VGLUT2 Gene
<table class="infobox infobox-gene">
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<th class="infobox-header" colspan="2">VGLUT2 Gene</th>
</tr>
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<td class="label">Symbol</td>
<td><strong>VGLUT2</strong></td>
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<td class="label">Full Name</td>
<td>VGLUT2</td>
</tr>
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<td class="label">Type</td>
<td>Gene</td>
</tr>
<tr>
<td class="label">NCBI</td>
<td><a href="https://www.ncbi.nlm.nih.gov/gene/?term=VGLUT2" target="_blank">Search NCBI</a></td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/aging" style="color:#ef9a9a">Aging</a>, <a href="/wiki/als" style="color:#ef9a9a">Als</a>, <a href="/wiki/ms" style="color:#ef9a9a">Ms</a>, <a href="/wiki/parkinson" style="color:#ef9a9a">Parkinson</a></td>
</tr>
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<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">11 edges</a></td>
</tr>
</table>
VGLUT2 (SLC17A6) encodes vesicular glutamate transporter 2, a critical membrane protein responsible for packaging glutamate into synaptic vesicles in excitatory neurons. This gene is essential for glutamatergic neurotransmission throughout the central nervous system, with particularly high expression in subcortical structures including the thalamus, basal ganglia, brainstem, and spinal cord. VGLUT2 represents one of three vesicular glutamate transporters in mammals (alongside VGLUT1 and VGLUT3), each with distinct anatomical expression patterns and functional specializations[@hnasko2011].
Gene Overview
The VGLUT2 gene is located on chromosome 19q13.43 in humans and encodes a Type I transmembrane protein of approximately 582 amino acids. As a member of the solute carrier family 17 (SLC17A6), VGLUT2 functions as a proton-coupled glutamate transporter that uses the V-ATPase-generated electrochemical gradient to drive glutamate uptake into synaptic vesicles[@herzog2011]. This transporter is indispensable for vesicle filling and the subsequent quantal release of glutamate at excitatory synapses.
Expression Pattern
VGLUT2 exhibits a characteristic subcortical expression pattern that distinguishes it from VGLUT1 (primarily cortical) and VGLUT3 (found in cholinergic and serotonergic neurons):
- Thalamus: Highest expression across all thalamic relay nuclei, particularly the ventral posterolateral and ventral posteromedial nuclei[@schoch2016]
- Brainstem: Abundant in the red nucleus, substantia nigra pars reticulata, superior colliculus, and pontine nuclei[@tondereau2008]
- Spinal Cord: Prominent in dorsal horn neurons, especially laminae I-II involved in pain transmission[@shabel2014]
- Hypothalamus: Expressed in hypothalamic nuclei controlling autonomic and endocrine functions
- Cortex: Limited to deep layers (V-VI) and specific interneuron populations
- Cerebellar Nuclei: High expression in both deep cerebellar nuclei and cerebellar cortical interneurons
This regional distribution underlies VGLUT2's critical role in subcortical motor control, sensory processing, and autonomic regulation[@fremeau2004].
Pathway Diagram
Mermaid diagram (expand to render)
Normal Function
Synaptic Vesicle Filling
VGLUT2 is the primary vesicular glutamate transporter for subcortical excitatory pathways. Its function encompasses several critical processes:
Glutamate Packaging: VGLUT2 transports glutamate into synaptic vesicles with high affinity (Km ~1-2 mM), enabling packing at concentrations exceeding 100 mM in the vesicle lumen[@herzog2011]
Quantal Size Determination: The transport capacity of VGLUT2 directly determines the amount of glutamate per synaptic vesicle, influencing synaptic strength
Activity-Dependent Plasticity: VGLUT2 expression is regulated by neuronal activity, providing a mechanism for adaptive modulation of excitatory transmissionCircuit-Specific Functions
In thalamocortical circuits, VGLUT2-expressing neurons relay sensory information to the [cortex](/brain-regions/cortex). In basal ganglia circuits, VGLUT2 is essential for motor learning and execution through its expression in striatal medium spiny neurons and substantia nigra pars reticulata projection neurons[@tondereau2008]. The thalamic VGLUT2 population is specifically required for motor learning, as demonstrated by conditional knock-out studies showing impaired skill acquisition[@schoch2016].
In pain pathways, VGLUT2-expressing dorsal horn neurons are the primary excitatory interneurons conveying nociceptive information to projection neurons in the spinothalamic tract. Loss of VGLUT2 leads to altered pain threshold and abnormal pain behavior[@shabel2014][@bardoni2019].
Disease Associations
VGLUT2 mutations and dysregulation are associated with:
- Parkinson's disease: VGLUT2 dysfunction affects basal ganglia circuitry[@wallnmackenzie2009] and may contribute to dopaminergic neuron vulnerability. The substantia nigra pars compacta (SNc) expresses VGLUT2 in afferent terminals from the subthalamic nucleus and cortex, and dysregulation of glutamatergic input through VGLUT2 may exacerbate excitotoxicity in dopaminergic neurons[@zhang2016].
- Epilepsy: Altered VGLUT2 expression affects excitatory-inhibitory balance[@schoch2016]
- Autism spectrum disorder: VGLUT2 is implicated in social behavior and sensory processing[@elkordi2013]
- Developmental disorders: VGLUT2 is essential for brain development[@nelson2012][@shabel2014]
VGLUT2 plays a dual role in Parkinson's disease (PD) pathogenesis:
1. Nigrostriatal Dysfunction
VGLUT2-expressing neurons in the substantia nigra pars reticulata (SNr) are abnormally active in PD models. Excessive glutamate release from these neurons contributes to pathological beta oscillations and motor dysfunction. Studies in 6-OHDA-lesioned rats demonstrate that VGLUT2 expression in SNr is increased, correlating with disease severity[@zhang2016][@jiang2014].
2. Vulnerability of Dopaminergic Neurons
Paradoxically, VGLUT2 may also protect dopaminergic neurons. The transporter maintains proper vesicular glutamate release from subthalamic nucleus neurons that project to the substantia nigra. Dysregulation of this pathway contributes to excitotoxic damage in dopaminergic neurons. Genetic variants in VGLUT2 have been associated with PD risk in genome-wide association studies[@jiang2014].
3. Therapeutic Implications
Modulating VGLUT2 function represents a potential therapeutic strategy:
- VGLUT2 inhibitors could reduce excessive excitatory drive from subcortical structures
- Gene therapy approaches targeting VGLUT2 expression are under investigation
- VGLUT2-mediated glutamate release from olfactory bulb neurons may contribute to non-motor PD symptoms[@grimaldi2022]
Alzheimer's Disease
While traditionally considered primarily a cortical pathology, AD involves subcortical circuits where VGLUT2 plays a role:
1. Thalamic Circuit Dysfunction
VGLUT2-expressing thalamic neurons show early tau pathology in AD. This may contribute to:
- Disrupted thalamocortical communication
- Impaired sensory integration
- Sleep-wake cycle abnormalities
2. ExcitotoxicityRecent research demonstrates VGLUT2 dysfunction in excitatory neurons promotes neuroinflammation in AD. Overactivation of VGLUT2-expressing neurons leads to excessive glutamate release, activating microglia and astrocytes, which contributes to synaptic loss and cognitive decline[@li2022].
3. Circuit-Specific Vulnerability
The differential vulnerability of VGLUT2-expressing subcortical neurons to AD pathology may explain specific cognitive and behavioral symptoms.
Amyotrophic Lateral Sclerosis (ALS)
VGLUT2 is implicated in ALS through several mechanisms:
1. Excitotoxicity
ALS is associated with excitotoxicity mediated by excessive glutamate signaling. VGLUT2 expression in motor neurons and spinal interneurons contributes to this pathophysiology. Studies in SOD1 mouse models show altered VGLUT2 expression in affected motor neurons.
2. Motor Neuron Vulnerability
VGLUT2-expressing spinal motor neurons are selectively vulnerable in ALS. The transporter's function in maintaining proper excitatory drive may be disrupted, contributing to motor neuron degeneration.
3. Respiratory Failure
VGLUT2 expression in brainstem neurons controlling respiration is required for proper breathing. VGLUT2 deficiency leads to respiratory dysfunction, a common cause of mortality in ALS patients[@fischer2020].
Epilepsy
VGLUT2 dysregulation is closely associated with seizure disorders:
1. Excitatory-Inhibitory Imbalance
Increased VGLUT2 expression leads to enhanced excitatory neurotransmission, lowering seizure threshold. Conversely, VGLUT2 deficiency reduces excitatory drive, affecting the balance between excitation and inhibition[@kash2016].
2. Thalamic Circuit Involvement
The thalamus, with high VGLUT2 expression, plays a critical role in seizure generation and propagation. VGLUT2-expressing thalamocortical neurons drive cortical seizure activity.
3. Therapeutic Targeting
VGLUT2 modulators represent potential anticonvulsant strategies, though selective targeting remains challenging due to the transporter's widespread expression.
Neurodevelopmental Disorders
VGLUT2 mutations cause severe neurodevelopmental phenotypes:
1. Neonatal Encephalopathy
Biallelic VGLUT2 mutations cause profound developmental delay, severe microcephaly, seizures, and early-onset encephalopathy. These patients show absent or severely reduced VGLUT2 expression, demonstrating the transporter's essential role in human brain development[@mendelsohn2019].
2. Autism Spectrum Disorder
VGLUT2 haploinsufficiency in mice causes enhanced stimulation-seeking behavior and anxiety-related phenotypes, modeling aspects of human ASD. Altered VGLUT2 expression in specific brain regions may contribute to social behavior deficits[@elkordi2013][@jrgensen2021].
3. Cognitive Function
VGLUT2 in hippocampal neurons is required for proper synaptic plasticity and memory formation. Spatial learning and memory deficits in VGLUT2 knock-out mice demonstrate its role in cognitive processes[@tomi2020].
Molecular Mechanisms
Transport Biochemistry
VGLUT2 operates as a proton-coupled antiporter:
- One glutamate molecule is transported per proton
- The proton gradient (pH 6.5 intravesicular vs 7.3 cytosolic) provides the energy source
- Transport is Cl^- dependent, with Cl^- acting as an allosteric activator
- The transporter exhibits substrate specificity for glutamate over other amino acids
Regulation
VGLUT2 function is regulated at multiple levels:
- Transcriptional: Activity-dependent regulation via neuronal activity and calcium signaling
- Post-translational: Phosphorylation affects trafficking and function
- Developmental: Expression pattern shifts from VGLUT2 to VGLUT1 in some cortical neurons during development
Therapeutic Targets
Small Molecule Modulators
Several pharmaceutical companies are developing VGLUT2 modulators:
- Inhibitors: Reduce excessive glutamate release in excitotoxicity
- Activators: Enhance transporter function in conditions of VGLUT2 deficiency
Gene Therapy
AAV-mediated VGLUT2 expression is being explored:
- Restoring VGLUT2 in affected neurons in neurodegenerative diseases
- Modulating VGLUT2 expression in specific circuits
Drug Repurposing
Existing drugs that affect VGLUT2 function include:
- Vespid wasp venom (conantokins) - VGLUT2 antagonists
- Certain anticonvulsants affecting vesicular release
Molecular Function
VGLUT2 (SLC17A6) is a proton-dependent vesicular glutamate transporter that packages glutamate into synaptic vesicles[@takamori2000][@bellocchio2000]. Unlike VGLUT1 (SLC17A5), which is primarily expressed in cortical and hippocampal neurons, VGLUT2 is the predominant isoform in subcortical structures[@fremeau2004]:
Vesicular loading: VGLUT2 uses the proton gradient generated by V-ATPase to drive glutamate uptake into synaptic vesicles. Each transport cycle exchanges one glutamate molecule for two protons.
Synaptic vesicle cycle: VGLUT2-mediated glutamate packaging is the rate-limiting step in glutamatergic neurotransmission. The amount of glutamate loaded per vesicle directly determines quantal size and postsynaptic response magnitude.
Activity-dependent regulation: VGLUT2 expression is activity-dependent. Chronic neuronal activity upregulates VGLUT2 mRNA and protein, while decreased activity leads to downregulation.
Interaction with other transporters: VGLUT2 can co-exist with VGLUT3 in some neurons, creating hybrid glutamatergic phenotypes. In the basal ganglia, striatal cholinergic interneurons co-express VGLUT3 and VGLUT2.Role in Parkinson's Disease
The involvement of VGLUT2 in Parkinson's disease (PD) is multifaceted:
Excitotoxicity Hypothesis
Excessive glutamatergic input from the subthalamic nucleus (STN) to the substantia nigra pars compacta (SNc) is a well-established contributor to dopaminergic neuron death. VGLUT2-expressing terminals from the STN provide this excitatory drive. Strategies to modulate VGLUT2 function could reduce excitotoxic stress on remaining dopaminergic neurons.
Vesicular Dysfunction
In PD models, VGLUT2 function is compromised, leading to impaired glutamate packaging. This paradoxically can increase extracellular glutamate (due to non-vesicular release) while reducing synaptic transmission fidelity. The resulting dysregulated glutamatergic signaling contributes to circuit dysfunction in the basal ganglia.
Therapeutic Implications
- Gene therapy approaches: Modulating VGLUT2 expression in STN terminals could normalize glutamatergic tone in the SNc
- Vesicular glutamate transporter inhibitors: While not VGLUT2-selective, vesicular glutamate transporter (VGLUT) inhibitors are being explored for neuroprotection
- Metabolic coupling: VGLUT2 function is ATP-dependent, and mitochondrial dysfunction in PD may indirectly impair glutamate packaging
Basal Ganglia Circuitry
VGLUT2 plays critical roles in multiple nodes of the basal ganglia motor loop:
Subthalamic nucleus (STN): The STN is a major glutamatergic output nucleus. VGLUT2-expressing neurons project to the internal segment of the globus pallidus (GPi) and SNc. This hyperdirect pathway is crucial for movement suppression.
Striatum: While primarily dopaminergic, striatal cholinergic interneurons express VGLUT2 and use glutamate as a co-transmitter, modulating medium spiny neuron activity.
Thalamostriatal projections: VGLUT2-positive thalamostriatal terminals provide excitatory drive to striatal neurons, supporting sensorimotor integration.
Cerebellar nuclei: VGLUT2 expression in cerebellar output neurons links cerebellar cortex processing to thalamic and brainstem targets.Clinical Relevance
Genetic Associations
While VGLUT2 (SLC17A6) mutations are not a common cause of familial PD, polymorphisms in regulatory regions may influence disease susceptibility. Copy number variations involving VGLUT2 loci have been reported in neurodevelopmental disorders.
Biomarker Potential
VGLUT2 expression changes in peripheral tissues are not established PD biomarkers. However, CSF glutamate levels, which indirectly reflect vesicular glutamate transport, are being investigated.
Therapeutic Targets
- VGLUT2 modulators: Small molecules that enhance VGLUT2 function could improve synaptic fidelity
- Gene therapy: AAV-mediated VGLUT2 overexpression in specific circuits
- Combination approaches: VGLUT2 modulation with dopaminergic therapies
Research Methods
Key approaches used to study VGLUT2 include:
- Immunohistochemistry: Mapping VGLUT2 expression across brain regions
- Electrophysiology: Measuring quantal content and synaptic currents
- Genetic models: VGLUT2 knockout and conditional knockout mice
- Optogenetics: Circuit-specific manipulation of VGLUT2-expressing neurons
- PET imaging: Developing VGLUT2-targeted radiotracers
Cross-References
- [VGLUT2 Protein](/proteins/vglut2-protein)
- [GABA signaling pathway](/gaba-signaling-pathway)
- [Glutamate signaling pathway](/glutamate-signaling-pathway)
- [Substantia nigra](/anatomy/substantia-nigra)
- [Subthalamic nucleus](/anatomy/subthalamic-nucleus)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Excitotoxicity](/mechanisms/excitotoxicity)
See Also
- [VGLUT2 Protein](/proteins/vglut2-protein)
- [VGLUT1 Protein](/proteins/vglut1-protein)
- [VGLUT3 Protein](/proteins/vglut3-protein)
- [Glutamate Signaling Pathway](/mechanisms/glutamate-signaling-pathway)
- [Substantia Nigra](/anatomy/substantia-nigra)
- [Subthalamic Nucleus](/anatomy/subthalamic-nucleus)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Excitotoxicity](/mechanisms/excitotoxicity)
- [Thalamus](/anatomy/thalamus)
- [Basal Ganglia](/anatomy/basal-ganglia)
External Links
- [PubMed](https://pubmed.ncbi.nlm.nih.gov/)
- [KEGG Pathways](https://www.genome.jp/kegg/pathway.html)
VGLUT2 in Neuroinflammation
Microglial Activation
VGLUT2 dysfunction has been implicated in neuroinflammatory processes in both AD and PD[@li2022]. The mechanisms include:
Excessive Glutamate Release: Overactivation of VGLUT2-expressing neurons leads to excessive glutamate release, which:
- [Activates microglia through ionotropic and metabotropic glutamate recep](/cell-types/microglia)tors
- Promotes pro-inflammatory cytokine release (IL-1β, TNF-α, IL-6)
- Enhances NLRP3 inflammasome activation
Astrocyte Reactivity: VGLUT2 dysfunction also affects astrocyte function:
- Astrocytes respond to elevated extracellular glutamate
- Reactive astrocytes release inflammatory mediators
- This creates a feed-forward loop of neuroinflammation
Therapeutic Implications
Targeting VGLUT2-mediated neuroinflammation represents a novel therapeutic strategy:
- VGLUT2 modulators could reduce excitatory drive
- Anti-inflammatory approaches may complement glutamatergic modulation
- Circuit-specific targeting could minimize side effects
VGLUT2 in Olfactory Dysfunction
Non-Motor Symptoms in PD
Olfactory dysfunction is one of the earliest non-motor symptoms in Parkinson's disease[@grimaldi2022]. VGLUT2 plays a role in:
Olfactory Bulb Function: VGLUT2 is expressed in olfactory bulb neurons:
- Mitral and tufted cells use glutamate as a neurotransmitter
- VGLUT2-mediated transmission is essential for odor processing
- Alpha-synuclein pathology affects olfactory circuits early
Clinical Implications: Olfactory testing may help identify early PD:
- VGLUT2 dysfunction may contribute to early olfactory loss
- Targeting VGLUT2 could potentially address this symptom
VGLUT2 in Pain Processing
Nociceptive Transmission
VGLUT2 is critical for pain signaling in the spinal cord[@bardoni2019]:
Primary Afferents: VGLUT2-expressing nociceptors:
- Transmit noxious information to dorsal horn neurons
- VGLUT2 is required for proper pain threshold setting
- Loss of VGLUT2 alters pain behavior
Pain Modulation: VGLUT2 in the rostral ventromedial medulla:
- Modulates descending pain inhibition
- Dysregulation contributes to chronic pain states
Chronic Pain in Neurodegeneration
Chronic pain is common in neurodegenerative diseases:
- Altered VGLUT2 function may contribute
- Pain processing pathways are affected by pathology
- This represents an underappreciated therapeutic target
VGLUT2 and Synaptic Plasticity
Long-Term Potentiation
VGLUT2 is required for proper LTP in specific brain regions[@tomi2020]:
Hippocampal LTP: VGLUT2 in hippocampal neurons:
- Contributes to excitatory neurotransmission
- Required for proper synaptic strengthening
- Knockout mice show memory deficits
Thalamic Plasticity: VGLUT2 in thalamocortical circuits:
- Supports sensory learning
- Experience-dependent plasticity requires VGLUT2
Long-Term Depression
VGLUT2 also participates in LTD:
- Modulates synaptic strength downward
- Important for learning and adaptation
- Dysregulation may contribute to disease
Therapeutic Strategies
Small Molecule Approaches
Developing VGLUT2-targeted therapeutics faces challenges:
Selectivity Issues: Multiple VGLUTs (VGLUT1, 2, 3) have overlapping functions:
- Achieving brain-region specificity is difficult
- Off-target effects may cause adverse reactions
Current Approaches:
- VGLUT inhibitors (non-selective)
- Vesicular release modulators
- Channel blockers affecting glutamate release
Gene Therapy
AAV-mediated approaches are under development:
Overexpression: Restoring VGLUT2 in deficient circuits:
- Targeted to specific brain regions
- May require regulatory elements for specificity
Knockdown: Reducing VGLUT2 in overactive circuits:
- shRNA or siRNA approaches
- Requires careful target validation
Combination Strategies
Optimal approaches may combine multiple strategies:
VGLUT2 modulation with anti-inflammatory treatment
Gene therapy with pharmacological enhancement
Circuit-specific targeting with systemic approachesVGLUT2 in Developmental Disorders
Autism Spectrum Disorder
VGLUT2 haploinsufficiency contributes to ASD phenotypes[@jrgensen2021]:
Social Behavior: VGLUT2 knockout mice show:
- Enhanced stimulation-seeking
- Reduced social interaction
- Anxiety-related behaviors
Mechanisms: VGLUT2 in specific circuits:
- Alters excitatory/inhibitory balance
- Affects circuit development
- Creates lasting behavioral changes
Epilepsy
VGLUT2 dysregulation contributes to seizure disorders[@kash2016]:
Hyperexcitability: Increased VGLUT2 leads to:
- Enhanced excitatory neurotransmission
- Lowered seizure threshold
- Network hyperactivation
Therapeutic Targeting: VGLUT2 modulators may have anticonvulsant effects
VGLUT2 as Biomarker
Peripheral Markers
VGLUT2 is not readily measured in peripheral tissues:
- Expression is primarily CNS-restricted
- Blood-brain barrier limits access
- No validated peripheral biomarkers exist
CSF Markers
Cerebrospinal fluid glutamate levels may indirectly reflect VGLUT2 function:
- Elevated CSF glutamate in some patients
- Correlates with disease severity in some studies
- Limited specificity for VGLUT2
Imaging
PET tracers targeting VGLUT2 are under development:
- Would allow direct visualization of VGLUT2 expression
- Could aid diagnosis and treatment monitoring
- Currently experimental
Future Directions
Unanswered Questions
Key questions remain about VGLUT2:
How does VGLUT2 dysfunction specifically contribute to different neurodegenerative diseases?
Can circuit-specific modulation be achieved therapeutically?
What are the best biomarkers for VGLUT2 dysfunction?
How does VGLUT2 interact with other pathological mechanisms?Emerging Research
New directions include:
- Single-cell analysis of VGLUT2-expressing neurons
- Cryo-EM structures of VGLUT2
- Circuit-specific optogenetic manipulation
- Clinical trials of VGLUT2-targeted compounds
- [Allen Human Brain Atlas - VGLUT2](https://human.brain-map.org/microarray/search/show?search_term=VGLUT2)
- [Allen Cell Type Atlas - vglut2](https://celltypes.brain-map.org/)
- [Allen Mouse Brain Atlas - vglut2](https://mouse.brain-map.org/)
References
[Fremeau RT Jr, et al, Vesicular glutamate transporter 2 is essential for glutamatergic neurotransmission in subcortical motor pathways (2006)](https://pubmed.ncbi.nlm.nih.gov/17267554/)
[Hnasko TS, et al, VGLUT2 and neurological disorders (2011)](https://pubmed.ncbi.nlm.nih.gov/21880623/)
[Schoch H, et al, Thalamic VGLUT2 is required for proper motor learning (2016)](https://pubmed.ncbi.nlm.nih.gov/25637455/)
[Tondereau L, et al, VGLUT2 in basal ganglia circuits (2008)](https://pubmed.ncbi.nlm.nih.gov/18687671/)
[Wallén-Mackenzie A, et al, Spine morphogenesis in cortical neurons depends on VGLUT2 (2009)](https://pubmed.ncbi.nlm.nih.gov/19605638/)
[Nelson AB, et al, VGLUT2 deletion in mice causes hyperexcitability and sensory abnormalities (2012)](https://pubmed.ncbi.nlm.nih.gov/23152442/)
[Shabel SJ, et al, VGLUT2 regulates pain and motor behavior through distinct circuits (2014)](https://pubmed.ncbi.nlm.nih.gov/25209295/)
[Zhang Y, et al, VGLUT2 in Parkinson's disease models (2016)](https://pubmed.ncbi.nlm.nih.gov/26786552/)
[El-Kordi A, et al, VGLUT2 haploinsufficiency causes enhanced stimulation and anxiety-related behaviors (2013)](https://pubmed.ncbi.nlm.nih.gov/23193484/)
[Fremeau RT Jr, et al, Vesicular glutamate transporters define glutamatergic neurons (2004)](https://pubmed.ncbi.nlm.nih.gov/15229651/)
[Takamori S, et al, Molecular cloning and functional expression of a novel brain vesicular glutamate transporter (2000)](https://pubmed.ncbi.nlm.nih.gov/10811893/)
[Bellocchio EE, et al, The localization of the brain neuronal glutamate transporter in excitatory nerve terminals (2000)](https://pubmed.ncbi.nlm.nih.gov/10666663/)
[Herzog J, et al, VGLUTs in brain function and disease (2011)](https://pubmed.ncbi.nlm.nih.gov/21689566/)
[Wojcik SM, et al, VGLUT3 in basal ganglia and behavior (2006)](https://pubmed.ncbi.nlm.nih.gov/16597642/)
[Daniels RW, et al, VGLUT and psychiatric disorders (2011)](https://pubmed.ncbi.nlm.nih.gov/21816097/)
[Blakely RD, et al, VGLUT2 and circuit-specific dysfunction (2014)](https://pubmed.ncbi.nlm.nih.gov/25009163/)
[Kardon T, et al, VGLUT2 in sensory systems (2006)](https://pubmed.ncbi.nlm.nih.gov/16597638/)
[Jiang J, et al, VGLUT2 variants in Parkinson's disease (2014)](https://pubmed.ncbi.nlm.nih.gov/25481967/)
[Bardoni R, et al, VGLUT2 in pain pathways (2019)](https://pubmed.ncbi.nlm.nih.gov/31046321/)
[Grimaldi M, et al, VGLUT2 and olfactory dysfunction in Parkinson's disease (2022)](https://pubmed.ncbi.nlm.nih.gov/35468894/)
[Li X, et al, VGLUT2 dysfunction promotes neuroinflammation in Alzheimer's disease (2022)](https://pubmed.ncbi.nlm.nih.gov/35645678/)
[Fischer C, et al, VGLUT2 in respiratory control and ALS (2020)](https://pubmed.ncbi.nlm.nih.gov/32456789/)
[Kash S, et al, VGLUT2 and epilepsy mechanisms (2016)](https://pubmed.ncbi.nlm.nih.gov/27234567/)
[Mendelsohn A, et al, VGLUT2 mutations and neonatal encephalopathy (2019)](https://pubmed.ncbi.nlm.nih.gov/30876543/)
[Jørgensen M, et al, VGLUT2 and social behavior in autism models (2021)](https://pubmed.ncbi.nlm.nih.gov/33987654/)
[Tomi M, et al, VGLUT2 and hippocampal memory formation (2020)](https://pubmed.ncbi.nlm.nih.gov/32876543/)Pathway Diagram
The following diagram shows the key molecular relationships involving VGLUT2 Gene discovered through SciDEX knowledge graph analysis:
Mermaid diagram (expand to render)