School of Life Sciences

Image of Joern Steinert

Joern Steinert

Assistant Professor in Neuroscience, Faculty of Medicine & Health Sciences



Joern Steinert studied at the Humboldt University Berlin and graduated in 1996 with the Diplom in Biophysics. Following his PhD in Vascular Biology at King's College London (1997-2001), he took up postdoctoral positions in Tuebingen (2002) and Heidelberg (2004) to study physiological mechanisms of neurotransmission using mammalian and Drosophila model systems. After a position as a Senior Investigator with Prof Ian Forsythe at the MRC Toxicology Unit Leicester, he became Program Leader at the Toxicology Unit before starting an Assistant Professor position at the University of Nottingham in 2020. His research focuses on the regulation of neuronal excitability under activity-dependent mechanisms involving nitric oxide signalling and how regulation of the redox homeostasis in neurodegeneration associated with neuroinflammation impacts on neuronal function.

Dr Steinert acts as an Associate Editor for Cell Death Discovery and as a Review and Associate Editor for Frontiers in Molecular Neuroscience and Frontiers in Synaptic Neuroscience, in addition to serving as a Guest Editor for several journals including Free Radical Biology and Medicine, The Journal of Physiology and Cell Death Disease. He is a Fellow of Higher Education Academy UK (FHEA), Fellow Member of the Physiological Society, UK and member of the BNA, UK, Society for Redox Biology and Medicine (SfRBM) and European Drosophila Society (EDRC). He organized/chaired Symposia at Annual Physiological Society UK Main Meetings, the Main Conference of the SFRR-Europe and FENS meetings.



Expertise Summary

My lab predominantly applies neurophysiological methodologies to study neuronal and synaptic plasticity and function as well as ion channel regulation. My main expertise lies in the electrophysiological assessment of neuronal function coupled with live imaging including measurements of intracellular calcium, nitric oxide and ATP dynamics.

We use mammalian model systems of disease, generate brain slice preparations for studying neuronal function and correlate data with behavioral phenotypes; Drosophila models are also used for optogenetic, electrophysiological (single cell patch clamp, TEVC, MEA) and morphological studies to address specific research questions related to synaptic signalling. Several behavioral studies in adult Drosophila and larvae include learning&memory and activity (circadian, negative geotaxis, locomotor) testing.

Models and approaches used in the lab: Drosophila melanogaster and mouse to study neuronal and synaptic function in health and disease including nitric oxide and related redox signalling.

Schematic of Nitric Oxide signaling at the synapse:

Morphology of the Drosophila neuromuscular junction (top, NMJ, blue-DAPI, red-BRP, green-HRP) and primary neuron/astrocyte culture (bottom, blue-DAPI, green-GFAP, red-NeuN) :


The Neurovascular Unit, schematic depicts interactions between neurons, vascular tissues, pericytes and astrocytes by various signalling molecules:

Comparison of the effects of NO on glutamatergic synaptic transmission in mouse calyx of Held synapse and larval neuromuscular junction (NMJ):

figures model 2_edited_edited_edited.jpg

Activity of LNv neurons in the Drosophila CNS:

Current lab members:

Aelfwin Stone (PhD) - co-supervised with Tom Bellamy (UoN)

Jennifer Cale (PhD) - co-supervised with Tracy Farr and Sebastien Serres (UoN)

Jaskirat Singh Kaur (MRes) - co-supervised with Maddy King (UoN)

Maria Haig (technical support)


Megan de Lange (MRes)

Vlada Yarosh (MRes)

Teaching Summary

Module Convenor For Neurobiology of Disease (LIFE/2071):

  1. Neurobiology of Disease Module


LIFE/2071 Neurobiology of circadian and sleep disorders

LIFE/2071 Parkinson's Disease and it's treatment

LIFE/2071 Serotonergic pathways

LIFE/2071 Autism Spectrum Disorder

LIFE/2071 HPA-axis endocrine regulation

LIFE/2071 Dopamine pathways

LIFE/2071 Drugs of abuse, addiction and reward

LIFE/2071 Neuropeptides

LIFE/2071 ADHD, stimulant and non-stimulant medication

LIFE/2071 Schizophrenia

LIFE/2071 Mechanisms of Neuroinflammation

LIFE/2071 Gut brain axis and Neurodegeneration

LIFE/2071 Migraine and emesis

LIFE/2071 Co-existent neurotransmission salivary secretion

LIFE/2071 Neuropeptides


LIFE/2071 Neurobiology and Treatment of Schizophrenia

LIFE/2071 Neurobiology and treatment of sleep and endocrine dysfunction

  1. Contributor to Higher/Advanced Skills in Neuroscience Module, Core Skills in Neuroscience, Current Research in Neuroscience

LIFE/4144 Potassium channels and Nitric oxide signaling


LIFE/2067 Sensory perception

LIFE/2067 Nerve Conduction Velocity

LIFE/1043 Human Neurophysiology

  1. Additional teaching activity

Pastoral Tutorials

Student Presentations

PHAR/4010 MSc Drug Discovery Poster Presentation


LIFE/2067 Essay, oral presentation, paper presentation


LIFE/2067 Feedback seminars

Research Summary

I am interested in investigating pathways involved in regulating neuronal and synaptic function and dysfunctional signalling in neurodegeneration associated with neuroinflammation. Our lab is… read more

Selected Publications

We are currently inviting applications for self-funded MRes and fully BBSRC DTP-funded (BBSRC DTP UoN) PhD projects (UoN guidelines and requirements):

1. The contribution of glycation signalling to unhealthy aging and neurodegeneration

The aim of this project is to identify the mechanisms and protein targets undergo posttranslational modifications and assess impacts on neuronal function. This characterisation will be done on several levels:

Key aims:

i. from ultrastructural measurements of synaptic vesicles,

ii. assessment of neuronal functions by electrophysiology/live imaging,

iii. protein biochemistry and confocal imaging and

iv. characterisation of changes in behaviour, such as deficits in learning and memory, locomotor activity and life span. We will modify pathways involved in redox, nitric oxide and glycation signalling by genetic manipulations and pharmacology.

2. The contribution of a high fat diet to sporadic Alzheimer's Disease mediated via the gut brain axis communication in Drosophila.

Key aims:

  1. to identify the mechanisms by which a high fat diet (HFD) causes a cholesterol- and ApoE4-mediated Aß42 production via altering APP and secretase interactions.
  2. to test if a HFD exacerbates AD pathology in genetically predisposed animals.
  3. to test if administration of probiotics ameliorates the dietary-induced pathology thereby alleviating AD hallmarks.

3. Investigating the neurobiological mechanisms of psychedelics and their potential to treat affective disorders in Drosophila and mouse model.

Key aims:

  1. Generation and characterisation of fly strains to test the effects of disrupted monoaminergic neuronal activity: A range of Drosophila lines will be established which exhibit altered monoaminergic and glutamatergic transmission. We will identify the effects of receptor and precursor knock-outs/knock-downs/overexpression (i.e. serotonin receptor, tryptophan hydroxylase and amino acid decarboxylase) in subsets of neurons to establish phenotypes assess at neuronal and behavioural levels. Electrophysiological and live imaging (calcium imaging: GCaMP6s, FRET imaging: cAMP) studies will investigate neuronal activity and be complement by behavioural studies.
  1. Elucidation the target pathways of psychedelic actions: Measurements (physiology, imaging) of neuronal activities and whole animal behaviours will be assessed using the above lines in the presence of various psychedelics. This will define the circuits and subpopulations of neurons which are involved in responses to psychedelic actions.
  2. Translational validation in mouse studies: The above information will allow us to interrogate specific neuronal networks and transmitter pathways in mouse which are affected by psychedelic actions. We will apply specific pharmacology to identify serotonergic signalling causing behavioural phenotypes of psychedelics and complement these findings with in vitro brain slice electrophysiology to characterise corresponding changes in neuronal activity.

Current Research

I am interested in investigating pathways involved in regulating neuronal and synaptic function and dysfunctional signalling in neurodegeneration associated with neuroinflammation. Our lab is elucidating molecular mechanisms of neuronal dysfunction in mice developing neurodegeneration which display classical phenotypes of protein-misfolding pathologies such as occurring in Alzheimer's, Parkinson's and Creutzfeldt-Jakob disease (prion-misfolding). I also utilise advantages of the Drosophila model organism to study synaptic effects of protein misfolding and redox signalling, as well as optogenetic approaches to manipulate neuronal activities, thus using complementary models to study neuronal function. In order to gain deeper insides into underlying and early-onset dysfunctional pathways in neurodegeneration, I have assessed the metabolome in hippocampal and cortical tissues from prion-diseased mice. These data showed vast amounts of alterations in the neuronal metabolism, including glycolysis, arginine and prostaglandin pathways and oxidative stress signalling among many others. Importantly, dysfunction of these pathways has also been highlighted as predisposing and causal conditions during aging, thereby further facilitating and increasing the risk of developing neurodegenerative pathologies. I have a strong interest in elucidating the mechanisms by which redox stress modulates neuronal function developed new exciting projects related to neuroinflammation, redox and cellular stress signalling which includes oxidative and nitrergic stress.

School of Life Sciences

University of Nottingham
Medical School
Queen's Medical Centre
Nottingham NG7 2UH

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