Calcium signalling is a critical process that plays a central role in neurotransmission, the communication between neurons at synapses. The influx of calcium ions into neurons is a key event that triggers various molecular processes, leading to the release of neurotransmitters, influencing synaptic plasticity, and other essential aspects of neuronal function. Calcium plays a central role in the release of neurotransmitters from the presynaptic neuron. When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium ions to enter the neuron. This increase in intracellular calcium concentration triggers the fusion of neurotransmitter-containing vesicles with the presynaptic membrane, leading to the exocytosis of neurotransmitters into the synaptic cleft. Neurotransmitters then bind to receptors on the postsynaptic neuron, initiating the transmission of the signal across the synapse. Calcium signalling is also intimately involved in synaptic plasticity, the ability of synapses to strengthen or weaken in response to activity. Long-term potentiation (LTP) and long-term depression (LTD) are two forms of synaptic plasticity that underlie learning and memory processes. Calcium influx through NMDA receptors, a subtype of glutamate receptors, is critical for the induction of LTP. The activation of these receptors allows calcium to enter the postsynaptic neuron, leading to intracellular signalling cascades that strengthen the synaptic connection. Calcium-Calmodulin-Dependent Protein Kinase II (CaMKII), a calcium-activated protein kinase abundant in the postsynaptic density of excitatory synapses, becomes activated by binding to calmodulin, a calcium-binding protein. Active CaMKII phosphorylates various target proteins, including AMPA receptors (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors), leading to an increase in their synaptic insertion. This process enhances the strength of excitatory synaptic transmission. Conversely, calcium-dependent signalling pathways are involved in LTD, which weakens the synaptic connection. Calcium entry through the NMDA receptors activates the calcium/calmodulin-dependent phosphatase calcineurin which dephosphorylates various target proteins, including AMPA receptors, leading to their internalization or removal from the synaptic membrane. This reduction in AMPA receptors at the synapse decreases the strength of excitatory synaptic transmission, thereby contributing to LTD. Calcium signalling also plays a role in modulating neurotransmitter release at the presynaptic terminal. Feedback mechanisms can regulate the amount of calcium influx into the presynaptic neuron, influencing the probability of neurotransmitter release. For instance, certain G-protein-coupled receptors (GPCRs) can inhibit or facilitate calcium entry through voltage-gated calcium channels, affecting synaptic transmission. Finally, in addition to its role in fast neurotransmission, calcium signalling is involved in neuromodulation, a process that modulates the excitability of neurons and synaptic transmission over longer timescales. Calcium can influence the expression and function of neurotransmitter receptors, ion channels, and other proteins involved in neuronal signalling. Neuromodulatory systems, such as those utilizing dopamine, acetylcholine, and serotonin, rely on calcium signalling to mediate their effects on neuronal excitability and synaptic transmission. We offer a large product range of research reagents for studying calcium signaling, including Calretinin antibodies, Calbindin antibodies, CamKII gamma antibodies, CAMKIV antibodies, and ADCY8 antibodies. Explore our full calcium signaling product range below and discover more, for less. Alternatively, you can explore our Calcium Binding Proteins, Calmodulin & CaMK, and Calcium Channels product ranges.