckli@glasgow.ac.uk, 0141 330 6237 

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Investigation of the somatosensory coding mechanism in the spinal cord

Supervisor: Dr Junichi Hachisuka

Project outline: Somatosensory information including pain and itch is conveyed through the spinal cord to the brain. However, the physiological and anatomical basis of somatosensory processing in the spinal cord is still largely unknown. Our goal is to understand how the spinal dorsal horn neurons differentiate various somatosensory stimuli, especially those associated with pain and itch. To tackle this question, we have developed a semi-intact somatosensory preparation that enables us to record the spinal dorsal horn neuron activity in response to natural stimulation of the skin. Combining this with molecular, genetic and anatomical approaches, we will examine the physiological properties of spinal cord neurons to the natural sensory stimuli.

Summary aim:To reveal the coding mechanism for somatosensory perception including pain and itch in spinal cord dorsal horn neurons.

Techniques to be used:

  • Whole-cell patch clamp recording
  • Retrograde neuronal tracing
  • Immunocytochemistry
  • Neuronal reconstruction
  • Behavioural testing


References:

  • Choi, S. et al. Parallel ascending spinal pathways for affective touch and pain. Nature (2020).
  • Hachisuka, J. et al. Semi-intact ex vivo approach to investigate spinal somatosensory circuits. Elife 5, 1–19 (2016).
  • Hachisuka, J., Koerber, H. R. & Ross, S. E. Selective-cold output through a distinct subset of lamina I spinoparabrachial neurons. Pain 161, 185–194 (2020).
  • Hachisuka, J. et al. Wind-up in lamina I spinoparabrachial neurons: A role for reverberatory circuits. Pain 159, 1484–1493 (2018).
  • Kardon, A. P. et al. Dynorphin acts as a neuromodulator to inhibit itch in the dorsal horn of the spinal cord. Neuron 82, 573–86 (2014).
  • Snyder, L. M. et al. Kappa Opioid Receptor Distribution and Function in Primary Afferents. Neuron 99, 1274-1288.e6 (2018).

Contact:

Dr Junichi Hachisuka (Junichi.Hachisuka@glasgow.ac.uk), Senior Lecturer, School of Psychology and Neuroscience, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ

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Synaptic circuitry of the spinal dorsal horn: unmasking the cellular basis of chronic pain

Supervisor: Dr. David I HughesAndrew.Todd@glasgow.ac.uk

Project outline: 

Chronic (persistent) pain affects approximately 20% of the global population, however, one in three of these patients do not respond to any form of 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.

Chronic pain can arise from the skin, from joints or from internal organs and in these projects, we will aim to identify circuits in the spinal cord that contribute to the development and maintenance of these conditions.

These projects will use a variety of molecular, cellular and systems level techniques to study somatosensory circuits in rodent models and determine how these change in pathological states.

Summary aim: 

To identify spinal circuits implicated in the development of chronic pain from the skin, from joints and from internal organs.

Techniques to be used: 

A variety of molecular, cellular and systems level techniques will be used, including

  • recovery surgical techniques
  • optogenetics, chemogenetics and targeted silencing
  • behavioural testing
  • general histological techniques and immunocytochemistry
  • confocal microscopy
  • transmission electron microscopy
  • image analysis using dedicated software (eg Neurolucida for confocal, Neurolucida Explorer, Meta Morph and Image J)

References:

  1. Hughes DI and Todd AJ. (2020). Inhibitory interneurons in the spinal dorsal horn. Special issue on Pain: Aligning New Approaches to Accelerate the Development of Analgesic Therapies. Neurotherapeutics 17: 874-885. (doi: 10.1007/s13311-020-00936-0)
  2. Boyle KA, Gradwell MA, Yasaka T, Dickie AC, Polgár E, Ganley RP, Orr DPH, Watanabe M, Abraira VE, Kuehn ED, Zimmerman AL, Ginty DD, Callister RJ, Graham BA, Hughes DI. (2019).  Defining a spinal microcircuit that gates myelinated afferent input: implications for tactile allodynia. Cell Reports 28 28: 526-540.e6. (doi: 10.1016/j.celrep.2019.06.040)
  3. 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)
  4. 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. Journal of Physiology 593: 4319-4339 (doi:10.1113/JP270855)
  5. 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)
  6. 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)

 Contact:

  • Dr David I Hughes (David.I.Hughes@glasgow.ac.uk), Senior Lecturer, School of Psychology and Neuroscience, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ

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Synaptic plasticity deficits in schizophrenia

Supervisor: Prof. Brian Morris

Project outline: Schizophrenia is a common and severe 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 (in utero), to cause the disease. We have recently identified a gene involved in glutamatergic signalling in the CNS that shows strong genetic association with schizophrenia. This gene becomes especially interesting, considering that it is also activated during maternal exposure to infection during pregnancy. 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 the extent to which the gene is involved in synaptic plasticity in the CNS, and in stress and immune responses, and 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

  • Neuronal and microglial cell cultures
  • gene transfection
  • immunofluorescence
  • RT-PCR
  • western blotting
  • mouse behavioural analysis.

References:

  1. 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)
  2. 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.
  3. Coffey, E. T. (2014). "Nuclear and cytosolic JNK signalling in neurons." Nature Reviews Neuroscience 15: 285-99
  4. Openshaw, R.L et al., (2019) “JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk” Journal of Neuroinflammation. 16: 18
  5. Bristow, G.C. et al (2020) “16p11 Duplication Disrupts Hippocampal-Orbitofrontal-Amygdala Connectivity, Revealing a Neural Circuit Endophenotype for Schizophrenia” Cell Reports, 31, 107536, https://doi.org/10.1016/j.celrep.2020.107536.

Contact:

  • Prof Brian Morris (Brian.Morris@glasgow.ac.uk),  Professor of Molecular Neurobiology, School of Psychology and Neuroscience, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ

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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: 

  • immunocytochemistry
  • confocal and electron microscopy
  • neuronal reconstruction
  • retrograde neuronal tracing
  • PCR (for genotyping).

References:

  1. Todd AJ (2010) Neuronal circuitry for pain processing in the dorsal horn. Nature Reviews of Neuroscience 11:823-836.
  2. 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.
  3. 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.

Contact:

  • Prof Andrew J Todd (andrew.todd@glasgow.ac.uk) MBBS, PhD, FSB, Professor of Neuroscience, School of Psychology and Neuroscience, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ;
  • Dr John S Riddell (john.riddell@glasgow.ac.uk) PhD, School of Psychology and Neuroscience, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ

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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: 

  • M/EEG
  • fMRI
  • ultra-high field (7T) fMRI
  • simultaneous EEG/fMRI
  • tES
  • pupillometry
  • multivariate pattern analysis
  • computational modelling

References:

  1. 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.
  2. 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.
  3. 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.

Contact:

  • Marios Philiastides, School of Psychology and Neuroscience , 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

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Synaptic plasticity deficits in schizophrenia

Supervisor: Prof. Brian Morris

Project outline: Schizophrenia is a common and severe 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 (in utero), to cause the disease. We have recently identified a gene involved in glutamatergic signalling in the CNS that shows strong genetic association with schizophrenia. This gene becomes especially interesting, considering that it is also activated during maternal exposure to infection during pregnancy. 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 the extent to which the gene is involved in synaptic plasticity in the CNS, and in stress and immune responses, and 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

  • Neuronal and microglial cell cultures
  • gene transfection
  • immunofluorescence
  • RT-PCR
  • western blotting
  • mouse behavioural analysis.

References:

  1. 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)
  2. 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.
  3. Coffey, E. T. (2014). "Nuclear and cytosolic JNK signalling in neurons." Nature Reviews Neuroscience 15: 285-99
  4. Openshaw, R.L et al., (2019) “JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk” Journal of Neuroinflammation. 16: 18
  5. Bristow, G.C. et al (2020) “16p11 Duplication Disrupts Hippocampal-Orbitofrontal-Amygdala Connectivity, Revealing a Neural Circuit Endophenotype for Schizophrenia” Cell Reports, 31, 107536, https://doi.org/10.1016/j.celrep.2020.107536.

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Overview

Discovering how the central nervous system functions normally and how it is affected by disease and injury present major challenges for biological and medical research in the 21st century. Over the last two decades there has been an explosion of interest in understanding the normal function of the brain illustrated by launching of the Human Brain Project and the Brain Initiative. In parallel the huge burden of neurological and psychiatric disorders on society and the current lack of effective treatments means there is an urgent need to develop new approaches.

Four centres of excellence

  • Neuroscience
  • Stroke and Brain Imaging
  • Cognitive Neuroimaging
  • Social Interaction

Via their interactions, our centres aim to understand brain networks at multiple levels of function, from cells to cognition with a strong emphasis on imaging and computational analyses of each level. Our translational efforts are directed at a range of disorders including pain, stroke, spinal cord injury, neurodevelopmental disorder and schizophrenia.

Our staff and students have access to world-class imaging infrastructure and supporting high-performance computing facilities. This provides strong unifying technological and methodological links across the different centres of the INP, including a state-of-the-art platform of cognitive imaging in humans, a high field small bore animal scanner, dedicated confocal and electron microscopy facilities, as well as cutting edge equipment to measure dynamic social signals.

A PhD programme in Neuroscience and Psychology is based on individual research projects covering an exciting range of topics including:

  • non-invasive multimodal brain imaging using fMRI
  • dynamics of auditory and visual processing
  • functions of brain oscillations
  • neuroendocrine effects on social interactions
  • neuromodulation via TMS
  • spinal cord and brainstem circuits in pain
  • molecular mechanisms of synaptic transmission and plasticity
  • neural control of respiration
  • schizophrenia
  • spinal cord injury
  • rett syndrome
  • imaging in acute stroke
  • stroke clinical trial and design
  • stem cells as treatment for stroke
  • experimental stroke
  • cortical circuits mediating perception and memory
  • circadian rhythms

Study options

PhD

  • Duration: 3/4 years full-time; 5 years part-time

Individual research projects are tailored around the expertise of principal investigators.

Integrated PhD programmes (5 years)

Applications for September 2022 intake are now closed. Applications will reopen in October 2022.

Our Integrated PhD allows you to combine masters level teaching with your chosen research direction in a 1+3+1 format. 

International students with MSc and PhD scholarships/funding do not have to apply for 2 visas or exit and re-enter the country between programmes. International and UK/EU students may apply.

Year 1

Taught masters level modules are taken alongside students on our masters programmes. Our research-led teaching supports you to fine tune your research ideas and discuss these with potential PhD supervisors. You will gain a valuable introduction to academic topics, research methods, laboratory skills and the critical evaluation of research data. Your grades must meet our requirements in order to gain entry on to a PhD research programme. If not, you will receive the masters degree only.

Years 2, 3 and 4

PhD programme with research/lab work, completing an examinable piece of independent research in year 4.

Year 5

Thesis write up.

MD (Doctor of Medicine)

  • Duration: 2 years full-time; 4 years part-time (for medically-qualified graduates only)

Entry requirements

A 2.1 Honours degree or equivalent.

English language requirements

For applicants whose first language is not English, the University sets a minimum English Language proficiency level.

International English Language Testing System (IELTS) Academic module (not General Training)

  • 6.5 with no sub-test under 6.0. 
  • Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test.

Common equivalent English language qualifications

All stated English tests are acceptable for admission to this programme:

TOEFL (ib, my best or athome)

  • 90 with minimum R 20, L 19, S 19, W 23. 
  • Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test, this includes TOEFL mybest.

PTE (Academic)

  • 60 with minimum 59 in all sub-tests.
  • Tests must have been taken within 2 years 5 months of start date. Applicants must meet the overall and subtest requirements using a single test.

Glasgow International College English Language (and other foundation providers)

  • 65%.
  • Tests are accepted for academic year following sitting.

University of Glasgow Pre-sessional courses

  • Tests are accepted for 2 years following date of successful completion.

Alternatives to English Language qualification

  • Degree from majority-English speaking country (as defined by the UKVI including Canada if taught in English).
  • Students must have studied for a minimum of 2 years at Undergraduate level, or 9 months at Master’s level, and must have completed their degree in that majority-English speaking country and within the last 6 years.
  • Undergraduate 2+2 degree from majority-English speaking country (as defined by the UKVI including Canada if taught in English).
  • Students must have completed their final two years study in that majority-English speaking country and within the last 6 years.

For international students, the Home Office has confirmed that the University can choose to use these tests to make its own assessment of English language ability for visa applications to degree level programmes. The University is also able to accept an IELTS test (Academic module) from any of the 1000 IELTS test centres from around the world and we do not require a specific UKVI IELTS test for degree level programmes. We therefore still accept any of the English tests listed for admission to this programme.

Pre-sessional courses

The University of Glasgow accepts evidence of the required language level from the English for Academic Study Unit Pre-sessional courses. We also consider other BALEAP accredited pre-sessional courses:

Fees and funding

Fees

2023/24

  • UK: To be confirmed by UKRI [22/23 fee was £4596]
  • International & EU: £27,930

Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.

Irish nationals who are living in the Common Travel Area of the UK, EU nationals with settled or pre-settled status, and Internationals with Indefinite Leave to remain status can also qualify for home fee status.

Alumni discount

We offer a 20% discount to our alumni on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed Junior Year Abroad, Exchange programme or International Summer School with us. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.

Possible additional fees

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

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2022/23 fees

  • UK: £4,596
  • International & EU: £23,950

Possible additional fees

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

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Funding

The iPhD  is not supported by University of Glasgow Scholarship/Funding

Support

The College of Medical, Veterinary and Life Sciences Graduate School provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
 
Our overarching aim is to provide a research training environment that includes:

  • provision of excellent facilities and cutting edge techniques
  • training in essential research and generic skills
  • excellence in supervision and mentoring
  • interactive discussion groups and seminars
  • an atmosphere that fosters critical cultural policy and research analysis
  • synergy between research groups and areas
  • extensive multidisciplinary and collaborative research
  • extensive external collaborations both within and beyond the UK 
  • a robust generic skills programme including opportunities in social and commercial training

Many of our project supervisors have strong academic connections with international collaborators in universities and research institutes across the world. Funds are available through the college of Medical, Veterinary and Life Sciences to allow visits to international laboratories where part of your project can be carried out, if you and your supervisor decide this would enhance your research and training. This provides an excellent opportunity for networking and increasing your scientific knowledge and skill set. Some supervisors also have strong links with industry. The university organises an open day to highlight career opportunities in industry related to our research.

Resources

We offer a wide range of cutting-edge research facilities. Our imaging centre is equipped with state of the art technology for multimodal human brain imaging (fMRI, MEG, TMS and EEG) with sophisticated analysis methods to study the functioning of the human brain. In the near future we will extend these facilities to include the unique Imaging Centre of Excellence at the new South Glasgow University Hospital which will include a world-leading £7m ultra high-field MRI scanner, a facility which will be unique in the UK.

Our laboratories have a wide range of resources and technical expertise for studies in experimental systems using cell culture, confocal microscopy, gene therapy, electrophysiology, 7 Tesla small bore experimental MRI, behavioural assessment. 

How to apply

Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor who will act as the main source of academic support and research mentoring. You may want to identify a potential supervisor and contact them to discuss your research proposal before you apply. Please note, even if you have spoken to an academic staff member about your proposal you still need to submit an online application form.

You can find relevant academic staff members with our staff research interests search.

Gather your documents

Before applying please make sure you gather the following supporting documentation:

  1. Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document.
  2. Degree certificates (and an official translation, if needed): scanned copy in colour of the original document.
  3. Two references on headed paper and signed by the referee. One must be academic, the other can be academic or professional. References may be uploaded as part of the application form or you may enter your referees contact details on the application form. We will then email your referee and notify you when we receive the reference.  We can also accept confidential references direct to rio-researchadmissions@glasgow.ac.uk, from the referee’s university or business email account.
  4. Research proposal, CV, samples of written work as per requirements for each subject area.

Unfortunately our Application and Applicant Self Service systems are currently unavailable. We will post updates on the availability of these systems as soon as possible on our Enquiry and Programme pages. We can assure you that no applicant will be disadvantaged in respect to deadlines as a result of these systems issues.

Contact us

Before you apply

PhD/MSc/MD: email mvls-gradschool@glasgow.ac.uk

iPhD: email mvls-iphd@glasgow.ac.uk

After you have submitted your application

PhD/MSc/MD/iPhD: contact our Admissions team

Any references may be submitted by email to: rio-researchadmissions@glasgow.ac.uk