<table class="infobox infobox-cell">
<tr>
<th class="infobox-header" colspan="2">Enteric Glial Cells</th>
</tr>
<tr>
<td class="label">Category</td>
<td>Enteric Nervous System</td>
</tr>
<tr>
<td class="label">Location</td>
<td>Throughout gastrointestinal tract</td>
</tr>
<tr>
<td class="label">Cell Types</td>
<td>Enteric glial cells (EGCs), enteric neurons</td>
</tr>
<tr>
<td class="label">Cell Markers</td>
<td>GFAP, S100B, Sox10, PLP1</td>
</tr>
<tr>
<td class="label">Neurotransmitters</td>
<td>ATP, GABA, Nitric oxide</td>
</tr>
<tr>
<td class="label">Taxonomy</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Cell Ontology (CL)</td>
<td>[CL:0007011](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_0007011)</td>
</tr>
<tr>
<td class="label">Database</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Cell Ontology</td>
<td>[CL:0007011](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_0007011)</td>
</tr>
<tr>
<td class="label">Cell Ontology</td>
<td>[CL:4040002](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_4040002)</td>
</tr>
</table>
<table class="infobox infobox-cell">
<tr>
<th class="infobox-header" colspan="2">Enteric Glial Cells</th>
</tr>
<tr>
<td class="label">Category</td>
<td>Enteric Nervous System</td>
</tr>
<tr>
<td class="label">Location</td>
<td>Throughout gastrointestinal tract</td>
</tr>
<tr>
<td class="label">Cell Types</td>
<td>Enteric glial cells (EGCs), enteric neurons</td>
</tr>
<tr>
<td class="label">Cell Markers</td>
<td>GFAP, S100B, Sox10, PLP1</td>
</tr>
<tr>
<td class="label">Neurotransmitters</td>
<td>ATP, GABA, Nitric oxide</td>
</tr>
<tr>
<td class="label">Taxonomy</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Cell Ontology (CL)</td>
<td>[CL:0007011](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_0007011)</td>
</tr>
<tr>
<td class="label">Database</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Cell Ontology</td>
<td>[CL:0007011](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_0007011)</td>
</tr>
<tr>
<td class="label">Cell Ontology</td>
<td>[CL:4040002](https://www.ebi.ac.uk/ols4/ontologies/cl/classes/http%253A%252F%252Fpurl.obolibrary.org%252Fobo%252FCL_4040002)</td>
</tr>
</table>
Enteric glial cells (EGCs) are a specialized population of neural crest-derived cells that reside within the enteric nervous system (ENS), often called the "second brain" due to their complexity and autonomy. First identified by Dogiel in 1899, enteric glia have evolved from being considered passive support cells to recognized active participants in gut motility, barrier function, immune modulation, and even behavior [1](https://pubmed.ncbi.nlm.nih.gov/10534239/). These cells form an extensive network throughout the gastrointestinal tract, with estimates suggesting that they outnumber enteric neurons by approximately 10:1 in most species. [@furness2003]
The recognition of enteric glia as active players in gastrointestinal physiology and pathology has revolutionized our understanding of gut-brain interactions. Critically, dysfunction of enteric glia is now implicated in neurodegenerative diseases including Parkinson's disease, where alpha-synuclein pathology originates in the gut and propagates to the brain via the vagus nerve. This gut-to-brain spread of neurodegeneration positions enteric glia as potentially critical players in disease initiation and progression. [@braak2003]
Enteric glia are heterogeneous, with distinct populations:
Enteric glial cells exhibit distinctive morphological features:
Enteric glia provide essential support for enteric neurons:
EGCs critically maintain intestinal barrier integrity:
Enteric glia actively regulate gut motility:
EGCs serve as immune-competile cells in the gut:
Enteric glia communicate with the brain via:
Enteric glia are centrally involved in Parkinson's disease pathogenesis:
While less studied, EGCs may contribute to Alzheimer's disease:
Enteric glia offer therapeutic opportunities:
The study of enteric glia has undergone dramatic transformation. Initially considered passive support cells analogous to CNS astrocytes, enteric glia are now recognized as sophisticated regulatory cells essential for gut function. The landmark review by Furness in 2000 established enteric glia as active participants in gastrointestinal physiology [1](https://pubmed.ncbi.nlm.nih.gov/10534239/).
The discovery of alpha-synuclein pathology in the gut of Parkinson's disease patients decades before motor symptoms, followed by Braak's hypothesis of prion-like propagation via the vagus nerve, has elevated enteric glia to a position of central importance in neurodegenerative disease research. Current efforts focus on understanding how EGC dysfunction initiates and propagates neurodegeneration.