Dr Mohammed A Nassar
School of Biosciences
Lecturer
Level 1 Tutor
+44 114 222 2392
Full contact details
School of Biosciences
Alfred Denny Building
Western Bank
Sheffield
S10 2TN
- Profile
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Brief career history
- 2010-present: Lecturer, School of Biosciences, the University of Sheffield, UK.
- 1999-2009: Senior postdoctoral Fellow, Molecular Nociception Group, Dept. of Biology, UCL, UK.
- 1998-99: Postdoctoral Fellow (Wellcome Prize Fellowship), Wellcome Laboratory for Molecular Pharmacology, Dept. of Pharmacology, UCL, UK.
- 1994-98: Postgraduate student (Wellcome Prize studentship), Wellcome Laboratory for Molecular Pharmacology, Dept. of Pharmacology, UCL, UK.
- Research interests
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My research is focused on primary sensory neurons which are part of the peripheral nervous system (PNS). Sensory neurons convey sensory information from both the internal (e.g. viscera, muscles and bones) and the external (skin) environments to the central nervous system (CNS).
Sensory neurons convey both innoxious and noxious stimuli. The latter is perceived in the CNA as pain. Inflammation and nerve injury sensitise sensory neurons which results in decreased pain thresholds.
My research interest lies in investigating the molecular changes in sensory neurons that are associated with pathological pain.
This is important in order to identify potential targets for new, effective and specific analgesic drugs. My lab uses a variety of methods based on molecular biology, cellular biology and functional assays.
- Publications
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Show: Featured publications All publications
Featured publications
Journal articles
- An unbiased and efficient assessment of excitability of sensory neurons for analgesic drug discovery. PAIN. View this article in WRRO
- Veratridine produces distinct calcium response profiles in mouse Dorsal Root Ganglia neurons. Scientific Reports, 7. View this article in WRRO
- Tamoxifen induces cellular stress in the nervous system by inhibiting cholesterol synthesis. Acta Neuropathologica Communications, 3(1). View this article in WRRO
- Mouse DRG Cell Line with Properties of Nociceptors. PLOS ONE, 10(6). View this article in WRRO
- Na+current properties in islet α- and β-cells reflect cell-specificScn3aandScn9aexpression. The Journal of Physiology, 592(21), 4677-4696.
- Pain without nociceptors? Nav1.7-independent pain mechanisms.. Cell Rep, 6(2), 301-312. View this article in WRRO
- Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nature Communications, 3. View this article in WRRO
- Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds.. J Neurosci, 30(32), 10860-10871.
- Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain. Molecular Pain, 6. View this article in WRRO
- The cell and molecular basis of mechanical, cold, and inflammatory pain.. Science, 321(5889), 702-705.
- Nerve Injury Induces Robust Allodynia and Ectopic Discharges in Nav1.3 Null Mutant Mice. Molecular Pain, 2. View this article in WRRO
- Parallel “Pain” Pathways Arise from Subpopulations of Primary Afferent Nociceptor. Neuron, 47(6), 787-793.
- Neuropathic Pain Develops Normally in Mice Lacking both Nav1.7 and Nav1.8. Molecular Pain, 1. View this article in WRRO
- Nociceptor-specific gene deletion using heterozygous NaV1.8-Cre recombinase mice. Pain, 113(1), 27-36.
- Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proceedings of the National Academy of Sciences, 101(34), 12706-12711.
All publications
Books
- Ion Channel Activities Implicated in Pathological Pain. John Wiley & Sons, Ltd.
Journal articles
- An unbiased and efficient assessment of excitability of sensory neurons for analgesic drug discovery. PAIN. View this article in WRRO
- Mice lacking Kcns1 in peripheral neurons show increased basal and neuropathic pain sensitivity. PAIN, 159(8), 1641-1651. View this article in WRRO
- NaV1.7 and pain: contribution of peripheral nerves.. Pain. View this article in WRRO
- Veratridine produces distinct calcium response profiles in mouse Dorsal Root Ganglia neurons. Scientific Reports, 7. View this article in WRRO
- Reduced excitability and impaired nociception in peripheral unmyelinated fibers from Nav1.9-null mice. PAIN, 158(1), 58-67.
- Use dependence of peripheral nociceptive conduction in the absence of TTXr sodium channel subtypes. Journal of Physiology, 594(19), 5529-5541.
- Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain. Toxins, 8(3), 78-78. View this article in WRRO
- Tamoxifen induces cellular stress in the nervous system by inhibiting cholesterol synthesis. Acta Neuropathologica Communications, 3(1). View this article in WRRO
- Mouse DRG Cell Line with Properties of Nociceptors. PLOS ONE, 10(6). View this article in WRRO
- Na+current properties in islet α- and β-cells reflect cell-specificScn3aandScn9aexpression. The Journal of Physiology, 592(21), 4677-4696.
- Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.. Pain, 155(10), 1962-1975.
- Pain without nociceptors? Nav1.7-independent pain mechanisms.. Cell Rep, 6(2), 301-312. View this article in WRRO
- Sodium channels and mammalian sensory mechanotransduction. Molecular Pain, 8. View this article in WRRO
- Mo1862 The Effect of Human Supernatants From IBS Patients on Neuronal Excitability and Sodium Channel Trafficking. Gastroenterology, 142(5).
- Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nature Communications, 3. View this article in WRRO
- Role of na
v 1.9 in activity-dependent axon growth in motoneurons. Human Molecular Genetics, 21(16), 3655-3667.
- Genetic ablation of delta opioid receptors in nociceptive sensory neurons increases chronic pain and abolishes opioid analgesia. PAIN, 152(6), 1238-1248.
- Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds.. J Neurosci, 30(32), 10860-10871.
- RET Signaling Is Required for Survival and Normal Function of Nonpeptidergic Nociceptors. JOURNAL OF NEUROSCIENCE, 30(11), 3983-3994.
- GRK2: A Novel Cell-Specific Regulator of Severity and Duration of Inflammatory Pain. JOURNAL OF NEUROSCIENCE, 30(6), 2138-2149.
- Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain. Molecular Pain, 6. View this article in WRRO
- Behavioral deficits and subregion-specific suppression of LTP in mice expressing a population of mutant NMDA receptors throughout the hippocampus. LEARNING & MEMORY, 16(10), 635-644.
- SENSORY AXON-DERIVED NEUREGULIN-1 IS REQUIRED FOR AXOGLIAL SIGNALLING AND NORMAL SENSORY FUNCTION BUT NOT FOR LONG TERM AXON MAINTENANCE. JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, 14, 51-51.
- Sensory Axon-Derived Neuregulin-1 Is Required for Axoglial Signaling and Normal Sensory Function But Not for Long-Term Axon Maintenance. JOURNAL OF NEUROSCIENCE, 29(24), 7667-7678.
- The cell and molecular basis of mechanical, cold, and inflammatory pain.. Science, 321(5889), 702-705.
- GTP up-regulated persistent Na(+) current and enhanced nociceptor excitability require Na(V)1.9. JOURNAL OF PHYSIOLOGY-LONDON, 586(4), 1077-1087.
- Nerve Injury Induces Robust Allodynia and Ectopic Discharges in Nav1.3 Null Mutant Mice. Molecular Pain, 2. View this article in WRRO
- Deletion of Annexin 2 Light Chain p11 in Nociceptors Causes Deficits in Somatosensory Coding and Pain Behavior. Journal of Neuroscience, 26(41), 10499-10507.
- Tamoxifen-inducible NaV1.8-CreERT2 recombinase activity in nociceptive neurons of dorsal root ganglia. genesis, 44(8), 364-371.
- Nociceptor-derived brain-derived neurotrophic factor regulates acute and inflammatory but not neuropathic pain. Molecular and Cellular Neuroscience, 31(3), 539-548.
- Parallel “Pain” Pathways Arise from Subpopulations of Primary Afferent Nociceptor. Neuron, 47(6), 787-793.
- Neuropathic Pain Develops Normally in Mice Lacking both Nav1.7 and Nav1.8. Molecular Pain, 1. View this article in WRRO
- Nociceptor-specific gene deletion using heterozygous NaV1.8-Cre recombinase mice. Pain, 113(1), 27-36.
- Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proceedings of the National Academy of Sciences, 101(34), 12706-12711.
- Absence of Whisker-Related Pattern Formation in Mice with NMDA Receptors Lacking Coincidence Detection Properties and Calcium Signaling. The Journal of Neuroscience, 23(6), 2323-2332.
- Recombinant nicotinic receptors, expressed in Xenopus oocytes, do not resemble native rat sympathetic ganglion receptors in single-channel behaviour.. The Journal of Physiology, 500(1), 123-138.
- Single-channel currents from recombinant NM DANRla /NR2D receptors expressed in Xenopus oocytes. Proceedings of the Royal Society of London. Series B: Biological Sciences, 263(1373), 1079-1086.
- Determination of NMDA NR1 subunit copy number in recombinant NMDA receptors. Proceedings of the Royal Society of London. Series B: Biological Sciences, 262(1364), 205-213.
- A P2X purinoceptor cDNA conferring a novel pharmacological profile. FEBS Letters, 375(1-2), 129-133.
- Sodium Channels in Primary Sensory Neurons: Relationship to Pain States, 159-172.
- Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels. Pflügers Archiv - European Journal of Physiology, 865-880. View this article in WRRO
Conference proceedings papers
- The Effect of Human Supernatants From IBS Patients on Neuronal Excitability and Sodium Channel Trafficking. GASTROENTEROLOGY, Vol. 142(5) (pp S702-S703)
- An unbiased and efficient assessment of excitability of sensory neurons for analgesic drug discovery. PAIN. View this article in WRRO
- Research group
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Postgraduate studentship opportunities
Project 1: Investigation of changes in the excitability of pain neurons in diabetes
Diabetes is a condition in which a person’s homeostatic mechanism to control blood sugar level is compromised, resulting in an inability to produce insulin and reduce sugar level. The incidence of diabetes is increasing worldwide, and peripheral neuropathy is one of the most common complications.
Diabetic neuropathy causes extreme pain. The cause of this is thought to be from microvascular injury of the vasa nervorum, the blood vessels which supply nerves. The resulting neuronal damage is thought to affect nociceptor excitability and make them more likely to respond to stimuli. We are interested in characterising diabetes-induced changes in nociceptor excitability.
Our research is currently focusing on the pain neurones of the db/db knockout mouse model.
Project 2: Drug screening for effective and safe reduction of the excitability of pain neurons
Our aim is to identify novel compounds, or a combination of existing compounds, that produce the biggest reduction in the excitability of pain neurons with a minimal effect on non-nociceptors. By targeting only nociceptor activity, this should produce effective analgesia in vivo, with minimal side effects.
The initial step of this process is to screen candidate compounds on cultured primary mouse DRG neurons. Only those which produce the desired effect are taken for further investigation.
References
- Mohammed, Z.A., et al., Veratridine produces distinct calcium response profiles in mouse Dorsal Root Ganglia neurons. Sci. Rep, 2017. 7: p. 45221.
- Mohammed, Z., K. Kaloyanova, and M.A. Nassar, An unbiased and efficient assessment of excitability of sensory neurons for analgesic drug discovery. Pain, 2020.
- Teaching activities
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Teaching experience
- 2015: Postgraduate Certificate in Learning and Teaching from the University of Sheffield (Fellow of The Higher Education Academy, FHEA)
Undergraduate
- BMS109 Cell & Molecular
- BMS109 Practical Classes
- BMS110 Research Topics in Biomedicine
- BMS303 Molecular Physiology of Ion Channels
- BMS319 Pharmacological Techniques
- Level 3 Practical and Dissertation Modules
Masters (MSc)
- BMS6084 Pharmacological Techniques
- Professional activities and memberships
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Postgraduate Certificate in Learning and Teaching from the University of Sheffield (Fellow of The Higher Education Academy, FHEA)