Secretory vesicles play a central role in neurotransmission, enabling the efficient release of neurotransmitters from the presynaptic neuron into the synaptic cleft. These membrane-bound vesicles contain neurotransmitters essential for communication between neurons. Neurotransmitters are synthesized in the cell body or axon terminals of the presynaptic neuron and packaged into secretory vesicles in a process known as vesicular packaging. The neurotransmitters are actively transported into these secretory vesicles by vesicular neurotransmitter transporters (VNTs). For example, the vesicular transporter for acetylcholine is the vesicular acetylcholine transporter (VAChT), whilst the vesicular transporter for dopamine is the vesicular monoamine transporter 2 (VMAT2). As neurotransmitters are transported into the vesicle, protons are pumped into the vesicle lumen by the vacuolar H+-ATPase pump, acidifying the vesicle interior which promotes the packing and storage of neurotransmitters. In some cases, neurotransmitters may form complexes with specific proteins, known as vesicular transport proteins, such as vesicular glutamate transporters (VGLUTs) or vesicular GABA transporters (VGATs), to facilitate their packaging and storage. Once neurotransmitters are packaged into secretory vesicles, they are sequestered and protected from enzymatic degradation within the cytoplasm of the presynaptic neuron. This storage prevents premature release and ensures that neurotransmitters are available for release in a regulated and controlled manner. The release of neurotransmitters from secretory vesicles into the synaptic cleft occurs by exocytosis. When an action potential reaches the presynaptic terminal, it triggers the opening of voltage-gated calcium channels, leading to an influx of calcium ions into the neuron. This rise in intracellular calcium concentration triggers the fusion of secretory vesicles with the presynaptic membrane, a process known as calcium-dependent exocytosis. As the vesicle fuses with the membrane, the neurotransmitter molecules are released into the synaptic cleft, where they can bind to receptors on the postsynaptic neuron and transmit the signal. After exocytosis, the fused vesicle becomes a part of the plasma membrane. To maintain subsequent neurotransmitter release and synaptic function, the components of the vesicle membrane, including proteins and lipids, need to be replenished. The recycling of vesicle components is achieved through endocytosis, a process in which the membrane of the vesicle is retrieved from the plasma membrane, forming a new vesicle that can be refilled with neurotransmitters for subsequent release. The number of secretory vesicles available for release and the rate of neurotransmitter release can be modulated by various factors. Calcium influx is a critical regulator of vesicle fusion and neurotransmitter release, and the strength of synaptic transmission is often correlated with the amount of calcium entering the presynaptic terminal. Additionally, presynaptic receptors and other intracellular signalling molecules can modulate the release of neurotransmitters. These regulatory mechanisms allow for the precise control of neurotransmission and synaptic plasticity. Different neurons may contain various types of secretory vesicles, each containing different neurotransmitters. For example, some neurons release small clear vesicles containing classical neurotransmitters, such as glutamate, GABA, and acetylcholine, whilst others release dense-core vesicles containing neuropeptides, which act as neuromodulators and have longer-lasting effects on synaptic function. We provide a large product catalogue of research reagents for studying secretory vesicles, including Synaptophysin antibodies, Rab5 antibodies, Synapsin I antibodies, SNAP25 antibodies, and Synaptotagmin 1 antibodies. Explore our full secretory vesicles product range below and discover more, for less. Alternatively, you can explore our SNAPs & SNAREs, Regulation, and Rabs product ranges.