Chris Bailey

Personal profile

Research interests

My research focuses on the neuronal changes caused by drugs of abuse, and how they relate to drug tolerance and addiction.

Opioid Tolerance

Morphine and related opiates such as heroin act by activating the µ-opioid receptor and are effective as analgesics, as well as being abused on the street. Following prolonged administration, tolerance occurs, whereby there is a need for escalating dose of that drug to maintain effect. This complicates pain-relief therapy as well as contributing to the social problems inherent in heroin addiction.

The mechanism(s) underlying opiate tolerance are poorly understood, but we have recently provided evidence that µ-opioid receptor desensitization may be a key process.

Interestingly, we have recently uncovered the fact that different ligands at the µ-opioid receptor can cause receptor desensitization and internalization by entirely different intracellular signalling mechanisms. On-going research is designed to investigate the precise molecular mechanisms underlying mu-opioid receptor desensitization and internalization, and determine precisely how these events relate to tolerance using behavioural methods.

Synaptic Plasticity and Drug Addiction

Intake of drugs of abuse such as heroin, cocaine and ethanol can result in compulsive drug use. Synaptic plasticity is thought to underlie memory formation, and as compulsive drug use is a learned behaviour, current interest in the field of drug addiction is focusing on the role of synaptic plasticity in the responses to drugs of abuse. On-going research is designed to gain a better understanding of the molecular processes underlying synaptic plasticity caused by drugs of abuse in areas of the brain such as the ventral tegmental area, nucleus accumbens and prefrontal cortex, how these processes can be modulated, and their effects on drug addiction.

Experimental Approaches

We use a combination of electrophysiological approaches and real-time cell imaging coupled with behavioural measures of reward, analgesia and respiratory depression.

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Projects

1 Not started
1 Active
10 Finished

Functional consequences of biased signalling at neuronal G protein-coupled receptors

Bailey, C.

1/10/17 → 30/09/21

Project: UK charity

New tools for acute spatiotemporal control of GPCR signalling in vivo

Bailey, C.

Biotechnology and Biological Sciences Research Council

1/11/20 → 31/10/23

Project: Research council

MRC Confidence in Concept - A New Series of Opioid Antagonists and Partial Agonists

Husbands, S., Bailey, C. & Bailey, S.

Medical Research Council

1/06/15 → 30/06/16

Project: Research council

Sex differences in effects of kappa opioid agonists and stress

Bailey, C., Bailey, S. & Ma, Q.

1/02/15 → 1/02/19

Project: Other

Motivational memory: role of nicotinic receptors in synaptic plasticity

Bailey, C., Palandri, J., Wonnacott, S. & Heal, D. J.

1/10/14 → 30/09/18

Project: Research council

Research Output

48 Article
8 Meeting abstract
2 Conference contribution
1 Chapter
2 More
- 1 Comment/debate
- 1 Editorial

A novel G protein-biased agonist at the δ opioid receptor with analgesic efficacy in models of chronic pain

Conibear, A. E., Asghar, J., Hill, R., Henderson, G., Borbely, E., Tekus, V., Helyes, Z., Palandri, J., Bailey, C. P., Starke, I., Williams, S., Kendall, D. & Kelly, E., 29 Feb 2020, In : Journal of Pharmacology and Experimental Therapeutics. 372, 2, p. 224-236 13 p.

Research output: Contribution to journal › Article

Open Access

3 Citations (Scopus)

Morphine-induced respiratory depression is independent of β-arrestin2 signalling

Kliewer, A., Gillis, A., Hill, R., Schmidel, F., Bailey, C., Kelly, E., Henderson, G., Christie, M. J. & Schulz, S., 12 Feb 2020, In : British Journal of Pharmacology.

Research output: Contribution to journal › Article

Open Access

7 Citations (Scopus)