This review discusses the control of cerebral blood flow by neurons and astrocytes, highlighting the role of neurotransmitter-mediated signaling, particularly glutamate, in regulating blood flow. It emphasizes that blood flow is not solely controlled by arterioles but also by capillaries, with astrocytes playing a key role in this process. The brain consumes a large proportion of the body's energy, and this energy is used to maintain ion gradients necessary for synaptic and action potentials. A lack of blood glucose and oxygen can lead to neuronal and glial injury, as seen in conditions like stroke and spinal cord injury. The brain has evolved neurovascular coupling mechanisms to increase blood flow to active neurons, a process known as functional hyperaemia. This process is influenced by various factors, including neurotransmitter signaling, metabolic messengers like adenosine and lactate, and the modulation of vascular smooth muscle by astrocytes. The review also discusses the role of arachidonic acid derivatives, such as prostaglandins and epoxyeicosatrienoic acids (EETs), in regulating blood flow. It highlights the importance of understanding these mechanisms for developing therapies for neurological disorders. The review also addresses the role of pericytes in regulating capillary diameter and the impact of oxygen levels on neurovascular signaling. Finally, it discusses the implications of these findings for functional imaging techniques like BOLD fMRI, which rely on functional hyperaemia to detect brain activity. The review concludes with a discussion of the role of neurovascular coupling in pathological conditions, such as spreading depression and ischaemia, and the potential for therapeutic interventions to improve blood flow and prevent neuronal damage.This review discusses the control of cerebral blood flow by neurons and astrocytes, highlighting the role of neurotransmitter-mediated signaling, particularly glutamate, in regulating blood flow. It emphasizes that blood flow is not solely controlled by arterioles but also by capillaries, with astrocytes playing a key role in this process. The brain consumes a large proportion of the body's energy, and this energy is used to maintain ion gradients necessary for synaptic and action potentials. A lack of blood glucose and oxygen can lead to neuronal and glial injury, as seen in conditions like stroke and spinal cord injury. The brain has evolved neurovascular coupling mechanisms to increase blood flow to active neurons, a process known as functional hyperaemia. This process is influenced by various factors, including neurotransmitter signaling, metabolic messengers like adenosine and lactate, and the modulation of vascular smooth muscle by astrocytes. The review also discusses the role of arachidonic acid derivatives, such as prostaglandins and epoxyeicosatrienoic acids (EETs), in regulating blood flow. It highlights the importance of understanding these mechanisms for developing therapies for neurological disorders. The review also addresses the role of pericytes in regulating capillary diameter and the impact of oxygen levels on neurovascular signaling. Finally, it discusses the implications of these findings for functional imaging techniques like BOLD fMRI, which rely on functional hyperaemia to detect brain activity. The review concludes with a discussion of the role of neurovascular coupling in pathological conditions, such as spreading depression and ischaemia, and the potential for therapeutic interventions to improve blood flow and prevent neuronal damage.