Nitric oxide (NO) signalling plays important roles in neurotransmission, influencing various aspects of neuronal communication and synaptic function. As a gaseous signalling molecule, NO is unique in its ability to diffuse freely across cell membranes, allowing for rapid and widespread effects on neighbouring cells. NO signalling is intimately involved in synaptic plasticity, which underlies learning and memory processes. NO is produced by nitric oxide synthase (NOS) in response to calcium influx into the postsynaptic neuron. It acts as a retrograde messenger, diffusing back to the presynaptic terminal, where it modulates neurotransmitter release. In the hippocampus, a brain region critical for memory formation, NO has been shown to play a role in long-term potentiation (LTP), a form of synaptic plasticity that strengthens synaptic connections. NO activates the enzyme guanylate cyclase in the presynaptic neuron, leading to an increase in cyclic guanosine monophosphate (cGMP) levels, which ultimately enhances neurotransmitter release and strengthens the synapse. By targeting specific proteins involved in vesicle fusion and release, NO can either facilitate or inhibit neurotransmission, depending on the context. For example, NO can enhance glutamate release in certain synapses, thereby increasing excitatory signalling in the brain. On the other hand, NO has been shown to inhibit acetylcholine release in certain neuronal circuits, leading to a decrease in excitability. Beyond its direct effects on synaptic transmission, NO signalling plays a critical role in regulating cerebral blood flow. Neuronal activity and the subsequent release of neurotransmitters can activate NOS in adjacent blood vessels, leading to the production of NO. NO then acts on smooth muscle cells in blood vessels, causing them to relax and dilate, increasing blood flow to active brain regions. This phenomenon, known as neurovascular coupling, ensures that the increased metabolic demands of active neurons are met with an adequate supply of oxygen and nutrients. NO signalling is also implicated in neuroprotection and neuronal survival. Under certain conditions, such as during inflammation or oxidative stress, NO production can be upregulated as part of the brain's defence mechanisms. In small amounts, NO can have protective effects against neurotoxic insults by neutralizing free radicals and reducing cellular damage. However, excessive uncontrolled NO production can lead to neurotoxicity, as seen in neurodegenerative diseases such as Alzheimer's and Parkinson's disease. NO signalling also acts as a neuromodulator, modifying the activity of neurons and synaptic transmission over longer timescales. By influencing various signalling pathways, NO can modulate the excitability of neurons and alter synaptic plasticity. It can also interact with other neurotransmitter systems, such as glutamate and dopamine, to shape neural network activity and behavioural responses. In the peripheral nervous system, NO signalling is involved in pain modulation. Neurons that release NO in the spinal cord can inhibit pain signals from reaching the brain. This mechanism, known as descending pain modulation, contributes to the body's ability to regulate pain perception and alleviate discomfort. We offer a wide product range of research reagents for studying nitric oxide, including eNOS antibodies, iNOS antibodies, GTP cyclohydrolase 1 antibodies, DYNLL1 antibodies, and eNOS ELISA Kits. Explore our full nitric oxide product range below and discover more, for less. Alternatively, you can explore our NOS product range.