Prenatal Excess Glucocorticoid Exposure and Adult Affective Disorders:A Role for Serotonergic and Catecholamine Pathways

Fetal glucocorticoid exposure is a key mechanism proposed to underlie prenatal ‘programming’ of adult affective behaviours such as depression and anxiety. Indeed, the glucocorticoid metabolising enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which is highly expressed in the placenta and the developing fetus, acts as a protective barrier from the high maternal glucocorticoids which may alter developmental trajectories. The programmed changes resulting from maternal stress or bypass or from the inhibition of 11β-HSD2 are frequently associated with alterations in the hypothalamic-pituitary-adrenal (HPA) axis. Hence, circulating glucocorticoid levels are increased either basally or in response to stress accompanied by CNS region-specific modulations in the expression of both corticosteroid receptors (mineralocorticoid and glucocorticoid receptors). Furthermore, early-life glucocorticoid exposure also affects serotonergic and catecholamine pathways within the brain, with changes in both associated neurotransmitters and receptors. Indeed, global removal of 11β-HSD2, an enzyme that inactivates glucocorticoids, increases anxiety‐ and depressive-like behaviour in mice; however, in this case the phenotype is not accompanied by overt perturbation in the HPA axis but, intriguingly, alterations in serotonergic and catecholamine pathways are maintained in this programming model. This review addresses one of the potential adverse effects of glucocorticoid overexposure in utero, i.e. increased incidence of affective behaviours, and the mechanisms underlying these behaviours including alteration of the HPA axis and serotonergic and catecholamine pathways

Can the effects of implementation intentions on exercise be enhanced using text messages?

Implementation intentions planning in advance the situation in which one will act, have been proposed to be an effective self-regulatory technique for changing health behaviour. Encouraging people to receive text message reminders of their implementation intentions should enhance their strength and, thus, it was predicted that this combined approach would be particularly effective in increasing exercise. Participants (N = 155) were randomly allocated to one of five conditions (implementation intentions and SMS, implementation intention, SMS or one of two control groups) then completed self-report measures of exercise behaviour and motivation. Four weeks later, they responded to similar items. Results suggested that the combined intervention increased exercise frequency significantly more than the other strategies including the implementation intention group. It is proposed, therefore, that implementation intention effects can be enhanced via plan reminders

'Apraxic dysgraphia' in a 15-year-old left-handed patient: disruption of the cerebello-cerebral network involved in the planning and execution of graphomotor movements

Apraxic agraphia is a peripheral writing disorder caused by neurological damage. It induces a lack or loss of access to the motor engrams that plan and programme the graphomotor movements necessary to produce written output. The neural network subserving handwriting includes the superior parietal region, the dorsolateral and medial premotor cortex and the thalamus of the dominant hemisphere. Recent studies indicate that the cerebellum may be involved as well. To the best of our knowledge, apraxic agraphia has not been described on a developmental basis. This paper reports the clinical, neurocognitive and (functional) neuroimaging findings of a 15-year-old left-handed patient with an isolated, non-progressive developmental handwriting disorder consistent with a diagnosis of "apraxic dysgraphia". Gross motor coordination problems were objectified as well but no signs of cerebellar, sensorimotor or extrapyramidal dysfunction of the writing limb were found to explain the apraxic phenomena. Brain MRI revealed no supra- and infratentorial damage but quantified Tc-99m-ECD SPECT disclosed decreased perfusion in the anatomoclinically suspected prefrontal and cerebellar brain regions crucially involved in the planning and execution of skilled motor actions. This pattern of functional depression seems to support the hypothesis that "apraxic dysgraphia" might reflect incomplete maturation of the cerebello-cerebral network involved in handwriting. In addition, it is hypothesized that "apraxic dysgraphia" may have to be considered to represent a distinct nosological category within the group of the developmental dyspraxias following dysfunction of the cerebello-cerebral network involved in planned actions