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Early-postnatal iron deficiency impacts plasticity in the dorsal and ventral hippocampus in piglets
Ellis Nelissen1, Jochen De Vry1, Alexandra Antonides2
1Dept. of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands.
Insights
Postnatal iron deficiency (ID) disrupts brain plasticity markers in piglets, affecting hippocampal function. This study reveals altered brain-derived neurotrophic factor (BDNF) and its receptor TrkB levels, impacting cognitive development.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Postnatal iron deficiency (ID) is linked to cognitive impairments.
- Plasticity markers like brain-derived neurotrophic factor (BDNF), p75 neurotrophin receptor (p75NTR), and tyrosine receptor kinase B (TrkB) are crucial for cognitive function.
- Understanding the molecular mechanisms underlying ID-induced cognitive deficits is essential.
Purpose of the Study:
- To investigate the impact of postnatal iron deficiency on plasticity markers (BDNF, p75NTR, TrkB) in piglets.
- To determine if alterations in these markers underlie iron deficiency-induced cognitive impairments.
Main Methods:
- Newborn piglets were fed either iron-depleted or iron-sufficient diets for four weeks.
- Iron repletion was administered eight weeks after the initial diet period.
- Protein levels of BDNF, p75NTR, TrkB, and phosphorylated CREB were analyzed in the hippocampus and prefrontal cortex using Western blotting.
Main Results:
- Iron deficiency led to decreased mature BDNF and proBDNF in the ventral hippocampus, with increases in the dorsal hippocampus.
- Phosphorylation of CREB mirrored the mature BDNF pattern in the hippocampus.
- TrkB levels were significantly decreased in both dorsal and ventral hippocampus but increased in the prefrontal cortex of iron-deficient piglets.
Conclusions:
- Postnatal iron deficiency disrupts hippocampal plasticity in piglets.
- Altered expression of BDNF and TrkB in the hippocampus suggests a mechanism for ID-induced cognitive impairments.
- These findings highlight the critical role of iron in early brain development and cognitive function.
Abstract:
In this study, we investigated whether alterations in plasticity markers such as brain-derived neurotrophic factor (BDNF), p75 neurotrophin receptor (p75NTR) and tyrosine receptor kinase B (TrkB) are underlying iron deficiency (ID)-induced cognitive impairments in iron depleted piglets. Newborn piglets were either fed an iron-depleted diet (21mg Fe/kg) or an iron-sufficient diet (88mg Fe/kg) for four weeks. Subsequently, eight weeks after iron repletion (190-240mg Fe/kg) we found a significant decrease in mature BDNF (14kDa) and proBDNF (18kDa and 24kDa) protein levels in the ventral hippocampus, whereas we found increases in the dorsal hippocampus. The phosphorylation of cAMP response element binding protein (CREB) follows the mature BDNF protein level pattern. No effects were found on BDNF and CREB protein levels in the prefrontal cortex. The protein levels of the high affinity BDNF receptor, TrkB, was significantly decreased in both dorsal and ventral hippocampus of ID piglets, whereas it was increased in the prefrontal cortex. Together, our data suggest a disrupted hippocampal plasticity upon postnatal ID.
