Susan Sontag has observed that every society seems to need one illness that attaches stigma and blame to its ‘victims’ – mental illness, particularly schizophrenia, appears to have taken this mantle over from AIDS. A review paper by Haghighat (pp. 207–215) proposes that stigmatisation is a fundamental human tendency – a vestige of our animal evolutionary heritage – and, consequently, anti-stigma campaigns must work on many different levels in order to be successful. The power of the mass media has greatly increased the impact of stigma. If every time we hear the word ‘schizophrenic’ on television there is news of another murder, a form of classical conditioning occurs. Cognitive, affective and cultural strategies are therefore needed to ‘desensitise’ the public's fear and anxiety. Crisp (pp. 197–199), in an accompanying editorial, favours legislative and political interventions and feels that people with mental illnesses, like those with physical disabilities, should be empowered to ‘fight their corner’ and test out the relevance of human rights and disability discrimination legislation for their own ends.

New research is dramatically altering our understanding of the molecular mechanisms underlying neuronal communication.

To elucidate the molecular mechanisms underlying the therapeutic effects of mood stabilisers.

Results from integrated clinical and laboratory studies are reviewed.

Chronic administration of lithium and valproate produced a striking reduction in protein kinase C (PKC) isozymes in rat frontal cortex and hippocampus. In a small study, tamoxifen (also a PKC inhibitor) had marked antimanic efficacy. Both lithium and valproate regulate the DNA binding activity of the activator protein 1 family of transcription factors. Using mRNA differential display, it was also shown that chronic administration of lithium and valproate modulates expression of several genes. An exciting finding is that of a robust elevation in the levels of the cytoprotective protein, bcl-2.

The results suggest that regulation of signalling pathways may play a major part in the long-term actions of mood stabilisers. Additionally, mood stabilisers may exert underappreciated neuroprotective effects.

Genetics is increasingly being used to explain human behaviours, with growing enthusiasm for what could be termed ‘genetic determinism’, which an ultra-Darwinist approach seeks to apply to all aspects of the human condition.

To consider the validity of the claims concerning the genetics of human behaviour and psychological distress.

A critical review of the current assumptions about the relative contributions of genetics and the environment.

Organisms are in constant interaction with their environment: that is, organisms select environments just as environments select organisms. Like organisms, environments evolve and are homeodynamic rather than homeostatic; both ‘genome’ and ‘envirome’ are abstractions from this continuous dialectic.

Although the presence of wide-ranging neuropsychological deficits in individuals with major depression is well established, few studies have investigated the nature of cognitive impairment in patients with bipolar disorder.

To review research of the neuropsychology of bipolar disorder, with special attention to the relationship between mood and cognitive functioning.

Literature review.

Findings generally demonstrate mania-related impairments on conventional neuropsychological tests, with direct comparisons of patients with mania and patients with depression failing to find group differences. More recent work has sought to differentiate these disorders by employing tasks with affective components. This research has demonstrated biases for processing positive and negative stimuli in patients with mania and depression, respectively.

Future studies, employing tasks that require cognitive and emotional processing, should improve our understanding of the deficits observed in depression and mania. Neuroimaging studies of the neural regions that underlie cognitive processing of affective meaning suggest that the medial and orbitofrontal prefrontal cortex may be particularly involved.