The neuro-symphony of stress.

The impact of stress on brain function is increasingly recognized. Various substances are released in response to stress and can influence distinct neuronal circuits, but the functional advantages of having such a diversity of stress mediators remain unclear. Individual neurotransmitter, neuropeptide and steroid stress mediators have specific spatial and temporal niches, but these niches also overlap. In addition, the effects of individual mediators on neuronal function and plasticity are integrated, and emerging evidence suggests that there is crosstalk between them. Together, this results in the stress instruments producing an orchestrated 'symphony' that enables fine-tuned responses to diverse challenges

The multiple personalities of h-channels.

Concepts regarding the function of the hyperpolarization-activated current (Ih) in shaping the excitability of single cells and neuronal ensembles have been evolving rapidly following the recent cloning of genes that encode the underlying 'h-channels' - the HCN genes. This article reviews new information about the transcriptional regulation of these channels, highlighting novel studies that demonstrate short- and long-term modulation of HCN expression, and linking this modulation to mechanisms of neurological diseases

The central corticotropin releasing factor system during development and adulthood.

Corticotropin releasing factor (CRH) has been shown to contribute critically to molecular and neuroendocrine responses to stress during both adulthood and development. This peptide and its receptors are expressed in the hypothalamus, as well as in limbic brain areas including amygdala and hippocampus. This is consistent with roles for CRH in mediating the influence of stress on emotional behavior and cognitive function. The expression of CRH and of its receptors in hypothalamus, amygdala and hippocampus is age-dependent, and is modulated by stress throughout life (including the first postnatal weeks). Uniquely during development, the cardinal influence of maternal care on the central stress response governs the levels of central CRH expression, and may alter the 'set-point' of CRH-gene sensitivity to stress in a lasting manner