Professor Brian Morris

Professor of Molecular Neurobiology (Centre for Cognitive Neuroimaging)

telephone: 01413305361
email: Brian.Morris@glasgow.ac.uk

R306 Level 3, West Medical Building, Glasgow G12 8QQ

Research interests

Schizophrenia - characterisation of neurobiological dysfunction, identification of genomic abnormalities, identification of novel drug candidates. Neuronal plasticity - role of protein signalling complexes, mRNA translation, (including dendritic mRNA), and gene transcription (including transcription factors) in sustaining late phase of long-term potentiation.

Professor Brian Morris is a neuroscientist, whose abilities helped attract YRING - a highly successful target and drug discovery Institute based within the Universities of Strathclyde and Glasgow, and funded by Mitsubishi Pharma Corporation of Japan - to Glasgow. His research interests are focussed on the causes of psychiatric disease, and the mechanisms of synaptic plasticity in the brain. For 10 years he was Co-Director of YRING. He is now a Co-Director of the Psychiatric Research Institute of Neuroscience in Glasgow (PsyRING) along with Professor Judith Pratt of the University of Strathclyde and Professor Robert Hunter of NHS, Greater Glasgow and Clyde.

Projects:
Genetic and genomic analysis of neuronal function in psychiatric diseases such as schizophrenia, and neurodegenerative diseases such as Parkinsonism and Alzheimer's disease; molecular and functional analysis of the mechanisms of synaptic plasticity in the CNS, in relation to learning and memory formation; investigation of the molecular mechanisms linking alterations in the neurochemical environment to sustained changes in neuronal gene expression.

The research uses a variety of cultured cells to study long-term changes in neuronal activity, studying this "plasticity" in terms of :

the cellular mechanisms (what extracellular and intracellular signals induce plasticity ?)
the functional consequences (what is the effect on cell function of a particular change in cellular biochemistry ?)

The studies are centred on understanding plasticity in three brain regions:

the cerebral cortex (subtle pathology and disconnectivity linked to psychiatric diseases such as schizophrenia)
the hippocampus (long-term changes are linked to mechanisms of learning and memory, and also to diseases such as Alzheimer's disease and epilepsy)
the basal ganglia (long-term changes are linked to motor control and also to diseases such as Parkinson's disease)

The experimental techniques used are designed to study the proteins and mRNAs expressed by the cultured cells, and to monitor the effect of altered expression of identified genes, for example by neuronal transfection.

The image shows a cultured hippocampal neurone transfected with a green fluorescent protein vector.

Neuronal function in psychiatric and neurodegenerative disease

Psychiatric and neurodegenerative diseases result from altered function of neurones and their connections in specific brain areas. For example, Parkinson's disease results from a loss of the dopamine-secreting cells in the substantia nigra at the base of the brain, while schizophrenia results from compromised function of a population of interconnected cells in the prefrontal cortex, temporal cortex and thalamus. The dysfunction of these cells is caused by a poorly understood combination of genetic and environmental influences.

In Parkinson's disease, the loss of the dopamine cells leads to abnormal activity in a network of brain regions known as the basal ganglia. Since this network controls aspects of movement, patients experience a variety of symptoms linked to loss of movement control. While drugs such as L-DOPA are effective, particularly in the early stages of the disease, unpleasant side-effects, combined with loss of efficacy in many cases, makes the search for novel treatments of great urgency.

In schizophrenia, impaired function of cortico-thalamic networks leads to "positive" symptoms such as hallucinations and delusions, "negative" symptoms such as depression, social withdrawal and inability to experience pleasure, along with deficits in cognitive processes. This impaired function is centred on the prefrontal cortex and associated areas. Highly localised damage to these areas is sufficient to produce the symptoms of the disease. Existing drugs deal effectively with the positive symptoms, but show little activity against the negative symptoms and cognitive deficits, and cause a number of unpleasant side-effects. Novel drugs with improved efficacy and reduced side-effect profiles are urgently required.

The research adopts a multidisciplinary approach to understanding the causes of these diseases, and hence identifying potential new and improved treatment strategies. Genetic, genomic, molecular, cellular and systems level techniques are employed.

Mechanisms of synaptic plasticity in the CNS

Neurones can alter aspects of their biochemical and morphological character in response to changes in their local environment or their level of activity. This plasticity allows them to adapt and survive in altered conditions, or assume a changed functional role. Three distinct temporal components of neuronal plasticity can usually be idebtified - a rapid phase, apparent within a few milliseconds and lasting for an hour or so, an intermediate phase, lasting for 2-3 hours, and a late phase lasting from 2-3 hours up to many weeks. These distinct temporal phases are sustained by entirely different cellular mechanisms.

Rapid phase:

In many cases, the trigger for the induction of synaptic plasticity is activation of the N-methyl-D-Aspartate (NMDA) class of ionotropic glutamate receptor. This is true for one of the best studies models of synaptic plasticity - long-term potentiation (LTP) in the hippocampus. In LTP, brief high-frequency stimulation of the neuronal connections leads to a long-lasting enhancement of the efficiency of synaptic transmission. This is believed to be related to the mechanisms of learning and memory.

Calcium entry through the stimulated NMDA receptor leads to activation of signalling intermediates such as protein kinase C, ERKs (extracellular-signal-regulated kinases) and Ca2+/calmodulin-dependent kinases. Many of these signalling events are compartmentalised within the dendritic spines that are the site of the excitatory input. However, the ways in which these signalling pathways interact, and how they exert their downstream effects, are not clear.
We have discovered that a small protein known as RhoB - a member of a large family of molecules that act as molecular switches, gating signalling cascades, particularly in relation to cancer - is activated during synaptic plasticity, and plays a key role in co-ordinating many of the lasting effects on the neurone. In addition, we have obtained new insight into the role of ERK, and its downstream effectors such as Msk1, in plasticity in the CNS.

Intermediate phase

Permanent memory formation is known to require the synthesis of new proteins in brain regions such as the hippocampus. Long-term potentiation (LTP) of synaptic transmission between hippocampal neurones represents a widely used cellular model of memory formation, and this LTP also requires protein synthesis. LTP is highly restricted to the synapse - the region of the cell where the incoming fibres make contact, yet protein synthesis takes place a relatively long distance away in the body of the cell. Hence it is not clear how the proteins that are newly synthesised in response to the activity in an incoming nerve fibre find their way specifically to the activated synapse, somewhere out on the branching network of neuronal dendrites.

One possibility is that the neuronal cell takes advantage of the presence of a few mRNAs out in the dendrites, far away from the cell body, but in the vicinity of the synapses (an enlarged portion of the dendrite is shown schematically here). We have recently shown that synaptic activity can increase the stability of these dendritic mRNAs in cultured neurones, making the mRNA levels rise in the dendrite, and hence increase synthesis of the corresponding proteins in a highly localised part of the cell in the region of the stimulation. This provides an elegant mechanism to link highly discrete presynaptic fibre activity to highly localised postsynaptic protein synthesis.

(Thanks to Ian Ramsden for artwork)

Late phase

The late phases of LTP are dependent on gene transcription and protein synthesis. A number of transcription factors - proteins that switch on or off specific genes in the genome - are activated by the above signalling pathways. Induction of plasticity at the activated synapse alters transcription factor activity in the cell nucleus. Two transcription factors with a particularly prominent role in synaptic plasticity and in learning and memory are CREB and zif268. Both mediate altered gene transcription in response to NMDA receptor stimulation. Our recent work has identified the target genes of zif268 in neurones - likely to be the genes that sustain the altered neuronal function in the long-term.
Surprisingly, these include a prominent set of genes encoding components of the proteasome - the cellular "waste disposal" system. This focusses attention on the possible role of targetted protein degradation in sustaining synaptic plasticity.

However, how, and to what extent, the products of the altered transcriptional activity are transported back to the activated synapse, is not clear.

Publications

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Number of items: 65.

2026

Yue, Liang, Craig, Michael T. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2026) Glucocorticoids modulate expression of perineuronal net component genes and parvalbumin during development of mouse cortical neurons. Molecular Neurobiology, 63(1), 205. (doi: 10.1007/s12035-025-05369-4) (PMID:41317238) (PMCID:PMC12664862) (Accepted for Publication)

2025

Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2025) Maximising translational value of the Iowa gambling task in preclinical studies through the use of the rodent touchscreen. Frontiers in Psychiatry, 16, 1518435. (doi: 10.3389/fpsyt.2025.1518435) (PMID:39931698) (PMCID:PMC11808010)

2024

Visocky, Vladimir, Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795, Dunlop, John, Brandon, Nick, Sakata, Shuzo and Pratt, Judith A. (2024) Site-specific inhibition of the thalamic reticular nucleus induces distinct modulations in sleep architecture. European Journal of Neuroscience, 59(4), pp. 554-569. (doi: 10.1111/ejn.15908) (PMID:36623837)

2023

Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Thomson, David M., Bristow, Greg C., Mitchell, Emma J., Pratt, Judith A., Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Dawson, Neil (2023) 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability. Communications Biology, 6, 557. (doi: 10.1038/s42003-023-04891-2) (PMID:37225770) (PMCID:PMC10209099)

2022

Kwon, Jaedeok, Arsenis, Christos, Suessmilch, Maria, McColl, Alison, Cavanagh, Jonathan ORCID: https://orcid.org/0000-0003-0640-8050 and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2022) Differential effects of toll-like receptor activation and differential mediation by MAP kinases of immune responses in microglial cells. Cellular and Molecular Neurobiology, 42(8), pp. 2655-2671. (doi: 10.1007/s10571-021-01127-x) (PMID:34297254) (PMCID:PMC9560989)

Willis, Ashleigh, Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2022) Enzymatic degradation of cortical perineuronal nets reverses GABAergic interneuron maturation. Molecular Neurobiology, 59(5), pp. 2874-2893. (doi: 10.1007/s12035-022-02772-z) (PMID:35233718)

Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2022) The schizophrenia risk gene Map2k7 regulates responding in a novel contingency-shifting rodent touchscreen gambling task. Disease Models and Mechanisms, 15(3), dmm049310. (doi: 10.1242/dmm.049310) (PMID:35275161) (PMCID:PMC8922023)

2021

Kwon, Jaedeok, Suessmilch, Maria, McColl, Alison, Cavanagh, Jonathan ORCID: https://orcid.org/0000-0003-0640-8050 and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2021) Distinct trans-placental effects of maternal immune activation by TLR3 and TLR7 agonists: implications for schizophrenia risk. Scientific Reports, 11, 23841. (doi: 10.1038/s41598-021-03216-9) (PMID:34903784) (PMCID:PMC8668921)

Thomson, David M., Mitchell, Emma J., Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2021) Mice lacking melatonin MT2 receptors exhibit attentional deficits, anxiety and enhanced social interaction. Journal of Psychopharmacology, 35(10), pp. 1265-1276. (doi: 10.1177/02698811211032439) (PMID:34304635) (PMCID:PMC8521347)

Willis, Ashleigh, Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2021) BDNF and JNK signalling modulate cortical interneuron and perineuronal net development: implications for schizophrenia-linked 16p11.2 duplication syndrome. Schizophrenia Bulletin, 47(3), pp. 812-826. (doi: 10.1093/schbul/sbaa139) (PMID:33067994)

2020

Mitchell, Emma J., Thomson, David M., Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Bristow, Greg C., Dawson, Neil, Pratt, Judith A. and Morris, Brian ORCID: https://orcid.org/0000-0003-4439-0795 (2020) Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions. Scientific Reports, 10, 12303. (doi: 10.1038/s41598-020-69130-8) (PMID:32704009) (PMCID:PMC7378168)

Almarzooq, Salsabil, Kwon, Jaedeok, Willis, Ashleigh, Craig, John and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2020) Novel alternatively-spliced exons of the VRK2 gene in mouse brain and microglial cells. Molecular Biology Reports, 47, pp. 5127-5136. (doi: 10.1007/s11033-020-05584-3) (PMID:32583282)

Bristow, Greg C., Thomson, David M., Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Mitchell, Emma J., Pratt, Judith A., Dawson, Neil and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2020) 16p11 duplication disrupts hippocampal-orbitofrontal-amygdala connectivity, revealing a neural circuit endophenotype for schizophrenia. Cell Reports, 31(3), 107536. (doi: 10.1016/j.celrep.2020.107536) (PMID:32320645)

Openshaw, Rebecca ORCID: https://orcid.org/0000-0002-0150-4353, Thomson, David M., Thompson, Rhiannon, Penninger, Josef M., Pratt, Judith A., Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Dawson, Neil (2020) Map2k7 haploinsufficiency induces brain imaging endophenotypes and behavioral phenotypes relevant to schizophrenia. Schizophrenia Bulletin, 46(1), pp. 211-223. (doi: 10.1093/schbul/sbz044) (PMID:31219577) (PMCID:PMC6942167)

2019

Pratt, Judith A., Morris, Brian ORCID: https://orcid.org/0000-0003-4439-0795 and Dawson, Neil (2019) Deconstructing Schizophrenia: advances in preclinical models for biomarker identification. In: Pratt, Judith and Hall, Jeremy (eds.) Biomarkers in Psychiatry. Series: Current topics in behavioral neurosciences (40). Springer: Cham, Switzerland, pp. 295-323. ISBN 9783319996417 (doi: 10.1007/7854_2018_48)

Openshaw, Rebecca L. ORCID: https://orcid.org/0000-0002-0150-4353, Kwon, Jaedeok, McColl, Alison, Penninger, Josef M., Cavanagh, Jonathan ORCID: https://orcid.org/0000-0003-0640-8050, Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2019) JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk. Journal of Neuroinflammation, 16(1), 18. (doi: 10.1186/s12974-019-1408-5) (PMID:30691477) (PMCID:PMC6350402)

2018

Willis, Ashleigh, Pratt, Judith A and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2018) Distortion of protein analysis in primary neuronal cultures by serum albumin from culture medium: a methodological approach to improve target protein quantification. Journal of Neuroscience Methods, 308, pp. 1-5. (doi: 10.1016/j.jneumeth.2018.07.002) (PMID:30033387)

2017

Pratt, Judith, Dawson, Neil, Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795, Grent-'T-Jong, Tineke ORCID: https://orcid.org/0000-0003-3177-5346, Roux, Frederic and Uhlhaas, Peter J. ORCID: https://orcid.org/0000-0002-0892-2224 (2017) Thalamo-cortical communication, glutamatergic neurotransmission and neural oscillations: a unique window into the origins of ScZ? Schizophrenia Research, 180, pp. 4-12. (doi: 10.1016/j.schres.2016.05.013) (PMID:27317361)

Openshaw, R. L. ORCID: https://orcid.org/0000-0002-0150-4353, Thomson, D.M., Penninger, J.M., Pratt, J.A. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2017) Mice haploinsufficient for Map2k7, a gene involved in neurodevelopment and risk for schizophrenia, show impaired attention, a vigilance decrement deficit and unstable cognitive processing in an attentional task: impact of minocycline. Psychopharmacology, 234(2), pp. 293-305. (doi: 10.1007/s00213-016-4463-y) (PMID:27774567) (PMCID:PMC5203862)

2015

Dawson, Neil, Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, Judith A. (2015) Functional brain connectivity phenotypes for schizophrenia drug discovery. Journal of Psychopharmacology, 29(2), pp. 169-177. (doi: 10.1177/0269881114563635) (PMID:25567554)

Dawson, N. et al. (2015) Altered functional brain network connectivity and glutamate system function in transgenic mice expressing truncated Disrupted-in-Schizophrenia 1. Translational Psychiatry, 5(5), e569. (doi: 10.1038/tp.2015.60) (PMID:25989143)

Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2015) The thalamic reticular nucleus: a functional hub for thalamocortical network dysfunction in schizophrenia and a target for drug discovery. Journal of Psychopharmacology, 29(2), pp. 127-137. (doi: 10.1177/0269881114565805)

2014

Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, Judith A. (2014) Novel treatment strategies for schizophrenia from improved understanding of genetic risk. Clinical Genetics, 86(5), pp. 401-411. (doi: 10.1111/cge.12485)

Winchester, Catherine L., Pratt, Judith A. and Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 (2014) Risk genes for schizophrenia: translational opportunities for drug discovery. Pharmacology and Therapeutics, 143(1), pp. 34-50. (doi: 10.1016/j.pharmthera.2014.02.003)

Dawson, Neil, McDonald, Martin, Higham, Desmond J., Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, Judith A. (2014) Subanesthetic ketamine treatment promotes abnormal interactions between neural subsystems and alters the properties of functional brain networks. Neuropsychopharmacology, 39(7), pp. 1786-1798. (doi: 10.1038/npp.2014.26)

Dawson, Neil, Xiao, Xiaolin, McDonald, Martin, Higham, Desmond J., Morris, Brian J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, Judith A. (2014) Sustained NMDA receptor hypofunction induces compromised neural systems integration and schizophrenia-like alterations in functional brain networks. Cerebral Cortex, 24(2), pp. 452-464. (doi: 10.1093/cercor/bhs322)

2013

Nomura, K. ORCID: https://orcid.org/0000-0002-5912-074X, Lee, M., Banks, C., Lee, G. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2013) An ASK1-p38 signalling pathway mediates hydrogen peroxide-induced toxicity in NG108-15 neuronal cells. Neuroscience Letters, 549, pp. 163-167. (doi: 10.1016/j.neulet.2013.05.045)

Gilfillan, L., Blair, A., Morris, B. ORCID: https://orcid.org/0000-0003-4439-0795, Pratt, J., Schweiger, L., Pimlott, S. ORCID: https://orcid.org/0000-0002-8396-3392 and Sutherland, A. ORCID: https://orcid.org/0000-0001-7907-5766 (2013) Synthesis and biological evaluation of novel 2,3-dihydro-1H-1,5-benzodiazepin-2-ones; potential imaging agents of the metabotropic glutamate 2 receptor. MedChemComm, 4(7), pp. 1118-1123. (doi: 10.1039/c3md00110e)

Dawson, N., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, J.A. (2013) Subanaesthetic ketamine treatment alters prefrontal cortex connectivity with thalamus and ascending subcortical systems. Schizophrenia Bulletin, 39(2), pp. 366-377. (doi: 10.1093/schbul/sbr144)

2012

Winchester, C.L., Ohzeki, H., Vouyiouklis, D.A., Thompson, R., Penninger, J.M., Yamagami, K., Norrie, J.D., Hunter, R., Pratt, J.A. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2012) Converging evidence that sequence variations in the novel candidate gene MAP2K7 (MKK7) are functionally associated with schizophrenia. Human Molecular Genetics, 21(22), pp. 4910-4921. (doi: 10.1093/hmg/dds331)

Steward, L.J., Kennedy, M.D., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, J.A. (2012) Chronic phencyclidine (PCP)-induced modulation of muscarinic receptor mRNAs in rat brain: Impact of antipsychotic drug treatment. Neuropharmacology, 62(3), pp. 1554-1563. (doi: 10.1016/j.neuropharm.2011.05.016)

Barberan, S., Mcnair, Kara ORCID: https://orcid.org/0000-0001-5013-2237, Iqbal, K., Smith, N.C., Prendergast, G.C., Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031, Cobb, S.R. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2012) Altered apoptotic responses in neurons lacking RhoB GTPase. European Journal of Neuroscience, 34(11), pp. 1737-1746. (doi: 10.1111/j.1460-9568.2011.07891.x)

Pratt, J., Winchester, C., Dawson, N. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2012) Advancing schizophrenia drug discovery: optimizing rodent models to bridge the translational gap. Nature Reviews Drug Discovery, 11(7), pp. 560-579. (doi: 10.1038/nrd3649)

2011

Forrest, C.M., Addae, J.I., Murthy, S., Darlington, L.G., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 and Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031 (2011) Molecular changes associated with hippocampal long-lasting depression induced by the serine protease subtilisin-A. European Journal of Neuroscience, 34(8), pp. 1241-1253. (doi: 10.1111/j.1460-9568.2011.07853.x)

Xiao, X., Dawson, N., MacIntyre, L., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795, Pratt, J.A., Watson, D.G. and Higham, D.J. (2011) Exploring metabolic pathway disruption in the subchronic phencyclidine model of schizophrenia with the Generalized Singular Value Decomposition. BMC Systems Biology, 5(72), pp. 1-20. (doi: 10.1186/1752-0509-5-72)

2010

Dawson, N., Thompson, R.J., McVie, A., Thomson, D.M., Morris, B. J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, J. A. (2010) Modafinil reverses phencyclidine-induced deficits in cognitive flexibility, cerebral metabolism, and functional brain connectivity. Schizophrenia Bulletin, 38(3), pp. 457-474. (doi: 10.1093/schbul/sbq090)

McNair, K., Spike, R., Guilding, C., Prendergast, G.C., Stone, T.W., Cobb, S.R. and Morris, B.J. (2010) A role for RhoB in synaptic plasticity and the regulation of neuronal morphology. Journal of Neuroscience, 30(9), pp. 3508-3517. (doi: 10.1523/JNEUROSCI.5386-09.2010) (PMID:20203211) (PMCID:PMC6634083)

Thomson, D.M., McVie, A., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, J.A. (2010) Dissociation of acute and chronic intermittent phencyclidine-induced performance deficits in the 5-choice serial reaction time task: influence of clozapine. Psychopharmacology, 213(4), pp. 681-695. (doi: 10.1007/s00213-010-2020-7)

2009

McDade, D.M., Conway, A.M., James, A.B. ORCID: https://orcid.org/0000-0003-4472-7095 and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2009) Activity-dependent gene transcription as a long-term influence on receptor signalling. Biochemical Society Transactions, 37(6), pp. 1375-1377. (doi: 10.1042/BST0371375)

2008

Egerton, A., Reid, L., McGregor, S., Cochran, S.M., Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, J.A. (2008) Subchronic and chronic PCP treatment produces temporally distinct deficits in attentional set shifting and prepulse inhibition in rats. Psychopharmacology, 198(1), pp. 37-49. (doi: 10.1007/s00213-008-1071-5)

2007

Conway, A.-M., James, A.B. ORCID: https://orcid.org/0000-0003-4472-7095, Zang, J. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2007) Regulation of neuronal cdc20 (p55cdc) expression by the plasticity-related transcription factor Zif268. Synapse, 61, pp. 463-468. (doi: 10.1002/syn.20387)

Clark, CJ, McDade, DM, OShaughnessy, T and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2007) Contrasting roles of neuronal Msk1 and Rsk2 in Bad phosphorylation and feedback regulation of Erk signalling. Journal of Neurochemistry, 102, pp. 1024-1034. (doi: 10.1111/j.1471-4159.2007.04601.x)

Guilding, C, McNair, K, Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031 and Morris, BJ (2007) Restored plasticity in a mouse model of neurofibromatosis type 1 via inhibition of hyperactive ERK and CREB. European Journal of Neuroscience, 25, pp. 99-105. (doi: 10.1111/j.1460-9568.2006.05238.x)

Suckling, C. et al. (2007) M-4 agonists/5HT(7) antagonists with potential as antischizophrenic drugs: Serominic compounds. Bioorganic and Medicinal Chemistry Letters, 17, pp. 2649-2655. (doi: 10.1016/j.bmcl.2007.01.093)

2006

James, A.B. ORCID: https://orcid.org/0000-0003-4472-7095, Conway, A.M. and Morris, B.J. (2006) Regulation of the neuronal proteasome by Zif268 (Egr1). Journal of Neuroscience, 26(5), pp. 1624-1634. (doi: 10.1523/JNEUROSCI.4199-05.2006)

Paterson, GJ, Ohashi, Y, Reynolds, GP, Pratt, JA and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2006) Selective increases in the cytokine, TNF alpha, in the prefrontal cortex of PCP-treated rats and human schizophrenic subjects: influence of antipsychotic drugs. Journal of Psychopharmacology, 20, pp. 636-642. (doi: 10.1177/0269881106062025)

2005

Alier, K.A. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2005) Divergent regulation of Pyk2/CAK beta phosphorylation by Ca2+ and cAMP in the hippocampus. Biochimica et Biophysica Acta: Molecular Cell Research, 1745, pp. 342-349. (doi: 10.1016/j.bbamcr.2005.04.003)

Egerton, A, Reid, L, McKerchar, CE, Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, JA (2005) Impairment in perceptual attentional set-shifting following PCP administration: a rodent model of set-shifting deficits in schizophrenia. Psychopharmacology, 179, pp. 77-84. (doi: 10.1007/s00213-004-2109-y)

James, A.B. ORCID: https://orcid.org/0000-0003-4472-7095, Conway, A.M. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2005) Genomic profiling of the neuronal target genes of the plasticity-related transcription factor-Zif268. Journal of Neurochemistry, 95, pp. 796-810. (doi: 10.1111/j.1471-4159.2005.03400.x)

Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795, Cochran, SM and Pratt, JA (2005) PCP: from pharmacology to modelling schizophrenia. Current Opinion in Pharmacology, 5, pp. 101-106. (doi: 10.1016/j.coph.2004.08.008)

Rakhit, S, Clark, CJ, OShaughnessy, CT and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2005) N-methyl-D-aspartate and brain-derived neurotrophic factor induce distinct profiles of extracellular signal-regulated kinase, mitogen- and stress-activated kinase, and ribosomal S6 kinase phosphorylation in cortical neurons. Molecular Pharmacology, 67, pp. 1158-1165. (doi: 10.1124/mol.104.005447)

Reynolds, LM, Cochran, SM, Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795, Pratt, JA and Reynolds, GP (2005) Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain. Schizophrenia Research, 73, pp. 147-152. (doi: 10.1016/j.schres.2004.02.003)

2004

Alier, KA and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2004) Differential regulation of MAP2 and alpha CamKII expression in hippocampal neurones by forskolin and calcium ionophore treatment. Molecular Brain Research, 122, pp. 10-16. (doi: 10.1016/j.molbrainres.2003.11.018)

James, A.B. ORCID: https://orcid.org/0000-0003-4472-7095, Conway, A.M., Thiel, G. and Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795 (2004) Egr-1 modulation of synapsin I expression: permissive effect of forskolin via cAMP. Cellular Signalling, 16, pp. 1355-1362. (doi: 10.1016/j.cellsig.2004.04.001)

OKane, EM, Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031 and Morris, BJ (2004) Increased long-term potentiation in the CA1 region of rat hippocampus via modulation of GTPase signalling or inhibition of Rho kinase. Neuropharmacology, 46, pp. 879-887. (doi: 10.1016/j.neuropharm.2003.11.020)

Steward, LJ, Kennedy, MD ORCID: https://orcid.org/0000-0002-0970-5264, Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, JA (2004) The atypical antipsychotic drug clozapine enhances chronic PCP-induced regulation of prefrontal cortex 5-HT2A receptors. Neuropharmacology, 47, pp. 527-537. (doi: 10.1016/j.neuropharm.2004.04.020)

2003

Cochran, SM, Kennedy, M ORCID: https://orcid.org/0000-0002-0970-5264, Mckerchar, CE, Steward, LJ, Pratt, JA and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2003) Induction of metabolic hypofunction and neurochemical deficits after chronic intermittent exposure to phencyclidine: Differential modulation by antipsychotic drugs. Neuropsychopharmacology, 28, pp. 265-275. (doi: 10.1038/sj.npp.1300031)

McDermott, CJ, Bradley, KN, McCarron, JG, Palmer, AM and Morris, BJ (2003) Striatal neurones show sustained recovery from severe hypoglycaemic insult. Journal of Neurochemistry, 86, pp. 383-393. (doi: 10.1046/j.1471-4159.2003.01853.x)

OKane, EM, Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031 and Morris, BJ (2003) Activation of Rho GTPases by synaptic transmission in the hippocampus. Journal of Neurochemistry, 87, pp. 1309-1312. (doi: 10.1046/j.1471-4159.2003.02102.x)

OKane, EM, Stone, T.W. ORCID: https://orcid.org/0000-0002-5532-0031 and Morris, BJ (2003) Distribution of Rho family GTPases in the adult rat hippocampus and cerebellum. Molecular Brain Research, 114, pp. 1-8. (doi: 10.1016/S0169-328X(03)00121-9)

2002

Burr, PB and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2002) Involvement of NMDA receptors and a p21(Ras)-like guanosine triphosphatase in the constitutive activation of nuclear factor-kappa-B in cortical neurons. Experimental Brain Research, 147, pp. 273-279. (doi: 10.1007/s00221-002-1180-z)

Cochran, SM, Fujimura, M, Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, JA (2002) Acute and delayed effects of phencyclidine upon mRNA levels of markers of glutamatergic and GABAergic neurotransmitter function in the rat brain. Synapse, 46, pp. 206-214. (doi: 10.1002/syn.10126)

Cochran, SM, McKerchar, CE, Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 and Pratt, JA (2002) Induction of differential patterns of local cerebral glucose metabolism and immediate-early genes by acute clozapine and haloperidol. Neuropharmacology, 43, pp. 394-407.

2001

Fuller, G, Veitch, K, Ho, LK, Cruise, L and Morris, BJ ORCID: https://orcid.org/0000-0003-4439-0795 (2001) Activation of p44/p42 MAP kinase in striatal neurons via kainate receptors and PI3 kinase. Molecular Brain Research, 89, pp. 126-132.

1997

Morris, B.J. ORCID: https://orcid.org/0000-0003-4439-0795, Simpson, C.S., Mundell, S., MacEachern, K. ORCID: https://orcid.org/0000-0002-7705-6956, Johnston, H.M. and Nolan, A.M. (1997) Dynamic changes in NADPH-diaphorase staining reflect activity of nitric oxide synthase: evidence for a dopaminergic regulation of striatal nitric oxide release. Neuropharmacology, 36(11-12), pp. 1589-1599. (doi: 10.1016/S0028-3908(97)00159-7) (PMID:9517430)

This list was generated on Thu Jan 15 21:08:56 2026 GMT.

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