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Published on: October 16, 2012
Iron deficiency affects acoustic startle response and latency, but not prepulse inhibition in young adult rats
Maggie S Burhans1, Catherine Dailey, Jason Wiesinger
1Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA.
Insights
Iron deficiency impacts the acoustic startle response (ASR) in rats, particularly in males, and affects neurotransmitter transporters. Sex differences significantly influence these behavioral and neurochemical changes.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Nutritional Neuroscience
Background:
- Iron deficiency is linked to altered dopamine and serotonin transporter function and receptor density.
- Human infant studies show iron deficiency is associated with delayed maturation and altered auditory evoked potentials.
Purpose of the Study:
- To investigate the functional integrity of responses to environmental cues in iron-deficient rats.
- To examine the effects of diet-induced iron deficiency on the acoustic startle response (ASR), prepulse inhibition (PPI), and latency to maximum startle (Tmax).
Main Methods:
- Male and female rats were fed either iron-deficient (ID) or iron-adequate (CN) diets from weaning to adulthood.
- The acoustic startle response (ASR), prepulse inhibition (PPI), and mean latency to maximum startle response (Tmax) were measured.
- Neurotransmitter transporter densities (dopamine, serotonin, norepinephrine) were analyzed in various brain regions.
Main Results:
- ID rats exhibited reduced ASR magnitude (20-60%) compared to CN rats, with no effect on PPI.
- Tmax was significantly longer in ID females (10-20%) but not males.
- Dopamine transporter density was reduced in specific brain regions in ID males, and serotonin transporter density differed in several regions.
- Norepinephrine transporter density was lower in the locus ceruleus of ID male rats.
Conclusions:
- Iron deficiency affects the startle response but not the inhibitory circuits of PPI.
- Sex significantly influences the behavioral and neurochemical effects of iron deficiency.
- Iron deficiency alters monoamine transporter systems, impacting responses to environmental stimuli, with notable sex-dependent effects.
Abstract:
Iron deficiency is associated with alterations in dopamine and serotonin transporters as well as changes in dopamine receptor (DR) density, monoamine concentrations, and in vivo extracellular contents of monoamines in terminal fields. Human infants with iron deficiency have both delayed maturation as well as lengthened central conduction times in auditory evoked potential studies. The current study utilizes the magnitude of the acoustic startle response (ASR), prepulse inhibition (PPI), and mean latency to maximum startle response (T(max)), to examine the functional integrity of response to environmental cues. Male and female rats consumed iron deficient (ID) or iron adequate (CN) diets from weaning until adulthood. ID rats of both sexes had 20-60% reductions in ASR when compared to CN rats but there was no effect on PPI. T(max) was significantly longer by 10-20% in females, but not males. Dopamine transporter density was significantly lower in putamen, nucleus accumbens, and olfactory tubercle in males, but not female rats while the serotonin transporter was significantly different from control animal density in five of 14 brain regions. Norepinephrine transporter density was lower in the locus ceruleus of ID male rats but was unaffected in ID female rats. Regression modeling of ASR with brain monoamine transporters and receptors showed hematocrit, norepinephrine transporter (NET) in dentate gyrus, and D1R in the nucleus accumbens account for nearly 49% of the variance in ASR. T(max) was not significantly associated with any of the independent variables. We conclude that iron deficiency affects the startle response, but not the inhibitory circuits involved in prepulse inhibition. Importantly, sex also strongly influenced these behavioral responses. Future studies, perhaps pharmacologic in nature, are necessary to ascertain whether iron deficiency modifies the contribution of monoaminergic systems to responses to environmental stimuli.
