Human herpesvirus 6 (HHV-6) induces dysregulation of glutamate uptake and transporter expression in astrocytes

[Violeta]

https://pubmed.ncbi.nlm.nih.gov/18247129/

This study demonstrates dysregulation of glutamate uptake in human astrocytes infected with both variants of HHV-6, A and B, with differential effects of HHV-6 in acute and persistently infected cells.

Whereas astrocytes acutely infected with HHV-6 demonstrated increased glutamate uptake, cells persistently infected with HHV-6A and HHV-6B demonstrated impaired glutamate uptake.

Functional dysregulation of glutamate uptake was associated with early increases in mRNA and protein expression of the glial glutamate transporter EAAT-2 followed by a sustained decrease in mRNA expression in astrocytes infected with both HHV-6A and HHV-6B.

Dysregulated glutamate uptake and transporter expression suggests a mechanism for dysregulation of glutamate levels in vivo and a potential mechanism for virus-associated neurologic disease.

 

[Violeta]

https://pubmed.ncbi.nlm.nih.gov/18247129/

This study demonstrates dysregulation of glutamate uptake in human astrocytes infected with both variants of HHV-6, A and B, with differential effects of HHV-6 in acute and persistently infected cells.

Whereas astrocytes acutely infected with HHV-6 demonstrated increased glutamate uptake, cells persistently infected with HHV-6A and HHV-6B demonstrated impaired glutamate uptake.

Functional dysregulation of glutamate uptake was associated with early increases in mRNA and protein expression of the glial glutamate transporter EAAT-2 followed by a sustained decrease in mRNA expression in astrocytes infected with both HHV-6A and HHV-6B.

Dysregulated glutamate uptake and transporter expression suggests a mechanism for dysregulation of glutamate levels in vivo and a potential mechanism for virus-associated neurologic disease.

Maintaining zinc levels within a narrow range is also essential for glutamatergic function; another important mechanism as the receptor interacts with zinc. Rodents with zinc deficiency demonstrate alterations in glutamatergic receptor function with reduced neuroplasticity and neurogenesis.

Another explanation for high glutamate release in zinc deficiency is enhanced activity of NMDA receptor. Zinc down-regulates the glutamate response by inhibiting NMDA receptors.

The present study suggests that zinc enhances GABA release via potentiation of AMPA/kainate receptors in the CA3 region, followed by a decrease in presynaptic glutamate release in the same region. Zinc seems to be an inhibitory neuromodulator of glutamate release.




And a study to read about zinc/glutamate.

Relationship between Zinc (Zn2+) and Glutamate Receptors in the Processes Underlying Neurodegeneration​

https://www.ncbi.nlm.nih.gov/pmc/ar...2,enhanced activity of glutamate transmission.