Whilst it is universally accepted that the energy support of the brain is glucose, the form in which the glucose is taken up by neurones is the topic of intense debate. In the last few decades, the concept of lactate shuttling between glial elements and neural elements has emerged in which the glial cells glycolytically metabolise glucose/glycogen to lactate, which is shuttled to the neural elements via the extracellular fluid. The process occurs during periods of compromised glucose availability where glycogen stored in astrocytes provides lactate to the neurones, and is an integral part of the formation of learning and memory where the energy intensive process of learning requires neuronal lactate uptake provided by astrocytes. More recently sleep, myelination and motor end plate integrity have been shown to involve lactate shuttling. The sequential aspect of lactate production in the astrocyte followed by transport to the neurones is vulnerable to interruption and it is reported that such disparate pathological conditions as Alzheimer’s disease, amyotrophic lateral sclerosis, depression and schizophrenia show disrupted lactate signalling between glial cells and neurones.

The ability to understand the relationship between the reversal potential and the membrane potential is a fundamental skill that must be mastered by students studying membrane excitability. To clarify this relationship, we have reframed a classic experiment carried out by Hodgkin and Katz, where we compare graphically the membrane potential at three phases of the action potential (resting potential, action potential peak, and afterhyperpolarization) to reversal potential for K+ ( EK), reversal potential for Na ( ENa), and membrane potential ( Em) (calculated by the Goldman Hodgkin Katz equation) to illustrate that the membrane potential approaches the reversal potential of the ion to which it is most permeable at that instant.