School of Psychology

Behavioural Neuroscience


How we learn and how we behave

The Behavioural Neuroscience group investigates psychological and neural mechanisms underlying behaviour and psychiatric and neurological disease.

Research includes cross-species studies of learning and attention in rodents and humans. Insights are applied to disorders including schizophrenia and drug addiction, and the group maintains close links with colleagues in Biomedical Sciences, Biosciences and Psychiatry.

Recent projects and publications 

Recently funded projects examine associative learning mechanisms and neural substrates (BBSRC, Wellcome Trust) and contribution of hippocampal dysfunction to schizophrenia symptoms (Royal Society), and prefrontal mechanisms underlying cognitive deficits (Leverhulme Trust Fellowship).


Tobias Bast
Associate Professor

My research examines how a brain circuit consisting of the hippocampus, prefrontal cortex and connected subcortical sites mediates and integrates important cognitive functions, including everyday-type memory (e.g., memory for places and events) and attention, and other behavioural processes (emotional, motivational, sensorimotor).

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In addition, I study how dysfunction in this neural circuit causes cognitive and behavioural deficits. My major approach to address these questions is to combine sophisticated behavioural testing with a wide range of in vivo neurobiological methods to analyse and manipulate brain function in rat models. A concise overview of main lines of research and key underlying ideas can be found in our recent reviews (Bast, 2011, Curr Opin NeurobiolBast et al., 2017, Br J Pharmacol).

Current lines of research

Hippocampo-prefrontal/subcortical interactions mediating the hippocampal learning-behaviour translation:Continuing work on the hippocampal learning-behaviour translation (Bast et al, 2009, PLoS Biol; also see press release), we aim to identify prefrontal and subcortical mechanisms underlying behavioural performance based on hippocampus-dependent rapid-place learning and to characterize how the hippocampus interacts with these sites. We have begun to collaborate with Stephen Coombes and colleagues (Mathematics, University of Nottingham) to synthesize relevant neurobiological findings into neuro-computational models.

Off balance - cognitive deficits caused by hippocampo-prefrontal neural disinhibition: Neural disinhibition, i.e. GABA dysfunction, in hippocampus and prefrontal cortex has been implicated in many brain disorders characterised by cognitive deficits, including schizophrenia, cognitive ageing and Alzheimer's disease. We aim to determine if and howprefrontal and hippocampal disinhibition disrupt cognition and behaviour and to explore new pharmacological treatment strategies. To this end, we study the neural-network effects and behavioural/cognitive deficits resulting from such disinhibition in rodent models (Pezze et al, 2014, J NeurosciMcGarrity et al, 2017, Cereb CortexBast et al., 2017, Br J Pharmacol; also see press releases: 201420162017)

Hippocampo-prefrontal-subcortical circuit and aversive stimulus processing - fear memory and pain: Previous research, including our own, revealed a key role for the hippocampo-prefrontal-subcortical circuit in fear memory (e.g., Bast et al, 2003, HippocampusPezze et al, 2003, Cereb CortexHeath et al, 2015, PsychopharmacologyWang et al, 2015, Hippocampus). I continue collaborative research into the role of this circuit in fear behaviour in collaboration with Carl Stevenson (Biosciences, University of Nottingham). Recently, I have also become interested in how this circuit is implicated in chronic pain conditions. We have translational studies on the way to examine how chronic pain affects components within the hippocampo-prefrontal-subcortical circuit, as well as the cognitive and behavioural functions mediated by these components (in collaboration with colleagues at the Arthritis Research UK Pain Centre and in Life Sciences, University of Nottingham).

New applications of translational brain imaging methods in rodents: Methods developed for the non-invasive imaging of the human brain (MRI and other metabolic imaging methods) could substantially complement the neurobiological approaches traditionally used to characterise brain structure and function in rodent models. I am involved in projects adapting such methods for new applications in rodent models.

Studies of human cognition, using translational behavioral tests similar to our rodent paradigms: We have adapted a key rodent test of hippocampus-dependent rapid place learning, the delayed-matching-to-place watermaze test (e.g., Bast et al, 2009, PLoS Biolda Silva et al., 2014, Learn Memory), for human testing, using a virtual maze on a computer. Studies using this new virtual maze task, and other translational behavioral tests, in human participants will facilitate translation of findings from rodent model studies to humans.

PDF files of selected publications can be found at:

Charlotte Bonardi
Associate Professor

My main interest is in associative learning, a process that seems to be designed to let us learn about the causal structure of the world around us, allowing us to predict and control our environment. It is clear that this type of learning is important for the most basic aspects of our daily life, and it is found throughout the animal kingdom.

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Some psychologists also argue that networks of associations might underlie more complex types of learning in human subjects, such as concept formation and language. If this view is correct, then it is important for us to have a thorough understanding of associative processes and the limits of what they can explain. My research is (paradoxically) mainly concerned with types of learning that are assumed not to be easily explained in terms of association formation: the aim is to examine whether modifications of associative theory could allow it to accommodate these apparently nonassociative phenomena.

My previous and current work addresses the following topics:


Conditional learning

In some circumstances a particular item can have different associates depending on the conditions in which it is presented: for example, for a bilingual person the sight of a sheep (say) is going to be associated with different verbal labels depending on the language that they are speaking.  It appears as though the context is switching between the different associations that have been formed.  This process, known as conditional learning (or occasion setting) cannot be explained in terms of simple associations.  I have developed an associative-type account of conditional learning, that makes specific predictions about how conditional cues function.  Some of my current research is aimed at testing this hierarchical account of conditional learning.


When a stimulus of a particular duration (e.g. 20 seconds) predicts a particular outcome, association formation allows learning that the stimulus predicts the outcome - but not learning when (i.e. outcome will occur 20 seconds after stimulus onset).  Learning about time in this way does occur, but most associative theories cannot easily explain it, and make relatively few predictions about the effects of the temporal characteristics of cues on associative learning phenomena.  In a collaboration with Dr Dómhnall Jennings (University of Newcastle), we are investigating the way in which associative theories can represent temporal cues, with a view to developing an associative account of timing effects. We are also, in collaboration with Dr Eduardo Alonso (City University) and Dr Esther Mondragón (Centre for Computational and Animal Learning Research), using simulations to evaluate whether our findings can be accommodated by associative theories.

Hippocampus and learning

Damage to the hippocampus produces a complex range of cognitive deficits, for example in spatial learning; however, association formation is usually said to be intact, implying that associative learning does not underly the skills that are affected by hippocampal damage.  However, our recent work suggests that certain sorts of associative learning can be impaired after hippocampal damage, implying that an associative learning impairment could mediate the effects if hippocampal damage on, for example, spatial learning.  We aim to investigate those aspects of associative learning that are impaired by hippocampal damage, and the extent to which this can explain the other, more complex effects of such damage (p conducted with Dr Eric Tam, now at the University of Oxford).  

When learning goes wrong Alzheimer's disease and schizophrenia

In some conditions learning is impaired, and we can use what we know about associative theory to analyse these deficits.  For example, schizophrenia is often characterised by high impulsivity, which might be evident as a deficit in inhibitory learning; in a collaboration with Dr Helen Cassaday we confirmed this possibility (work conducted with Dr Zhimin He); related effects were observed in participants with certain types of personality disorder associated with impulsivity deficits.  Schizophrenia is also said to be characterised by a deficit in performance on tasks employing task-setting cues - which are formally equivalent to conditional cues (see above); this leads to the question whether such deficits are also evident in subjects with high schizotypy.  Finally, Alzheimer's disease is characterised by a wide range of cognitive impairments, and yet many of these have not been precisely characterised in associative terms.  In collaboration with Dr Marie-Christine Pardon (School of Biomedical Sciences) and Mr Paul Armstrong, I am currently conducting a series of studies whose long term aim is to analyse the cognitive deficits in a genetically modified strain of mouse that is regarded as a translational model of Alzheimer's disease, and examine their underlying neurobiological correlates.

Learning and Addiction

Human drug seeking has been analysed in terms of classical conditioning: the ability of environmental cues to become associated with the effects of the drug can make them provoke drug-seeking behaviour. The mechanism underlying this process has been modelled by an effect called Pavlovian-instrumental transfer (PIT): if you have two outcomes, chocolate and tobacco, each produced by a different (drug-seeking response), then a conditioned stimulus that signals e.g. chocolate, will increase the level of the chocolate-seeking response more than the tobacco-seeking response (and vv). However, there is still relatively little understanding of how this effect is mediated, and this project would address this. 

Helen Cassaday
Professor of Behavioural Neuroscience

My group investigate the underlying biology of associative learning processes, fundamental to normal cognition, in laboratory rats and mice. The animal learning theories can also be applied to our understanding of age-related cognitive decline, as well as to human diseases in which associative processes are disordered.

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When there is a time gap between events, we are less able to make a connection between them in learning and later memory. Thus it is harder to keep track of things that could in fact be causally related, in order - for example - to know that even distant engine noise can predict a future hazard or to anticipate dinner based on the smell of raw ingredients. The ability successfully to bridge a time gap between events is known to deteriorate with age in humans and other animals. This line of work (funded by the BBSRC) aims to identify the neural substrates of trace conditioning, and to compare these with those of delay-dependent forgetting measured in other procedures.

In schizophrenia, we find that learning occurs inappropriately, about stimuli that would normally be treated as irrelevant, redundant or in some other way indistinct. This line of work (funded by the MRC and Wellcome Trust) has focused on the neural substrates of selective learning. Recent work compared the effects of localised treatments within nucleus accumbens on latent inhibition, based on past experience with the cue or ‘acquired salience’, and cue competition through overshadowing, based on relative intensity of the cue or ‘intrinsic salience’.

To promote translation of these findings to our understanding of human disorder, a number of my graduate students (Ellen Migo, Ebrahim Kantini, Zhimin He, Meghan Thurston, Becci Gould) have also successfully established associative learning procedures suitable for use with human participants.

In addition to projects on selective learning mechanisms and their dysfunction, we have shown the validity of a non-invasive objective measure of stress in laboratory mice (Ann Fitchett, BBSRC-funded studentship, welfare remit).

Mark Haselgrove
Associate Professor

My research examines the mechanisms and properties of learning in humans and non-human animals. I am particularly interested in understanding how animals attend to and represent stimuli within the world. Most of my research has employed techniques such as appetitive Pavlovian conditioning with rats, and autoshaping with pigeons. More recently I have become interested in the relationship between schizotypy and cue competition in humans.

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See my Google Scholar Profile HERE and my academic family tree HERE.

Paula Moran
Associate Professor & Reader in Behavioural Neuroscience

My expertise is in psychopharmacology. I use animal and human translational models to understand the biology of schizophrenia and Alzheimer's disease. The aim of this research is to find new ways to treat the symptoms of these disorders.

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I was awarded my PhD from national University of Ireland. Following 6 years as a scientist in the pharmaceutical industry where I worked on a number of drug discovery projects for Alzheimers Disease and Schizophrenia. I moved back to academia through an EU research fellowship at the Institute of Psychiatry in London.I was Senior lecturer at University of Leicester before joining the School of Psychology Nottingham as associate Professor and Reader. I am currently external affairs officer for the British Association for Psychopharmacology and a member of the scientific advisory panel for psychosis and related disorders for the European College of Neuropsychopharmacology.
Jasper Robinson
Associate Professor
I'm currently examining recognition memory in people using eye-tracking. The procedure is an evolution of 'object recognition' memory tasks using in rodents, which have been used to examine the neural substrates of recognition memory. My current interest is in testing competing psychological hypotheses of recognition, which I describe here (Robinson & Bonardi, 2015).

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Past Research

Peter Jones, Emma Whitt and I examined mechanisms of rats' novelty/familiarity discrimination in a BBSRC-funded grant & PhD studentship. Our main findings were:

  • That despite the parallels between 'spontaneous object recognition' and simple, orienting-response, habituation procedures, lesions of the perirhinal cortex reduced rats' object recognition but did not affect habituation. This could be because they rely on different processes (declarative memory versus stimulus → response learning).
  • The reduction of object memory in rats with manipulations of the perirhinal cortex has been claimed to be the result of a failure to discriminate novelty from familiarity; however, other accounts of this deficit are available. We found direct evidence of the failure of novelty/familiarity discrimination in an auditory generalisation task in rats.

Future Research

Acquired equivalence experiments demonstrate that people (and rats and pigeons, for that matter) confuse stimuli that have signalled the same outcomes in the past. For example, when rats learn that both a tone and a white noise signal food deliver, they are now more likely to transfer new learning about the tone to the white noise. Analogous experiments with people have demonstrated that older people show this acquired equivalence effect less strongly (Robinson & Owens, 2013), which we interpret as providing evidence about dynamic processes within a three-layer network that supports learning. We plan to test predictions of this account.

School of Psychology

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