Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid

• Aquaporin-1 (AQP1) is a water channel expressed in the choroid plexus.
• Reactive astrocytes also express AQP1 under some pathological conditions.
• 3-Nitropropionic acid (3NP) is a neurotoxin that causes degeneration of striatum.
• AQP1 was expressed in astroglia and neurons of rat striatum after 3NP treatment.
• Induced AQP1 may play a pivotal role in water homeostasis in the striatum.

Aquaporin-1 (AQP1) is a water channel expressed in the choroid plexus and participates in forming cerebrospinal fluid. Interestingly, reactive astrocytes also express AQP1 in the central nervous system under some pathological conditions. On the other hand, 3-nitropropionic acid (3NP) is a mitochondrial toxin that causes selective degeneration of striatum; however, its chemical preconditioning is neuroprotective against cerebral ischemia. We previously reported that mild 3NP application is accompanied with numerous reactive astrocytes in rat striatum devoid of typical necrotic lesions. Therefore, we studied whether AQP1 in the rat striatum could be upregulated with reactive astrocytosis using the 3NP model. Immunohistochemical or immunofluorescence analysis showed that reactive astrocytosis in the striatum, which upregulates glial fibrillary acidic protein and glutamine synthetase, was induced by mild doses of 3NP administration. Intriguingly, after 3NP treatment, AQP1 was intensely expressed not only by the subpopulation of astroglia but also by neurons. The AQP1 immunoreactivity became more intensified at the early-subtoxic stage (ES: 24–48 h), but not as much in the delayed-subtoxic stage (DS: 96–120 h). In contrast, AQP4 expression in the striatum was downregulated after 3NP treatment, in particular during the ES stage. AQP1 upregulation/AQP4 downregulation induced under subtoxic 3NP treatment may play a pivotal role in water homeostasis and cell viability in the striatum.