This section summarises the psychology and neurobiology of stress responses in humans. It considers the adaptive value of stress in enabling humans to detect real or perceived threats in the environment and, through learning, to build resilience through helpful coping responses. The conditions that favour ‘toxic’ forms of stress to prevail and so cause chronic metabolic, inflammatory and cognitive disorders are highlighted and discussed from the perspective of dysregulated cortisol signalling.

Neurodevelopment begins in utero and continues throughout life. At each stage of development – from neurulation to adulthood – neural architecture is continuously and adaptively remodelled in response to experience. This experience-driven neural plasticity reaches its zenith during the early years of life, conferring an enormous potential for learning but also an innate vulnerability to the harmful effects of stress. In this section, we describe how brain development is shaped by sensory input, gonadal steroid hormones and experience over the lifespan. We cover concepts such as ‘bloom’ (synaptic overproliferation) and ‘prune’ (synaptic pruning), and present the evidence for critical periods of neuroplasticity for learning in humans. We specify critical periods for hormone-dependent organisational and activational effects from birth to adolescence, including sexually dimorphic neural plasticity. We also highlight specific examples of neuroplasticity during postnatal development and childhood such as language acquisition that may recruit activity-dependent plasticity mechanisms analogous to those that underlie the formation of ocular dominance columns in the primary visual cortex.

In this section, we describe key functions of neurons in the brain that synthesise and release noradrenaline (NA), serotonin (5-hydroxytryptamine; 5-HT), dopamine (DA), and acetylcholine (ACh). As classic ‘neuromodulators’, these widely researched neurotransmitter systems ascend from posterior and ventral regions of the braillopregna by optimising the performance of brain networks without inhibiting or exciting neurons directly. Traditionally considered in the context of ‘non-specific’ arousal states (i.e. sleep and wakefulness) and the ‘reticular activating system’ (), the ascending neurotransmitter systems contribute to a surprisingly diverse array of behavioural and cognitive functions via specific pathways in the brain. These pathways arise from discrete clusters of neurons in the midbrain and forebrain (Figure 4.6.1). As the loci for clinically effective drugs to treat neuropsychiatric conditions such as depression, schizophrenia, and attention deficit hyperactivity disorder, the ascending neurotransmitter systems are a major success story for the ‘receptor revolution’ in neuropsychiatry. For more on the synaptic physiology of these neurotransmitters, see Section 2.4.