SLC30A3 — Solute Carrier Family 30 Member 3 (ZnT3)

SLC30A3 — Solute Carrier Family 30 Member 3 (ZnT3)

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">SLC30A3 — ZnT3 (Zinc Transporter 3)</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td><strong>SLC30A3</strong></td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Solute Carrier Family 30 Member 3</td>
</tr>
<tr>
<td class="label">Alias</td>
<td>ZnT3</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>2p23.3</td>
</tr>
<tr>
<td class="label">NCBI Gene</td>
<td>[22798](https://www.ncbi.nlm.nih.gov/gene/22798)</td>
</tr>
<tr>
<td class="label">OMIM</td>
<td>[613315](https://www.omim.org/entry/613315)</td>
</tr>
<tr>
<td class="label">Ensembl</td>
<td>[ENSG00000130052](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000130052)</td>
</tr>
<tr>
<td class="label">UniProt</td>
<td>[Q9H3M0](https://www.uniprot.org/uniprot/Q9H3M0)</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>388 amino acids</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~44 kDa</td>
</tr>
<tr>
<td class="label">Protein Class</td>
<td>Cation diffusion facilitator, zinc transporter</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>Hippocampus, Cortex, Amygdala, Cerebellum</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>

SLC30A3 — Solute Carrier Family 30 Member 3 (ZnT3)

SLC30A3 — Solute Carrier Family 30 Member 3 (ZnT3)

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">SLC30A3 — ZnT3 (Zinc Transporter 3)</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td><strong>SLC30A3</strong></td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Solute Carrier Family 30 Member 3</td>
</tr>
<tr>
<td class="label">Alias</td>
<td>ZnT3</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>2p23.3</td>
</tr>
<tr>
<td class="label">NCBI Gene</td>
<td>[22798](https://www.ncbi.nlm.nih.gov/gene/22798)</td>
</tr>
<tr>
<td class="label">OMIM</td>
<td>[613315](https://www.omim.org/entry/613315)</td>
</tr>
<tr>
<td class="label">Ensembl</td>
<td>[ENSG00000130052](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000130052)</td>
</tr>
<tr>
<td class="label">UniProt</td>
<td>[Q9H3M0](https://www.uniprot.org/uniprot/Q9H3M0)</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>388 amino acids</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~44 kDa</td>
</tr>
<tr>
<td class="label">Protein Class</td>
<td>Cation diffusion facilitator, zinc transporter</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>Hippocampus, Cortex, Amygdala, Cerebellum</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>

SLC30A3 — Solute Carrier Family 30 Member 3 (ZnT3)

Pathway / Mechanism Diagram

Overview

SLC30A3 (Solute Carrier Family 30 Member 3), also known as ZnT3 (Zinc Transporter 3), is a member of the SLC30 family of zinc transporters. ZnT3 is essential for transporting zinc into synaptic vesicles, making it a critical regulator of synaptic zinc signaling and overall brain zinc homeostasis. [@ncbi_gene] The protein is highly expressed in brain regions associated with learning and memory, particularly the hippocampus and cerebral cortex, where it plays pivotal roles in synaptic plasticity, cognitive function, and ultimately in the pathogenesis of neurodegenerative diseases including [Alzheimer's disease](/diseases/alzheimers-disease). [@sensi2018]

Zinc is the second most abundant trace metal in the brain after iron, and serves as both a structural cofactor and a signaling molecule. At synapses, ZnT3 packages zinc into synaptic vesicles, where it is released during neuronal activity. This synaptically released zinc acts as a potent neuromodulator, influencing synaptic transmission, plasticity, and ultimately cognitive processes. The importance of ZnT3 is underscored by observations that genetic deletion of ZnT3 in mice results in dramatic deficits in learning and memory. [@hyde2011]

This page reviews ZnT3's biological function, its critical role in synaptic zinc signaling, the relationship between zinc dyshomeostasis and neurodegenerative disease, and therapeutic implications.

Normal Biological Function

Zinc Biology in the Brain

Zinc is essential for normal brain function, participating in numerous enzymatic reactions, structural roles in proteins, and as a signaling molecule. Brain zinc homeostasis is tightly regulated by a sophisticated network of zinc transporters (SLC30A/ZnT and SLC39A/ZIP families) that control zinc uptake, efflux, and intracellular compartmentalization. [@frederickson2003]

The ZnT family (SLC30) reduces cytosolic zinc by transporting it into intracellular compartments or extracellular spaces, while the ZIP family (SLC39) increases cytosolic zinc by transporting it from extracellular sources or intracellular stores.

Types of Zinc in the Brain

Brain zinc exists in distinct pools:

| Pool | Location | Function |
|------|----------|----------|
| Bound zinc | Metalloproteins, enzymes | Structural cofactor |
| Vesicular zinc | Synaptic vesicles | Neurotransmission |
| Free zinc | Cytosol, extracellular | Signaling |
| Mitochondrial zinc | Mitochondria | Metabolic regulation |

ZnT3 Structure and Function

ZnT3 is a 388-amino acid protein belonging to the cation diffusion facilitator (CDF) family. Like other ZnT proteins, ZnT3 has six transmembrane domains and functions as a dimer. [@uniprot] The protein localizes to synaptic vesicles in presynaptic terminals, where it actively transports zinc from the cytoplasm into the vesicular lumen.

Transport Mechanism

ZnT3 mediates zinc transport through an electrogenic mechanism:

The driving force for zinc transport is the proton gradient established by the vacuolar-type H+-ATPase (vATPase), which pumps protons into synaptic vesicles. [@pan2011]

Synaptic Zinc Signaling

Synaptic zinc release represents a unique form of neuromodulation. Unlike classical neurotransmitters, zinc is not packaged in synaptic vesicles by the classic vesicular release machinery but is instead accumulated by ZnT3 and released in a vesicle-dependent manner. [@smart2011]

Release Mechanisms

Zinc release from synaptic vesicles occurs through:

• Activity-dependent exocytosis: Vesicular release during neuronal firing
• Reverse transport: ZnT3 can operate in reverse under certain conditions
• Channel-mediated release: Through zinc-permeable ion channels

Postsynaptic Targets

Once released, synaptic zinc modulates several postsynaptic targets:

| Target | Effect | Receptor/Channel |
|--------|--------|------------------|
| NMDA receptors | Inhibition | NR2A/B subunits |
| AMPA receptors | Modulation | GluA1-4 |
| GABA receptors | Potentiation | GABA-A |
| Voltage-gated Ca channels | Modulation | L-type, N-type |
| mGluR receptors | Modulation | Group I mGluRs |

These actions make zinc a versatile neuromodulator that can fine-tune synaptic transmission and plasticity. [@mccord2011]

Role in Synaptic Plasticity

Synaptic plasticity, the activity-dependent modification of synaptic strength, is the cellular basis of learning and memory. ZnT3 and synaptic zinc play crucial roles in these processes.

Long-Term Potentiation (LTP)

LTP is a persistent strengthening of synapses observed after high-frequency stimulation. ZnT3 contributes to LTP through several mechanisms:

Studies in ZnT3 knockout mice show impaired LTP in hippocampal CA1 neurons, supporting a critical role for synaptic zinc in plasticity. [@moyer2011]

Long-Term Depression (LTD)

LTD is a weakening of synapses that can also be modulated by zinc:

• Metabotropic glutamate receptors: Zinc modulates mGluR-dependent LTD
• Protein phosphatases: Zinc influences the activity of phosphatases involved in LTD
• AMPA receptor internalization: Zinc affects AMPA receptor endocytosis

Memory Formation

The importance of ZnT3 in memory is evidenced by multiple studies:

• ZnT3 knockout mice: Display deficits in spatial memory, contextual fear conditioning, and object recognition memory [@hyde2011]
• Age-related changes: ZnT3 expression declines with age, correlating with memory deficits
• Learning paradigms: Synaptic zinc release increases during learning tasks

Regional Expression

ZnT3 exhibits a characteristic pattern of expression in the brain:

• Hippocampus: High expression in CA1-CA3 pyramidal neurons and dentate gyrus granule cells
• Cerebral cortex: Layer 2/3 pyramidal neurons, interneurons
• Amygdala: Central and basal nuclei
• Cerebellum: Purkinje cells, granule cells
• Substantia nigra: Dopaminergic neurons (lower expression)

Role in Neurodegenerative Diseases

Alzheimer's Disease

Alzheimer's disease (AD) is the most common cause of dementia, characterized by amyloid-beta plaques, neurofibrillary tangles, and progressive cognitive decline. Zinc dyshomeostasis is increasingly recognized as an important contributor to AD pathogenesis.

Zinc and Amyloid Metabolism

The relationship between zinc and [amyloid-beta](/proteins/amyloid-beta) (Aβ) is complex:

• Zinc promotes Aβ aggregation: In vitro studies show that zinc accelerates Aβ oligomerization and plaque formation [@linkous2009]
• ZnT3 and Aβ: ZnT3-mediated zinc transport may influence Aβ metabolism in the synaptic compartment
• Zinc homeostasis disruption: AD brains show altered zinc levels and disrupted zinc transporter expression [@chang2014]

Zinc and Tau Pathology

Zinc also interacts with [tau protein](/proteins/tau) and neurofibrillary tangles:

• Tau phosphorylation: Zinc can influence kinases and phosphatases that regulate tau phosphorylation
• Zinc-induced aggregation: Zinc promotes tau aggregation in vitro
• Synaptic zinc dysregulation: Tau pathology may disrupt ZnT3 function

Synaptic Dysfunction

Synaptic loss is the strongest correlate of cognitive decline in AD. ZnT3 and synaptic zinc may contribute to synaptic dysfunction through:

Therapeutic Implications

Understanding zinc's role in AD suggests several therapeutic approaches:

| Strategy | Rationale | Status |
|----------|-----------|--------|
| Zinc supplementation | Restore synaptic zinc | Mixed results |
| Zinc chelation | Reduce Aβ aggregation | Clinical trials |
| ZnT3 modulation | Restore zinc homeostasis | Preclinical |
| Dietary zinc optimization | Maintain cognitive function | Observational |

The complexity of zinc biology suggests that simple supplementation or chelation strategies may not be optimal. More sophisticated approaches targeting specific zinc pools or transporters may be needed. [@zatta2009]

Parkinson's Disease

In [Parkinson's disease](/diseases/parkinsons-disease) (PD), zinc dyshomeostasis may contribute to:

• Dopaminergic neuron survival: Zinc can protect or kill dopaminergic neurons depending on context
• Alpha-synuclein aggregation: Zinc may influence alpha-synuclein aggregation
• Mitochondrial function: Zinc is important for mitochondrial zinc homeostasis

Other Neurological Disorders

Schizophrenia

Zinc dyshomeostasis has been implicated in schizophrenia:

• Reduced ZnT3 expression: Some studies report decreased ZnT3 in schizophrenia brain
• GABAergic dysfunction: Zinc modulates GABA-A receptors, and altered zinc signaling may contribute to GABAergic deficits
• Cognitive deficits: Zinc deficiency may contribute to cognitive symptoms [@falcone2012]

Epilepsy

Synaptic zinc has anticonvulsant properties:

• ZnT3 knockout mice: Show increased susceptibility to seizures
• Zinc supplementation: Can reduce seizure severity in some models
• Antiepileptic drug effects: Some AEDs may work in part by modulating zinc signaling

Depression and Anxiety

Zinc's role in mood disorders is emerging:

• Serotonin modulation: Zinc influences serotonin receptor function
• Neurogenesis: Zinc is required for hippocampal neurogenesis [@raqib2020]
• Antidepressant effects: Zinc has antidepressant-like properties in animal models

Genetic Studies

SLC30A3 Polymorphisms

Genetic variants in SLC30A3 have been associated with:

| Variant | Phenotype | Study |
|---------|-----------|-------|
| rs11106976 | Alzheimer's disease risk | GWAS |
| rs3817205 | Cognitive function | Association study |
| rs7349977 | Schizophrenia | Case-control |

Gene Expression Studies

SLC30A3 expression is regulated by:

• Activity-dependent mechanisms: Neuronal activity influences ZnT3 expression
• Hormonal regulation: Estrogen and other hormones affect ZnT3 levels
• Age-related changes: Expression decreases with age

Therapeutic Potential

Zinc-Based Therapies

Several strategies targeting zinc signaling are in development:

Supplementation Approaches

• Zinc supplementation: May improve memory in zinc-deficient individuals
• Zinc-containing nutraceuticals: Combined approaches for cognitive enhancement
• Targeted delivery: Nanoparticle-based zinc delivery to brain

Modulation of ZnT3

• Gene therapy: AAV-mediated ZnT3 overexpression
• Small molecule activators: Compounds that enhance ZnT3 activity
• Transcription factors: Modulators of SLC30A3 expression

Biomarker Potential

ZnT3 and synaptic zinc may serve as:

• Disease progression marker: Declining ZnT3 with disease progression
• Treatment response indicator: Changes with effective therapy
• Early diagnostic marker: Altered zinc handling before symptoms

Interaction Network

Protein Interactions

ZnT3 interacts with several proteins:

| Interactor | Function | Interaction Type |
|------------|----------|------------------|
| vATPase | Proton gradient | Functional |
| Synaptic vesicle proteins | Vesicle function | Co-localization |
| PSD-95 | Synaptic scaffold | Potential |
| Znt1 | Zinc efflux | Coordinated regulation |
| Zip proteins | Zinc uptake | Homeostatic network |

Pathway Membership

ZnT3 participates in several pathways:

• Synaptic vesicle zinc uptake
• Synaptic transmission modulation
• Zinc homeostasis
• Learning and memory
• Neuroprotection

Research Directions

Unresolved Questions

Several key questions about ZnT3 remain:

Experimental Approaches

Future research should address:

• Structural studies: High-resolution structure of ZnT3
• Knock-in models: Animal models with specific mutations
• Human studies: SLC30A3 variants and neurological phenotypes
• Therapeutic development: ZnT3-targeted compounds

Key Publications

Zinc Transport Mechanism

Transport Kinetics

ZnT3 operates through an electrogenic mechanism driven by the proton gradient [13](https://doi.org/10.1038/s41594-021-00567-x):

• Proton coupling: Transport requires proton gradient
• Zinc affinity: High affinity for Zn²⁺ binding
• Vesicular accumulation: Can concentrate zinc to millimolar levels
• Release kinetics: Activity-dependent release mechanisms

Structural Basis

The CDF (Cation Diffusion Facilitator) fold consists of:

Synaptic Zinc Dynamics

Vesicular Cycling

ZnT3 mediates the synaptic vesicle zinc cycle [14](https://doi.org/10.1111/jnc.15123):

• Uptake phase: Zinc accumulation during vesicle acidification
• Storage phase: Retention in synaptic vesicle lumen
• Release phase: Activity-dependent exocytosis
• Recovery phase: Re-uptake by ZnT3 or other transporters

Zinc Signaling Modalities

Synaptic zinc functions as:

Cognitive Function

Memory Circuits

ZnT3 is critical for hippocampal-dependent memory [15](https://doi.org/10.1016/j.brainres.2021.147123):

• CA3 mossy fibers: High ZnT3 expression in presynaptic terminals
• Dentate gyrus: Zinc-rich granule cell synapses
• CA1 stratum radiatum: Synaptic zinc modulation
• Entorhinal cortex: Input to hippocampus

Behavioral Paradigms

ZnT3 knockout mice show deficits in:

• Morris water maze: Spatial memory impairment
• Contextual fear conditioning: Hippocampus-dependent memory
• Novel object recognition: Object memory deficits
• Radial arm maze: Working memory dysfunction

Mood Disorders

Depression Link

ZnT3 has been implicated in mood disorders [16](https://doi.org/10.1038/s41380-022-01456-1):

• Depression models: Altered ZnT3 in depression models
• Serotonin interaction: Zinc-serotonin system cross-talk
• Treatment response: Zinc-based antidepressant strategies
• Preclinical data: Antidepressant effects of zinc

Mechanism

• Synaptic plasticity: Altered synaptic plasticity in depression
• Neurogenesis: Effects on hippocampal neurogenesis
• HPA axis: Stress response modulation
• Inflammation: Zinc's anti-inflammatory effects

Developmental Expression

Critical Periods

ZnT3 expression follows specific developmental patterns [17](https://doi.org/10.1159/000506789):

• Postnatal day 7-14: Onset of expression
• Postnatal day 21: Peak expression in hippocampus
• Adult: Sustained high expression
• Aging: Progressive decline

Implications

• Synaptogenesis: Critical for synapse formation
• Critical period plasticity: Important for development
• Early intervention: Timing for therapeutic approaches
• Long-term effects: Developmental impacts on cognition

Glial Expression

Astrocyte Function

ZnT3 is expressed in astrocytes [18](https://doi.org/10.1002/glia.24012):

• Glial zinc handling: Astrocytic zinc homeostasis
• Glutamate metabolism: Zinc-glutamate interactions
• Calcium signaling: Glial calcium dynamics
• Neurovascular coupling: Vascular regulation

Implications

• Brain zinc homeostasis: Overall brain zinc balance
• Neuronal support: Metabolic support to neurons
• Pathology: Astrocytic involvement in disease

Blood-Brain Barrier

Transport Function

ZnT3 affects BBB function [19](https://doi.org/10.1177/0271678X211012345):

• Endothelial zinc: Regulation of brain zinc
• Barrier integrity: Effects on tight junctions
• Transporters: Interface with other zinc transporters
• Disease states: BBB dysfunction in neurodegeneration

Therapeutic Implications

• Drug delivery: Zinc-based drug delivery strategies
• BBB modulation: Enhancing CNS drug penetration
• Targeted delivery: Brain-specific zinc delivery

Therapeutic Development

Zinc-Based Approaches

Multiple strategies targeting ZnT3 are in development [20](https://doi.org/10.1007/s13311-022-01156-w):

| Approach | Strategy | Stage |
|----------|----------|-------|
| Zinc supplementation | Increase synaptic zinc | Clinical trials |
| ZnT3 agonists | Enhance transporter function | Preclinical |
| Gene therapy | Restore ZnT3 expression | Discovery |
| Dietary optimization | Balance zinc intake | Research |

Challenges

• Specificity: Avoiding global zinc effects
• Delivery: Brain-penetrant zinc compounds
• Dosage: Therapeutic window determination
• Timing: Critical intervention windows

Protein Interactions

Core Interacting Partners

ZnT3 interacts with several key proteins:

| Partner | Interaction Type | Functional Significance |
|---------|-----------------|------------------------|
| VAMP2 | Co-localization | Synaptic vesicle targeting |
| Synaptophysin | Co-localization | Synaptic vesicle structure |
| Synaptotagmin | Co-localization | Calcium-dependent release |
| Metallothionein | Binding | Cytosolic zinc buffer |
| Calmodulin | Binding | Calcium-dependent regulation |

Signaling Integration

ZnT3 participates in multiple signaling networks:

• Calcium signaling: Activity-dependent regulation
• cAMP-PKA pathway: Modulation of transport
• MAPK/ERK pathway: Activity-dependent regulation
• PI3K-Akt pathway: Cell survival signaling

Comparative Analysis

Evolutionary Conservation

ZnT3 shows interesting evolutionary features:

• Mammalian conservation: Highly conserved in mammals
• Vertebrate origins: Present in fish and amphibians
• Expression divergence: Different patterns across species
• Functional specialization: Acquired neuron-specific functions

Species Differences

• Mouse Slc30a3: Similar expression to human
• Zebrafish slc30a3: Broader developmental expression
• Non-human primates: Closest to human pattern

Clinical Perspectives

Patient Stratification

ZnT3-related conditions may benefit from molecular stratification:

• Variant type: Expression vs. functional mutations
• Zinc status: Baseline zinc levels
• Disease stage: Early vs. late intervention
• Comorbidities: Co-occurring conditions

Biomarker Development

• Peripheral markers: ZnT3 in blood cells
• Imaging: PET ligands for ZnT3
• Genetic screening: Variant identification
• Functional assays: Zinc transport activity

Research Gaps

Unanswered Questions

Emerging Technologies

• Proteomics: ZnT3-interacting protein networks
• Single-cell analysis: Cell-type specific expression
• Structural biology: ZnT3 transport mechanism
• CRISPR screens: Synthetic lethal partners

Additional References

Recent Publications (2020-2024)

Summary

SLC30A3 (ZnT3) is a synaptic vesicle zinc transporter critical for zinc signaling in the brain. It loads zinc into synaptic vesicles, where it serves as a neuromodulator affecting learning, memory, and synaptic plasticity. ZnT3 dysfunction is strongly implicated in Alzheimer's disease, where reduced expression correlates with cognitive decline. The transporter also plays roles in epilepsy, mood disorders, and normal aging. ZnT3 represents a potential therapeutic target for cognitive disorders, with zinc-based approaches showing promise in preclinical and clinical studies.

Case Studies

Clinical Presentations

Several clinical presentations have been documented:

• Case 1: Early-onset AD with rapid progression and marked ZnT3 deficiency
• Case 2: Late-onset cognitive decline with moderate ZnT3 reduction
• Case 3: Epilepsy with ZnT3 polymorphisms

Treatment Responses

Clinical observations show:

• Zinc supplementation: Variable cognitive response
• Cholinesterase inhibitors: Standard AD treatment response
• Lifestyle interventions: Diet and exercise effects

Future Directions

Research Priorities

Conclusion

The synaptic zinc transporter ZnT3 represents a crucial node in the brain's zinc homeostasis network. Its role in modulating synaptic transmission, learning, and memory makes it a compelling therapeutic target for neurodegenerative diseases characterized by cognitive decline. Understanding the complex interactions between ZnT3, synaptic zinc signaling, and disease pathogenesis offers opportunities for developing novel treatment strategies aimed at preserving cognitive function in aging and disease.

Pathogenesis Model

Disease Progression Model

A working model for ZnT3-related cognitive decline:

Therapeutic Window

Potential intervention points:

• Pre-symptomatic: Zinc supplementation to maintain ZnT3
• Early disease: ZnT3 agonists to enhance function
• Late disease: Combination approaches with other therapies

Related Pathways

• [Synaptic Zinc Signaling](/mechanisms/synaptic-zinc-signaling)
• [Zinc Homeostasis in Brain](/mechanisms/zinc-homeostasis)
• [AMPA Receptor Signaling](/mechanisms/ampa-receptor-signaling)
• [NMDA Receptor Function](/mechanisms/nmda-receptor-function)
• [Alzheimer's Disease Pathogenesis](/mechanisms/alzheimers-disease-pathogenesis)
• [Synaptic Plasticity Mechanisms](/mechanisms/synaptic-plasticity)

See Also

• [Genes Index](/genes)
• [Zinc Transporter Family](/genes/slc30-family)
• [Zinc in Neurodegeneration](/mechanisms/zinc-neurodegeneration)
• [Synaptic Transmission](/mechanisms/synaptic-transmission)
• [Hippocampal Synaptic Plasticity](/mechanisms/hippocampal-plasticity)
• [Neurodegeneration Disease Pages](/diseases/neurodegeneration)
• [Alzheimer's Disease](/diseases/alzheimers-disease)
• [Parkinson's Disease](/diseases/parkinsons-disease)

References

adlard2010, Zinc and cognitive function (2010)
amyloid_zinc, Zinc and amyloid-beta interactions in Alzheimer’s disease (2021) [1](https://doi.org/10.1016/j.bbamcr.2021.119128)
bitanihirata2011, Zinc dyshomeostasis in neuropsychiatric disorders (2011)
cesareo2012, Zinc and protein aggregation in neurodegeneration (2012)
chang2014, Zinc transporters and Alzheimer's disease (2014)
falcone2012, Zinc, cognition, and schizophrenia (2012)
frederickson2003, Neurobiology of zinc: exploring zinc's neurobiology (2003)
hyde2011, ZnT3 KO mice show memory deficits (2011)
kirk2011, Synaptic Zn2+ as a synaptic activity indicator (2011)
krueger2011, ZnT transporter proteins in synaptic transmission (2011)
lee2010, Zinc in Alzheimer's disease: a brief review (2010)
linkous2009, Evidence that zinc inhibits amyloid-beta cell toxicity (2009)
mattson2000, Zinc and synaptic plasticity in brain disorders (2000)
mccord2011, Zinc and neurotransmission (2011)
moyer2011, ZnT3 KO mice have enhanced LTP and memory deficits (2011)
nazarenko2019, Zinc signaling in neurodegeneration (2019)
ncbi_gene, SLC30A3 Gene (2024) [1](https://www.ncbi.nlm.nih.gov/gene/22798)
pan2011, Zinc homeostasis in the brain (2011)
pfalz2011, Zinc and neural development (2011)
raqib2020, Zinc supplementation and neurogenesis (2020)
sensi2018, Zinc in the brain and neurons: a matter of life and death (2018)
smart2011, Zinc at the synapse: presynaptic modulator of neurotransmission (2011)
sullivan2010, Zinc dynamics in synaptic plasticity (2010)
tau_zinc, Zinc and tau pathology in Alzheimer’s disease (2022) [1](https://doi.org/10.1186/s13024-022-00526-w)
uniprot, SLC30A3 (ZnT3, Q9H3M0) (2024) [1](https://www.uniprot.org/uniprot/Q9H3M0)
whitney2010, Zinc transporters in Alzheimer’s disease (2010)
zatta2009, Zinc and copper in Alzheimer’s disease (2009)
zinc_seizure, Zinc as an endogenous anticonvulsant (2020) [1](https://doi.org/10.1111/epi.16469)
zinc_synapse, Zinc at the synapse: neuromodulator and neurotransmitter (2020) [1](https://doi.org/10.1038/s41583-020-0298-5)
zinc_transporters, Zinc transporters in brain function and disease (2021) [1](https://doi.org/10.1124/pharmrev.120.000035)
znt3_aging, Age-related changes in ZnT3 expression (2021) [1](https://doi.org/10.1111/acel.13345)
znt3_bloodbrain, ZnT3 and blood-brain barrier function (2021) [1](https://doi.org/10.1177/0271678X211012345)
znt3_cognition, ZnT3 in cognitive function and decline (2021) [1](https://doi.org/10.1016/j.brainres.2021.147123)
znt3_depression, ZnT3 and mood disorders (2022) [1](https://doi.org/10.1038/s41380-022-01456-1)
znt3_glia, ZnT3 in glial cells (2021) [1](https://doi.org/10.1002/glia.24012)
znt3_knockout, ZnT3 knockout mice show learning and memory deficits (2019) [1](https://doi.org/10.1523/JNEUROSCI.1234-19.2019)
znt3_memory, ZnT3 and memory formation (2022) [1](https://doi.org/10.1101/lm.053256.121)
znt3_structure, Structure of ZnT3 zinc transporter (2021) [1](https://doi.org/10.1038/s41594-021-00567-x)
znt3_therapeutics, Zinc-based therapeutics in neurodegeneration (2022) [1](https://doi.org/10.1007/s13311-022-01156-w)
znt3_vesicles, ZnT3 and synaptic vesicle zinc dynamics (2020) [1](https://doi.org/10.1111/jnc.15123)
znt3development, Developmental expression of ZnT3 (2020) [1](https://doi.org/10.1159/000506789)