Sex- and histamine-dependent long-term cognitive effects of methamphetamine exposure

Summer F. Acevedo, Iwan J P De Esch, Jacob Raber

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

As prenatal methamphetamine (MA) exposure results in long-term hippocampus-dependent cognitive deficits, the increased MA use in women of childbearing age is of great concern. As mice are most commonly used in genetic models, we started to study the potential effects of neonatal MA exposure in female and male mice on brain function 3 months later. As histamine (HA) might mediate some effects of MA in adulthood, we also tested whether in neonates HA might mediate the long-term effects of MA using HA H3 receptor agonists and antagonists. Stimulation of HA H3 receptors by H 3 agonists inhibits HA synthesis and release, whereas inhibition of H3 receptors by H3 receptor antagonists increases HA release. MA (5 mg/kg), the H3 receptor antagonist thioperamide (5 mg/kg), and the H3 receptor agonist immepip (5 mg/kg) alone or in the presence of MA (5 mg/kg) were administered once daily from postnatal days 11 to 20 and the mice were tested at 3 months of age. Here we show that in mice exposure to MA early in life causes sex-dependent impairments in object recognition, spatial learning, and memory in the water maze, and pre-pulse inhibition in adulthood. HA mediates these impairments. Increasing HA release mimicked, whereas inhibiting HA release blocked the long-term detrimental MA effects. This model could be used to determine the role of genetic and environmental factors in MA-dependent cognitive impairments and to develop therapeutic strategies to inhibit them.

Original languageEnglish (US)
Pages (from-to)665-672
Number of pages8
JournalNeuropsychopharmacology
Volume32
Issue number3
DOIs
StatePublished - Mar 2007

Fingerprint

Methamphetamine
Histamine
Histamine H3 Receptors
Histamine Release
Histamine Agonists
thioperamide
Histamine H3 Antagonists
Genetic Models
Hippocampus
Newborn Infant

Keywords

  • Methamphetamine
  • Mouse
  • Neonatal
  • Open field
  • Prepulse inhibition
  • Water maze

ASJC Scopus subject areas

  • Pharmacology

Cite this

Sex- and histamine-dependent long-term cognitive effects of methamphetamine exposure. / Acevedo, Summer F.; De Esch, Iwan J P; Raber, Jacob.

In: Neuropsychopharmacology, Vol. 32, No. 3, 03.2007, p. 665-672.

Research output: Contribution to journalArticle

Acevedo, Summer F. ; De Esch, Iwan J P ; Raber, Jacob. / Sex- and histamine-dependent long-term cognitive effects of methamphetamine exposure. In: Neuropsychopharmacology. 2007 ; Vol. 32, No. 3. pp. 665-672.
@article{838e1d51eaf446348ca7ed373c8b5fdb,
title = "Sex- and histamine-dependent long-term cognitive effects of methamphetamine exposure",
abstract = "As prenatal methamphetamine (MA) exposure results in long-term hippocampus-dependent cognitive deficits, the increased MA use in women of childbearing age is of great concern. As mice are most commonly used in genetic models, we started to study the potential effects of neonatal MA exposure in female and male mice on brain function 3 months later. As histamine (HA) might mediate some effects of MA in adulthood, we also tested whether in neonates HA might mediate the long-term effects of MA using HA H3 receptor agonists and antagonists. Stimulation of HA H3 receptors by H 3 agonists inhibits HA synthesis and release, whereas inhibition of H3 receptors by H3 receptor antagonists increases HA release. MA (5 mg/kg), the H3 receptor antagonist thioperamide (5 mg/kg), and the H3 receptor agonist immepip (5 mg/kg) alone or in the presence of MA (5 mg/kg) were administered once daily from postnatal days 11 to 20 and the mice were tested at 3 months of age. Here we show that in mice exposure to MA early in life causes sex-dependent impairments in object recognition, spatial learning, and memory in the water maze, and pre-pulse inhibition in adulthood. HA mediates these impairments. Increasing HA release mimicked, whereas inhibiting HA release blocked the long-term detrimental MA effects. This model could be used to determine the role of genetic and environmental factors in MA-dependent cognitive impairments and to develop therapeutic strategies to inhibit them.",
keywords = "Methamphetamine, Mouse, Neonatal, Open field, Prepulse inhibition, Water maze",
author = "Acevedo, {Summer F.} and {De Esch}, {Iwan J P} and Jacob Raber",
year = "2007",
month = "3",
doi = "10.1038/sj.npp.1301091",
language = "English (US)",
volume = "32",
pages = "665--672",
journal = "Neuropsychopharmacology",
issn = "0893-133X",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - Sex- and histamine-dependent long-term cognitive effects of methamphetamine exposure

AU - Acevedo, Summer F.

AU - De Esch, Iwan J P

AU - Raber, Jacob

PY - 2007/3

Y1 - 2007/3

N2 - As prenatal methamphetamine (MA) exposure results in long-term hippocampus-dependent cognitive deficits, the increased MA use in women of childbearing age is of great concern. As mice are most commonly used in genetic models, we started to study the potential effects of neonatal MA exposure in female and male mice on brain function 3 months later. As histamine (HA) might mediate some effects of MA in adulthood, we also tested whether in neonates HA might mediate the long-term effects of MA using HA H3 receptor agonists and antagonists. Stimulation of HA H3 receptors by H 3 agonists inhibits HA synthesis and release, whereas inhibition of H3 receptors by H3 receptor antagonists increases HA release. MA (5 mg/kg), the H3 receptor antagonist thioperamide (5 mg/kg), and the H3 receptor agonist immepip (5 mg/kg) alone or in the presence of MA (5 mg/kg) were administered once daily from postnatal days 11 to 20 and the mice were tested at 3 months of age. Here we show that in mice exposure to MA early in life causes sex-dependent impairments in object recognition, spatial learning, and memory in the water maze, and pre-pulse inhibition in adulthood. HA mediates these impairments. Increasing HA release mimicked, whereas inhibiting HA release blocked the long-term detrimental MA effects. This model could be used to determine the role of genetic and environmental factors in MA-dependent cognitive impairments and to develop therapeutic strategies to inhibit them.

AB - As prenatal methamphetamine (MA) exposure results in long-term hippocampus-dependent cognitive deficits, the increased MA use in women of childbearing age is of great concern. As mice are most commonly used in genetic models, we started to study the potential effects of neonatal MA exposure in female and male mice on brain function 3 months later. As histamine (HA) might mediate some effects of MA in adulthood, we also tested whether in neonates HA might mediate the long-term effects of MA using HA H3 receptor agonists and antagonists. Stimulation of HA H3 receptors by H 3 agonists inhibits HA synthesis and release, whereas inhibition of H3 receptors by H3 receptor antagonists increases HA release. MA (5 mg/kg), the H3 receptor antagonist thioperamide (5 mg/kg), and the H3 receptor agonist immepip (5 mg/kg) alone or in the presence of MA (5 mg/kg) were administered once daily from postnatal days 11 to 20 and the mice were tested at 3 months of age. Here we show that in mice exposure to MA early in life causes sex-dependent impairments in object recognition, spatial learning, and memory in the water maze, and pre-pulse inhibition in adulthood. HA mediates these impairments. Increasing HA release mimicked, whereas inhibiting HA release blocked the long-term detrimental MA effects. This model could be used to determine the role of genetic and environmental factors in MA-dependent cognitive impairments and to develop therapeutic strategies to inhibit them.

KW - Methamphetamine

KW - Mouse

KW - Neonatal

KW - Open field

KW - Prepulse inhibition

KW - Water maze

UR - http://www.scopus.com/inward/record.url?scp=33847058102&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847058102&partnerID=8YFLogxK

U2 - 10.1038/sj.npp.1301091

DO - 10.1038/sj.npp.1301091

M3 - Article

C2 - 16710318

AN - SCOPUS:33847058102

VL - 32

SP - 665

EP - 672

JO - Neuropsychopharmacology

JF - Neuropsychopharmacology

SN - 0893-133X

IS - 3

ER -