My Journey: 1. A Career in Neuroscience

Outlines my neuroscience career, from a three-year Postdoctoral Fellowship with Nobel Laureate Arvid Carlsson in Sweden to running my own research laboratory for 14 years in the UK. Our laboratory’s research was focused on the regulation and function of brain dopamine systems, with a particular interest in addiction. In 2000, I closed my laboratory, as I did not think that neuroscience research was helping people overcome addiction. (3,492 words)

1. Learning About Drugs and the Brain

In the third year of my Psychology undergraduate degree at the City of London Polytechnic (now London Guildhall University) in the mid-1970s, I did not know whether I wanted to go on to become a Clinical Psychologist or conduct research in Psychopharmacology (study of brain function, and the effects of drugs on brain and behaviour).

I loved my undergraduate Abnormal Psychology course—although I now hate the words ‘abnormal’ psychology—and decided that I ultimately wanted to help people overcome psychological problems.

I also loved learning about the brain and the relationship between brain neurotransmitters and behaviour, both normal and ‘abnormal’, in my Psychopharmacology course. My third-year undergraduate project focused on an animal model of depression, and I spent a good deal of time conducting research with my laboratory rats, so much so that my girlfriend at the time (and later wife) told me that I was beginning to resemble one. 

Despite the limited amount of relevant information I had at hand at that stage of my life, I decided that the most interesting and potentially important way forward was to better understand brain neurotransmitters and their relationship to behaviour. I had been convinced by a lecturer of the importance of biological dysfunction underlying mental health problems such as depression—the so-called medical, or disease model, of mental health.

Visiting family in Australia during my PhD, 1979.

I remember one of my friends passionately arguing with me about this model and my proposed way forward; she saw the medical model as reductionist in nature, and the use of drugs to alleviate the complexity of psychological problems not only a waste of time, but also potentially causing even more problems for the person in need of help. And what relevance did the laboratory rat have to man?!

However, I was so wrapped up in what I was doing, I was not going to change my mind. 

2. PhD and Postdoctoral Training 

I started to apply for PhD places in various Psychology departments around the UK and was fortunate enough to be offered a PhD place at the University of Reading in 1976. I ended up building my own laboratory—my PhD supervisor, Professor David Warburton (R.I.P), had given up animal research and was now conducting human research—and spent four years working on a project focused on understanding brain mechanisms of reward, in particular brain dopamine systems, in the laboratory rat. 

During this time, I read a great deal about dopamine (DA) and its role in behaviour and in clinical problems such as schizophrenia and Parkinson’s Disease. I was fascinated by the work of Professor Arvid Carlsson (R.I.P) and his colleagues in the Department of Pharmacology at the Medical School in Göteborg, Sweden.

Arvid Carlsson was awarded the Nobel Prize in Physiology or Medicine in 2000.

Back in the late 1950s, Arvid was the scientist who first demonstrated DA to be a neurotransmitter, showed it played a key role in motor control, and claimed that l-Dopa would be an effective treatment for Parkinson’s disease. 

I applied to work with Arvid as a postdoctoral fellow in his laboratory, and he accepted my request contingent on me obtaining funding to support my travel and living expenses.

I submitted a funding application to the European Science Foundation (ESF) in France for a three-month Training Fellowship, outlining a project focused on studying a new way of reducing DA function that could have important implications for ameliorating psychiatric and neurological conditions associated with hyperactive DA systems, e.g. schizophrenia and tardive dyskinesia [1]. I was thrilled to later receive a letter stating that my funding application was successful.

I travelled to Göteborg near the end of September 1981. My research was so exciting that I worked for at least 12 hours a day for most of the three months. One of the drugs I was working with, synthesised by Arvid’s team of medicinal chemists, showed a profile in animal models that suggested it would ameliorate schizophrenic symptoms without inducing the motor side effects induced by almost all antipsychotic drugs (DA receptor antagonists). My research soon became focused on why our drug acted in the way it did, seemingly exerting differential effects on different DA-containing systems in the brain.   

I returned to the UK for Christmas, having submitted an application to renew my ESF Training Fellowship for a further three months. That application was successful. In fact, I ended up spending three years working with Arvid’s team, thank to further financial support from the Swedish Institute, Arvid’s laboratory, and the UK Science Research Council, the latter awarding me a two-year Overseas Postdoctoral Fellowship starting in September 1982.

Swedish work colleague and close friend Stephan Hjorth on return from skiing trip to the French Alps.

I continued my work with novel DA receptor agonists developed by Arvid’s medicinal chemists, one of which, (-)-3-PPP (preclamol), exhibited a unique profile (at that time), exerting either agonist or antagonist effects depending on the DA receptor population with which it interacted, and the sensitivity of that receptor population.

The drug, which we realised was what is known as a partial receptor agonist, acted at as antagonist at postsynaptic DA receptors in normal animals, but as an agonist at the same receptor population in animals which had most of their DA neurons destroyed, a condition mimicking Parkinson’s disease. 

As a result of our research, we suggested that (-)-3-PPP, and other drugs later discovered to exhibit the same profile, might, paradoxically, be effective in reducing symptoms of schizophrenia (by reducing DA function) and ameliorating symptoms of Parkinson’s disease (by increasing DA function).

In addition to publishing a number of articles focused on these drugs, we developed a new theory of drug-receptor interactions based on their actions which I outlined in two review articles I wrote with my colleagues Stephan Hjorth and Arvid Carlsson. Drug companies from around the world initiated drug discovery programmes based on our team’s ideas and numerous research publications.

Kungsportsavenyen, Göteborg. I loved visiting here on summer evenings.

My research not only involved studying behaviour, but also using neurochemical and electrophysiological techniques, the latter involving recording the electrical activity of individual DA cells in the anaesthetised rat. I was particularly enthralled with the latter technique, showing how drugs injected intravenously (thereby affecting the whole brain) or microiontophoretically (delivered directly onto the cell which I was recording from) altered the electrical activity of different DA-containing cell populations. Electrophysiological techniques would play an important role in my future neuroscience research career.

During this time, I spent three months in the latter part of 1983 working in Professor Steve Bunney’s laboratory at the Department of Pharmacology, Yale University School of Medicine in New Haven, Connecticut, USA, working on a collaborative electrophysiology project focused on the drugs I had been working with in Göteborg. 

I loved my time in Sweden—not just because of my work, but also because of my wonderful friends, the social activities I engaged in (like sailing and skiing), and the country itself.

Co-author of my most cited paper and a best mate, Francis (Frank) J. White R.I.P.

After leaving Sweden in late 1984, I worked for two years in a new research centre (Centre for Cell Biology) at Sinai Hospital in Detroit, USA, studying the regulation of different DA-containing systems in the brain. I believed that this form of research was important, given that different populations of DA neuron innervated and regulated different brain areas involved in motor control, emotional behaviour, and cognition. Could we pharmacologically influence abnormal cognitive function (arising in a clinical condition like schizophrenia) without impacting negatively on motor control?

During this time, I wrote a seminal review, with my great friend the Francis (Frank) J White (R.I.P), on the D1/D2 dopamine receptor classification, which became one of the most cited articles in the dopamine field at the time.

I was also involved in collaborative projects with Matthew Galloway and Bev Kovacic of Lafayette Clinic, Wayne State University, which focused on the effects of (-)-3-PPP, and its enantiomeric twin (+)-3-PPP, in an in vitro model of dopamine release in the rat brain, and in a model of tardive dyskinesia (a side effect in humans resulting from long-term administration of antipsychotic drugs) in the Cebus Apella monkey.

The results in the latter study showed the promising clinical potential of the partial agonist (-)-3-PPP, the drug I had devoted so much time researching while I was working with Arvid Carlsson.

3. My Research Laboratory

I returned to the UK at the end of 1986 to take up a prestigious five-year Advanced Research Fellowship awarded by the Science and Engineering Research Council and set up my own research laboratory (involving behavioural and electrophysiological techniques) in the Department of Psychology at the University of Reading.

Although I had the same status as a lecturer in the department, I did not have to teach. However, I supervised the research of a number of Masters and PhD students and postdoctoral fellows. We had a great spirit in the laboratory, and I was thrilled to have such a wonderful team.

Our electrophysiological research was focused on the regulation of different DA-containing systems in the brain, whilst our behavioural work was becoming increasingly oriented towards understanding the role of DA and DA receptors in drug addiction. We continued to work with one of the partial DA receptor agonists that our team in Göteborg had developed, but as UK research councils were not interested in funding this work, I eventually terminated this research programme. [2]

When I received the Young Scientist Award from the British Association for Psychopharmacology in 1988, I had to smile… I was 34 years old! My good friend Frank White won a similar Young Scientist Award in the US the same year.

A review article and new theory from my neuroscience days. Just a short title!?

In 1992, I was awarded a five-year Wellcome Trust University Award and decided to move my laboratory to the Department of Psychology at the University of Wales Swansea (now known as Swansea University). Again, I did not have to teach undergraduates, but I ran the department’s PhD programme.

I was lucky enough to live on the beautiful Gower Peninsula and have an office at the University on the ninth floor overlooking Swansea Bay. An unrivalled view in British academia! 

Over time, our team’s behavioural and electrophysiological research became increasingly focused on the neural mechanisms underlying addiction. The laboratory did very well—attracting good research funding and generating numbers of high-quality science publications—and I was excited by what we were doing.

I had a team of enthusiastic postdoctoral fellows and PhD students. We had also developed a new theory on brain mechanisms underlying addiction, which received favourable publicity from the science community. The review was complicated—suggested by the title and abstract—but ‘hey’, the brain is complex.

However, despite our academic success, I was beginning to feel that something wasn’t quite right.

4. Becoming Disillusioned 

At the time, the National Institute of Drug Abuse (NIDA) was receiving large sums of government money to fund neuroscience research focused on drug and alcohol addiction in the US. NIDA considered addiction to be a brain disease and addictive drugs were thought to ‘hijack’ the brain’s reward system, which was said to use DA as a neurotransmitter.

It was argued that addiction was a medical disorder, and people suffering from addiction were in need of treatment. NIDA continually promoted the idea that scientists would discover brain mechanisms underlying addiction and their work would lead to improved treatment for addiction. Scientists and treatment practitioners were the solution to a problem suffered by millions of people!   

However, as the end of the millennium approached, I realised that I had become a frustrated neuroscientist! Whilst our research was going well, and I could tell a good story about brain mechanisms underlying drug addiction, I did not feel that I (nor any other neuroscientist) was actually helping anyone overcome their addiction. I did not believe that addiction could be ‘cured’ by a drug.

I was also conscious of the fact that I, and the vast majority of neuroscientists I knew, had never spent quality time with people suffering from drug and alcohol problems. Did we neuroscientists understand the true nature of addiction?

Moreover, I was also beginning to question the medical model of mental health care, the belief that psychological distress has a biological cause. Was schizophrenia caused by overactivity of brain DA systems? Moreover, given the side-effects of long-term treatment with antipsychotic drugs (DA receptor antagonists), were these drugs causing more harm than good? Were drugs used to treat other mental health problems actually effective in a beneficial way? I now believe that long-term administration of psychiatric drugs causes more harm than good. 

5. A Major Career Change

In the late 1990s, I was approached by the Welsh Development Agency, which was concerned with furthering the economic development of Wales, to develop an educational website focused on illicit drugs and alcohol. Their rationale was that drug and alcohol problems, and addiction, were impacting on communities in Wales, negatively affecting the wellbeing of individuals, families, and whole communities, and stunting economic growth.

I started to explore what was going in Wales, in order to gain some insights into the nature of the drug and alcohol problem in the ‘real world’. I spent time with Sue Morgan, Director of the Welsh Drug and Alcohol Unit, and her team in Cardiff. Sue recognised my enthusiasm and passion… and no doubt my naivety! 

I was intrigued by addiction and wanted to know how people overcame the problem. One obvious way to understand the nature of addiction, and recovery from addiction, was to talk with people who had overcome a serious substance use problem.

I met some addiction treatment agency workers in Swansea, some of whom were in recovery from addiction, and they introduced me to some of the people they were helping. I was soon inspired by a small group of recovering people, not just by their bravery in overcoming their personal problems, but also by their strong desire to help other people. 

I set up an initiative called WIRED (later to become Wired In)—I will use the name Wired In throughout these writings article to avoid confusion—and a charity Wired International Ltd. In 2000, I was fortunate enough to win a tender to evaluate all projects supported by the Drug and Alcohol Treatment Fund in Wales (cf. Chapter X). I was now also working in the addiction field with humans, rather than just with laboratory rats, dealing with the complexities of human thinking, feelings, and behaviour, as well as society as a whole.

Late in 2000, I was awarded a Personal Chair (Professorship) in Psychology by my university. It was a tradition there that anyone awarded a Personal Chair give an Inaugural Lecture about their research to members of the university and general public. The university Vice Chancellor then hosted a dinner for family and friends of the new Professor. I was due to give my Inaugural Lecture in December, but I had to cancel to attend an event that was far more important. My former colleague and mentor in Sweden, Professor Arvid Carlsson, had been awarded the 2000 Nobel Prize in Physiology or Medicine for his research. 

Two of my best mates in Sweden, Erik Pileblad (left) and Kjell Svensson, 2000.

I was inited to attend two celebratory events in Göteborg—one a civic reception in town, and the other a departmental party—so my Inaugural Lecture was postponed until 1st February 2001. I had not seen many of my friends in Göteborg for over a decade, so the civic reception was a chance to renew old friendships. I was greatly touched at the departmental celebration when my former colleagues told me they were also celebrating my promotion to Professor. I felt a little embarrassed when I informed them that I was giving up neuroscience research. I needn’t have worried. They fully understood my decision and wished me well after I had explained why I was ‘changing career’. 

It certainly wasn’t an easy, lightly-taken decision  to change career from conducting neuroscience research in laboratory animals (for nearly 25 years) to working with humans in the community. I loved studying brain function and writing (and reading) science papers on this topic, training PhD students and postdoctoral fellows, working in the laboratory (when I had time), and even writing research grants for funding our work. I enjoyed attending science conferences around the world and meeting old friends who were running successful laboratories.

However, I just didn’t feel I was contributing to helping mankind in some way or other, something that was important to me.   

I had to gradually wind down my neuroscience laboratory over time, to ensure that all my team had finished their research work and, where relevant, gained their PhDs. My right-hand man in the laboratory and great friend Paul Overton, with whom I had collaborated so closely over the years, was offered a lectureship in the Department of Psychology, University of Sheffield. I gave him all our laboratory equipment he needed, so he could set up a new laboratory with little delay. Paul later became Head of that department. 

Revealing Daily Dose during my Professorial Inaugural Lecture, 2001.

During my Professorial Inaugural lecture, I explained to my audience that I was changing ‘career’, from neuroscience to working in the community in the addiction field. I also explained that whilst I had been very productive as a neuroscientist, generating over 60 peer-reviewed articles, including a number of highly-cited review articles, my ‘audience’ was very small—other neuroscientists working in the field.

In shifting field, my research and other activities would gain a much larger audience, one which would also be much more varied—people with a substance use problem and their families, practitioners, policy makers, academic researchers, and members of the general public—particularly if I used the internet as a core tool for disseminating our content. My new activities could have much more of a social impact than my neuroscience research.

I then told them that I was now going to officially launch Daily Dose, a new drug and alcohol news portal, I had developed in collaboration with website designer Ash Whitney from Cilfrew, near Neath, and initially funded by the Welsh Development Agency. The next moment Daily Dose probably became the largest website (at least physically) in the world as I revealed it on the large screen in the main lecture theatre in the university.


[1] Tardive dyskinesia, which can be irreversible, is a movement disorder characterised by involuntary and abnormal movements of the jaw, lips and tongue. Typical symptoms include facial grimacing, sticking out the tongue, sucking or fish-like movements of the mouth. The disorder is caused by long-term use of most of the DA receptor antagonists used to ‘treat’ people diagnosed as suffering from schizophrenia. In some cases, the condition is irreversible.

[2] University researchers have to apply for research grants from government research councils, charities and other sources to hire staff and purchase equipment, consumable and laboratory animals. The university also receives a percentage of the grants to cover their costs. The sort of research I did was expensive and research grants were highly competitive. At the time I was conducting neuroscience research in the UK, research councils were more interested in funding research focused on addiction than on psychiatric and neurological disorders, so this eventually became a focus of my team’s research.

[3] Looking at the NIDA website today, I see the following: ‘As a result of scientific research, we know that addiction is a medical disorder that affects the brain and changes behavior.’ Addiction is also described as a ‘brain disorder’, and is ‘like other diseases, such as heart disease’. So scientists have worked out that addiction changes behaviour. Wow, how amazing! Not!! By definition, addiction is a change in behaviour. Addiction is not a disease like heart disease. And drugs do not ‘hijack’ the brain, as has been frequently touted by NIDA.

Addiction is not a medical disorder. Addiction is a problem that has biological, psychological and sociological elements. By touting addiction as a medical disorder, NIDA is implying that a medical solution involving treatment is required for people to overcome addiction. In their website section entitled Treatment and Recovery, it is argued that, ‘Research shows that when treating addictions to opioids (prescription pain relievers or drugs like heroin or fentanyl), medication should be the first line of treatment, usually combined with some form of behavioral therapy or counseling.’ Medication should not always be the first line of treatment.

> 2. Learning About Addiction Treatment – My WGCADA Experience, Part 1

> ‘My Journey’ chapter links (and biography)