The Long-Term Behavioural Effects of Maternal Creatine Supplementation in a Spiny Mouse Model of Birth Asphyxia.
Study Goal
The researchers aimed to determine whether maternal creatine supplementation could mitigate behavioral deficits in spiny mice offspring caused by birth asphyxia.
Results Summary
Maternal creatine supplementation reduced anxiety-like behavior in neonatal offspring and negated some asphyxia-induced deficits, though it also led to reduced object exploration and increased body weight in adolescence/adulthood.
Population
Pregnant spiny mice and their offspring.
Effective Dosage
5% w/w creatine monohydrate in daily diet.
Duration
From gestational day 20 until delivery (approximately 18 days).
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
birth asphyxia | increase | locomotor deficits | spiny mice offspring | - | displayed | #1 |
birth asphyxia | increase | anxiety-like behaviour | spiny mice offspring at PND 3-7 | - | displayed | #2 |
birth asphyxia | decrease | novel object discrimination | spiny mice offspring at PND 18 | - | impaired | #3 |
antenatal creatine exposure | decrease | anxiety-like behaviour | spiny mice pups at PND 3 | - | reduced | #4 |
antenatal creatine exposure | decrease | asphyxia-induced anxiety-like behaviour | spiny mice pups at PND 3 | - | amelioration of | #5 |
creatine and asphyxia exposure | decrease | reduced object exploration | spiny mice offspring in adolescence/adulthood | - | showed | #6 |
antenatal creatine | decrease | anxiety-like behaviour | spiny mice offspring at adolescence | - | led to sustained reductions in | #7 |
antenatal creatine | increase | body weight | spiny mice offspring | - | increased | #8 |
antenatal creatine exposure following maternal dietary creatine supplementation | decrease | anxiety-like behaviour | spiny mice offspring | - | decreased | #9 |
antenatal creatine exposure | decrease | behavioural abnormalities caused by birth asphyxia | spiny mice offspring in the neonatal period | - | negated | #10 |
INTRODUCTION: Birth asphyxia-induced encephalopathy is a major cause of long-term neurological morbidity, including cognitive and motor deficits. A proposed treatment is maternal creatine supplementation for prophylactic neuroprotection. This study examined how maternal creatine supplementation with or without birth asphyxia affected the behaviour of spiny mice offspring. METHODS: On day 20 of gestation (mid-gestation; term = 39 days), dams were randomly allocated to either a daily diet containing 5% w/w creatine monohydrate or remained on standard rodent chow. On gestational day 38, dams underwent either control caesarean section where offspring were delivered and recovered immediately, or birth asphyxia whereby the pregnant uterus was excised and placed in a saline bath for 7.5 min, inducing global hypoxia. All offspring were then cross-fostered to a lactating dam. Behavioural assessments were then completed on recovered offspring from neonatal to adolescent/adult ages (postnatal day [PND] 3-41) using the open-field, elevated plus maze, and novel object recognition test. RESULTS: Offspring that underwent birth asphyxia displayed locomotor deficits and increased anxiety-like behaviour at PND 3-7 in the open-field test (p < 0.05) and impaired novel object discrimination at PND 18 (p < 0.05). Antenatal creatine exposure reduced anxiety-like behaviour irrespective of asphyxia in pups at PND 3, indicating an amelioration of the asphyxia-induced anxiety-like behaviour. In adolescence/adulthood, creatine and asphyxia-exposed offspring showed reduced object exploration (p < 0.0001). Antenatal creatine led to sustained reductions in anxiety-like behaviour in the elevated plus maze at adolescence and increased body weight, regardless of birth asphyxia exposure (p < 0.05). CONCLUSION: Antenatal creatine exposure following maternal dietary creatine supplementation decreased anxiety-like behaviour in spiny mice offspring. This change negated behavioural abnormalities caused by birth asphyxia in the neonatal period, though it may have broader influences on long-term emotional and information processing in offspring which warrants further investigation.