Glutamatergic Neurons
Glutamatergic Neurons - Related Videos
04:27
Co-culturing Glutamatergic Neurons and Pediatric High-Grade Glioma Cells
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2025
This video showcases a technique for co-culturing glutamatergic neurons and pediatric high-grade glioma (pHGG) cells within a microfluidic device. Human induced pluripotent stem cells are introduced into the microfluidic system and incubated to promote their differentiation into mature cortical glutamatergic neurons. Following this, the pHGG cells are introduced onto the mature neurons, establishing a co-culture and enabling interactions between neurons and pHGG cells.
02:41
Assessing Glutamatergic Neurons and Glioma Cells Interactions in a Co-Culture
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2025
This video demonstrates the assessment of neuronal electrical activity in a co-culture of hiPSC-derived cortical glutamatergic neurons and glioma cells using a microfluidic device with multielectrode arrays.
10:49
The Specification of Telencephalic Glutamatergic Neurons from Human Pluripotent Stem Cells
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Cited by 38 •
2013
This procedure yields telencephalic neurons by going through checkpoints which are similar to those observed during human development. The cells are allowed to spontaneously differentiate, are exposed to factors which push them towards the neural lineage, are isolated, and are plated onto coverslips to allow for terminal differentiation and maturation.
09:40
Isolation of Sensory Neurons of Aplysia californica for Patch Clamp Recordings of Glutamatergic Currents
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Cited by 5 •
2013
We describe the dissection of the nervous system of the marine sea hare Aplysia after anesthesia, the isolation of neurons for short term-tissue culture, and recordings of single cell ion currents via the patch clamp technique.
10:57
Primary Cell Culture of Purified GABAergic or Glutamatergic Neurons Established through Fluorescence-activated Cell Sorting
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Cited by 9 •
2019
This protocol describes a cell sorting based method for the purification and culture of fluorescent GABAergic or glutamatergic neurons from the neocortex and hippocampus of postnatal mice or rats.
FAQs
When an action potential reaches the presynaptic terminal, calcium enters the terminal and triggers glutamate release into the synaptic cleft. This links electrical activity in the transmitting neuron to chemical communication with neighboring cells. The calcium-dependent release step is therefore essential for converting presynaptic excitation into a signal that can alter the receiving neuron’s activity.
AMPA and NMDA receptors are ionotropic receptors, meaning they participate directly in the rapid synaptic response that promotes depolarization. Metabotropic glutamate receptors belong to a different receptor class and contribute through signaling processes rather than the same direct ion-channel mechanism. Considering these receptor types separately helps explain how one transmitter can support both immediate excitation and longer-lasting cellular effects.
Glutamatergic signaling can extend beyond a brief change in membrane voltage because receptor activation may promote lasting modifications in synaptic strength. These changes alter how effectively a synapse responds to later activity, providing a cellular basis for neural plasticity. In neuroscience, this mechanism is important because plasticity connects momentary synaptic events with persistent changes associated with learning and memory.
Researchers examine how glutamate release and receptor activation change neuronal depolarization and synaptic strength. These measurements or observations help connect cellular signaling with neural plasticity, the capacity of nervous-system connections to change. Because learning and memory depend on such lasting changes in synaptic function, glutamatergic neurons provide an important framework for investigating how experience can modify neural circuits.
Their excitatory signaling makes glutamatergic neurons relevant to disorders in which neural activity or synaptic function becomes disrupted. Studies can focus on glutamate release, receptor activation, depolarization, or longer-term changes in synaptic strength. In epilepsy and stroke research, this framework helps investigators relate altered excitatory communication to disease-related changes in nervous-system function without treating the neurons as an isolated phenomenon.
They provide a way to examine how excitatory communication affects neighboring cells and how synaptic changes develop over time. Investigators can relate receptor-mediated signaling to neural plasticity, then consider how disturbances in those processes may accompany neurodegeneration or other disorders involving excitatory signaling. This makes the system useful for connecting molecular communication, synaptic function, and broader neurological outcomes.