Methylphenidate improves cognitive deficits produced by infantile iron deficiency in rats

Wael M.Y. Mohamed, Erica L. Unger, Sarita K. Kambhampati, Byron Jones

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

In humans, iron deficiency early in life produces persistent, impaired cognition. Dietary iron replacement does not ameliorate these problems and to date, no attempt to treat these individuals pharmacologically has been reported. The aim of this work was to test the hypothesis that rats made iron deficient in early infancy exhibit cognitive deficits similar to those seen in humans at adolescence. A second aim was to investigate whether the deficit could be treated pharmacologically. Sprague-Dawley rats were made iron deficient (ID) starting at postnatal day 4 by being placed with iron-deficient dams (vs. control). At weaning, all pups were placed on an iron-sufficient diet for the remainder of the study. At 45 days of age, the animals were tested for attention set shifting. After testing, the animals were assigned to one of three methylphenidate (MePh) dose groups, 1, 5 or 10. mg/kg, p.o., vs. vehicle control and treated daily for 15 days prior to a second round of attention set shift testing and continued throughout testing. The results showed that ID rats performed more poorly than controls overall on attentional set-shift testing. MePh improved ID rats' performance and lower doses were more effective than higher doses. This is the first demonstration that MePh can improve cognitive deficits produced by early ID in animals. These findings may open the possibility of pharmacotherapy to treat the persistent cognitive difficulties in children who were severely iron deficient in early infancy.

Original languageEnglish (US)
Pages (from-to)146-152
Number of pages7
JournalBehavioural Brain Research
Volume216
Issue number1
DOIs
StatePublished - Jan 1 2011

Fingerprint

Methylphenidate
Iron
Dietary Iron
Weaning
Cognition
Sprague Dawley Rats
Diet
Drug Therapy

All Science Journal Classification (ASJC) codes

  • Behavioral Neuroscience

Cite this

Methylphenidate improves cognitive deficits produced by infantile iron deficiency in rats. / Mohamed, Wael M.Y.; Unger, Erica L.; Kambhampati, Sarita K.; Jones, Byron.

In: Behavioural Brain Research, Vol. 216, No. 1, 01.01.2011, p. 146-152.

Research output: Contribution to journalArticle

Mohamed, Wael M.Y. ; Unger, Erica L. ; Kambhampati, Sarita K. ; Jones, Byron. / Methylphenidate improves cognitive deficits produced by infantile iron deficiency in rats. In: Behavioural Brain Research. 2011 ; Vol. 216, No. 1. pp. 146-152.
@article{6d23d282da4942199d6e9b06b1df086a,
title = "Methylphenidate improves cognitive deficits produced by infantile iron deficiency in rats",
abstract = "In humans, iron deficiency early in life produces persistent, impaired cognition. Dietary iron replacement does not ameliorate these problems and to date, no attempt to treat these individuals pharmacologically has been reported. The aim of this work was to test the hypothesis that rats made iron deficient in early infancy exhibit cognitive deficits similar to those seen in humans at adolescence. A second aim was to investigate whether the deficit could be treated pharmacologically. Sprague-Dawley rats were made iron deficient (ID) starting at postnatal day 4 by being placed with iron-deficient dams (vs. control). At weaning, all pups were placed on an iron-sufficient diet for the remainder of the study. At 45 days of age, the animals were tested for attention set shifting. After testing, the animals were assigned to one of three methylphenidate (MePh) dose groups, 1, 5 or 10. mg/kg, p.o., vs. vehicle control and treated daily for 15 days prior to a second round of attention set shift testing and continued throughout testing. The results showed that ID rats performed more poorly than controls overall on attentional set-shift testing. MePh improved ID rats' performance and lower doses were more effective than higher doses. This is the first demonstration that MePh can improve cognitive deficits produced by early ID in animals. These findings may open the possibility of pharmacotherapy to treat the persistent cognitive difficulties in children who were severely iron deficient in early infancy.",
author = "Mohamed, {Wael M.Y.} and Unger, {Erica L.} and Kambhampati, {Sarita K.} and Byron Jones",
year = "2011",
month = "1",
day = "1",
doi = "10.1016/j.bbr.2010.07.025",
language = "English (US)",
volume = "216",
pages = "146--152",
journal = "Behavioural Brain Research",
issn = "0166-4328",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Methylphenidate improves cognitive deficits produced by infantile iron deficiency in rats

AU - Mohamed, Wael M.Y.

AU - Unger, Erica L.

AU - Kambhampati, Sarita K.

AU - Jones, Byron

PY - 2011/1/1

Y1 - 2011/1/1

N2 - In humans, iron deficiency early in life produces persistent, impaired cognition. Dietary iron replacement does not ameliorate these problems and to date, no attempt to treat these individuals pharmacologically has been reported. The aim of this work was to test the hypothesis that rats made iron deficient in early infancy exhibit cognitive deficits similar to those seen in humans at adolescence. A second aim was to investigate whether the deficit could be treated pharmacologically. Sprague-Dawley rats were made iron deficient (ID) starting at postnatal day 4 by being placed with iron-deficient dams (vs. control). At weaning, all pups were placed on an iron-sufficient diet for the remainder of the study. At 45 days of age, the animals were tested for attention set shifting. After testing, the animals were assigned to one of three methylphenidate (MePh) dose groups, 1, 5 or 10. mg/kg, p.o., vs. vehicle control and treated daily for 15 days prior to a second round of attention set shift testing and continued throughout testing. The results showed that ID rats performed more poorly than controls overall on attentional set-shift testing. MePh improved ID rats' performance and lower doses were more effective than higher doses. This is the first demonstration that MePh can improve cognitive deficits produced by early ID in animals. These findings may open the possibility of pharmacotherapy to treat the persistent cognitive difficulties in children who were severely iron deficient in early infancy.

AB - In humans, iron deficiency early in life produces persistent, impaired cognition. Dietary iron replacement does not ameliorate these problems and to date, no attempt to treat these individuals pharmacologically has been reported. The aim of this work was to test the hypothesis that rats made iron deficient in early infancy exhibit cognitive deficits similar to those seen in humans at adolescence. A second aim was to investigate whether the deficit could be treated pharmacologically. Sprague-Dawley rats were made iron deficient (ID) starting at postnatal day 4 by being placed with iron-deficient dams (vs. control). At weaning, all pups were placed on an iron-sufficient diet for the remainder of the study. At 45 days of age, the animals were tested for attention set shifting. After testing, the animals were assigned to one of three methylphenidate (MePh) dose groups, 1, 5 or 10. mg/kg, p.o., vs. vehicle control and treated daily for 15 days prior to a second round of attention set shift testing and continued throughout testing. The results showed that ID rats performed more poorly than controls overall on attentional set-shift testing. MePh improved ID rats' performance and lower doses were more effective than higher doses. This is the first demonstration that MePh can improve cognitive deficits produced by early ID in animals. These findings may open the possibility of pharmacotherapy to treat the persistent cognitive difficulties in children who were severely iron deficient in early infancy.

UR - http://www.scopus.com/inward/record.url?scp=78149407464&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78149407464&partnerID=8YFLogxK

U2 - 10.1016/j.bbr.2010.07.025

DO - 10.1016/j.bbr.2010.07.025

M3 - Article

VL - 216

SP - 146

EP - 152

JO - Behavioural Brain Research

JF - Behavioural Brain Research

SN - 0166-4328

IS - 1

ER -