The cell surface membrane comprises an insulating lipid bilayer in which specialised proteins are embedded. This supports the membrane potential difference between intracellular and extracellular fluids brought about by their differing Na+, K+ and Cl- concentrations, their respective Nernst potentials for electrochemical equilibrium, and their relative membrane permeabilities. The concentration distributions arise from metabolically dependent active ion transport through membrane Na+-K+ ATPase activity, first demonstrated using radioactive tracers in cephalopod giant axons. In intact cells, these factors are combined with the Donnan distribution properties for intracellular and extracellular ions, reflecting the presence of impermeant intracellular charged protein, to determine the resting potential. The intact cell thereby forms an osmotically and electrically balanced system with relatively increased intracellular K+ and extracellular Na+ concentrations separated by a membrane across which there is a stable negative resting potential. The latter provides the electrophysiological background upon which cell excitation events are superimposed.

Nervous systems are a characteristic feature of higher animals. Their sensory components convey incoming information from the internal and external environment; their motor components convey instructions for reactions to such stimuli to their effector organs. Vertebrates possess both central and peripheral nervous systems, including an autonomic division concerned with homeostasis of the internal environment. The nerve cell is the anatomical, functional and trophic unit of nervous system function. Its cell body radiates dendritic and axonal nerve fibres that respectively transmit incoming information and the departing results of its processing. In contrast to non-myelinated nerve fibres, myelinated nerve fibres are ensheathed by glial cells in the central and Schwann cells in the peripheral nervous systems. Peripheral but not central nerves show a capacity for regeneration along their basement membranes thereby regaining their peripheral attachments. This property has attracted significant interest in connection with clinical repair following nerve injury.

Skeletal muscle contraction can be characterised under either isometric or isotonic conditions of constant length or load. These demonstrate an inverse, Hill, relationship between initial shortening velocity and load. The muscle contraction timecourse exceeds that of its initiating electrical and intracellular Ca2+ changes. Repetitive stimulation consequently produces summation and tetanic fusion of successive muscle twitches. All these variants of contractile activity incur energy expenditure immediately supplied by ATP breakdown, replenished successively from creatine phosphate, carbohydrate and lipid energy supplies. Continued activity leads to energetic depletion, and osmotic and electrolyte imbalances all contributing to fatigue. However, cellular H+ buffering mechanisms mitigate the osmotic and pH effects of the associated lactate production. Na+-K+-ATPase activity buffers the inward Na+ and outward K+ fluxes accompanying electrical activity, and their osmotic effects. Long-term increases in muscle activity exert positive trophic effects. In contrast, ageing is associated with sarcopaenia which contributes importantly to clinical frailty.

Excitation-contraction coupling refers to the events connecting surface membrane excitation and initiation of mechanical activity. It involves a steeply voltage-dependent Ca2+ release from its intracellular sarcoplasmic reticular store. The resulting cytosolic Ca2+ elevation, leading to troponin activation, is detectable through absorbance or fluorescence properties of intracellularly introduced optically sensitive dyes. The initiating transverse tubular depolarisation is sensed by intramembrane dihydropyridine receptors at triad junctions with terminal cisternal sarcoplasmic reticulum. Their underlying configurational changes were demonstrated and characterised through their associated intramembrane charge movements employing pharmacological agents known to modify excitation-contraction coupling. This separated a steeply voltage-dependent qγ transition allosterically and co-operatively coupled to opening of sarcoplasmic reticular ryanodine receptor Ca2+ release channels. These events and the associated Ca2+ release reverse with membrane repolarisation. Sarcoplasmic reticular Ca2+-ATPase activity then returns the released Ca2+ from cytosol to its sarcoplasmic reticular store. Clinical ryanodine receptor disorders cause malignant hyperthermia, important in anaesthetic practice.

Studies demonstrating, characterising and thereby clarifying our understanding of nerve function began from the experimental availability of electophysiological methods for recording and stimulation of bio-electric signals. The classical recording methods were developed to measure intracellular potentials directly from cephalopod giant axons, skeletal muscle fibres and other excitable cell types. These consistently demonstrated strongly negative resting potentials and monophasic action potentials in response to stimulation, whose detailed waveforms varied with different excitable tissue types through a wide range of species. Measurement of extracellular potential differences between different recording sites in the nervous system permitted study both of electrical events occurring at a point, and their propagation along lengths of nerve. This demonstrated and characterised the observed compound action potentials. It separated their components by conduction velocity attributing this to their different fibre diameters and degrees of myelination. It also demonstrated their threshold excitation, all-or-none and refractoriness properties.

Central nervous system function depends on synaptic transmission involving either chemical-transmitter-mediated or direct electrical coupling between neurones. Transmitter activation of excitatory and inhibitory synapses respectively produce postsynaptic membrane depolarisation and hyperpolarisation in turn increasing or decreasing likelihoods of action potential firing by the targetted neuron. Further variants of neuron-neuron interactions include inhibition at the level of presynaptic terminals and G-protein dependent slow synaptic potentials. Some central nervous system synapses additionally show longer-term potentiation or depression phenomena with repeated activity produced by intracellular signaling mechanisms; these may underly memory. Finally, direct electrical synaptic connections between cells can synchronise firing between neurones. Release of K+ and transmitter glutamate by central neurones during intense electrical activity potentially perturbs their extracellular environment. This is normally corrected by transport activity in their closely related glial cells. Malfunctions in this buffering function predisposes to cortical spreading depression phenomena clinically associated with migraine aura.

Arrhythmias, frequently diagnosed through their characteristic electrocardiographic abnormalities, pose major public health problems contributing significant clinical morbidity and mortality. They result from breakdown of the normally orderly sequence of electrical activation through the heart. Although initiated by triggering events, they are sustained by the presence of re-entrant substrate arising from compromised, or heterogeneities in, action-potential conduction and/or recovery. These situations can arise from abnormal surface ion channel, Ca2+ homeostatic, cardiomyocyte metabolic function and/or cardiac remodelling or anatomical abnormalities. They proved amenable to study in genetically modified murine systems recapitulating clinically demonstrated abnormalities in their underlying biomolecules. These mirrored the features and mechanisms underlying human pro-arrhythmic conditions, including sinus node disorder, atrial arrhythmias, the Brugada and long QT syndromes, catecholaminergic polymorphic ventricular tachycardia, energetic and ion homeostatic disorders, and longer-term fibrotic or hypertrophic change. This led to recent classifications of arrhythmic mechanisms in different clinical situations, potentially modernising their management.

Culture as shared values/beliefs and behavioral scripts not only influences human behavior and cognition but modulates the underlying brain activity as well. Cultural impacts on the human brain have been investigated by cultural neuroscience research that examines cultural group differences in brain activities involved in specific cognitive/affective processes. The findings, however, do not allow inference of causal relationships between specific cultural values/beliefs and brain activity. Cultural priming approach tests how brain activities underlying various cognitive/affective processes are modulated by recent exposure to specific cultural symbols or activation of specific cultural values/beliefs. Increasing evidence indicates that cultural priming leads to subsequent changes of brain activities in response to perception, attention, reward, self-reflection, etc. The findings suggest that culture provides a key frame in which the human brain develops and functions to mediate multiple cognitive and affective processes.

It has become manifest across the biological sciences that culture is a dynamic component of human brain–body formation and experience. Culture is essential to understanding questions of neuroplasticity, emotional development, interoception, epigenetics, predictive coding, facial recognition, empathy, and so on, yet culture itself is often reduced by those sciences that have come to depend on it. It is "the exterior," or it is "input." The "world," insofar as it introduces contingency to what it is to be human, is not in itself understood as contingent. What happens when culture – both a cause and an effect of human formation – is itself situated, disrupted, historicized? Historians hold the keys to a radical interdisciplinary engagement that complicates the question of culture in ways complementary to the biological disruption of interiority. The cultural brain is an historical artefact. Acknowledging this should change the kinds of questions asked by those who study the brain.