Long-term effects of methamphetamine exposure on cognitive function and muscarinic acetylcholine receptor levels in mice

Siegel, Jessica A.; Craytor, Michael J.; Raber, Jacob

doi:10.1097/fbp.0b013e32833e7e44

Cited by 39 publications

(46 citation statements)

References 106 publications

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“…Adolescent MA exposure also did not affect memory in either the novel object recognition test or the Morris water maze. Adult MA exposure induces long-term impairments in object recognition memory in rats [70–72] and adult and neonatal MA exposure impairs novel object recognition memory and water maze memory performance later in life in rodents [16, 46, 73–75]. However, consistent with our findings, adolescent MA exposure does not impair novel object recognition or memory in the Morris water maze [20].…”

Section: Discussionsupporting

confidence: 86%

Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice

Buck

Morris

Weber

et al. 2017

Behavioural Brain Research

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The neurotoxic effects of methamphetamine (MA) exposure in the developing and adult brain can lead to behavioral alterations and cognitive deficits in adults. Previous increases in the rates of adolescent MA use necessitate that we understand the behavioral and cognitive effects of MA exposure during adolescence on the adolescent brain. Adolescents using MA exhibit high rates of nicotine (NIC) use, but the effects of concurrent MA and NIC in the adolescent brain have not been examined, and it is unknown if NIC mediates any of the effects of MA in the adolescent. In this study, the long-term effects of a neurotoxic dose of MA with or without NIC exposure during early adolescence (postnatal day 30-31) were examined later in adolescence (postnatal day 41-50) in male C57BL/6J mice. Effects on behavioral performance in the open field, Porsolt forced swim test, and conditioned place preference test, and cognitive performance in the novel object recognition test and Morris water maze were assessed. Additionally, the effects of MA and/or NIC on levels of microtubule associated-2 (MAP-2) protein in the nucleus accumbens and plasma corticosterone were examined. MA and NIC exposure during early adolescence separately decreased anxiety-like behavior in the open field test, which was not seen following co-administration of MA/NIC. There was no significant effect of early adolescent MA and/or NIC exposure on the intensity of MAP-2 immunoreactivity in the nucleus accumbens or on plasma corticosterone levels. These results show that early adolescent MA and NIC exposure separately decrease anxiety-like behavior in the open field, and that concurrent MA and NIC exposure does not induce the same behavioral change as either drug alone.

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Section: Discussionsupporting

confidence: 86%

Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice

Buck

Morris

Weber

et al. 2017

Behavioural Brain Research

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“…Previous research shows that female mice are more vulnerable to the long-term cognitive and neurotoxic effects of postnatal MA exposure [29, 30, 46]. Females also have a higher propensity of using MA during adolescence [10] and show a greater plasma corticosterone release following neonatal and adult MA exposure [22, 47] compared to males.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Effects of Early Adolescent Methamphetamine Exposure on Depression-Like Behavior and the Hypothalamic Vasopressin System in Mice

Joca

Zuloaga²,

Raber³

et al. 2014

Dev Neurosci

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Methamphetamine (MA) has neurotoxic effects on the adult human brain that can lead to deficits in behavior and cognition. However, relatively little research has examined the behavioral or neurotoxic effects of MA in adolescents. The rising rates of adolescent MA use make it imperative that we understand the long-term effects of MA exposure on the adolescent brain and how these effects may differ from those seen in adults. In this study, the long-term effects of MA exposure during early adolescence on behavior and the vasopressin system in the paraventricular nucleus of the hypothalamus in late adolescent and adult male and female C57BL/6J mice were examined. MA exposure increased depression-like behavior in the Porsolt forced swim test in both late adolescent and adult male and female mice. Late adolescent male mice exposed to MA also showed a decrease in the number of vasopressin-immunoreactive neurons in the paraventricular nucleus compared to sex-matched saline-treated controls. Thus, similar to humans exposed to MA during adolescence, mice exposed to MA during adolescence show increased depression-like behavior later in life. These changes in behavior may be related to MA-induced alterations in vasopressin and the hypothalamic-pituitary-adrenal axis, especially in males.

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“…For instance, the cholinergic system is altered (increasedM1mAChR number) in mice with developmental Meth-induced novel object and novel place recognition deficits (Siegel et al 2010). Histamine and its receptors are also altered by Meth use and is involved in the cognitive deficits following both developmental and adult exposure to the drug (Acevedo & Raber, 2011; Noda et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Neonatal (+)-methamphetamine exposure in rats alters adult locomotor responses to dopamine D1 and D2 agonists and to a glutamate NMDA receptor antagonist, but not to serotonin agonists

Graham

Amos‐Kroohs

Braun

et al. 2012

International Journal of Neuropsychopharmacology

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AbstractNeonatal exposure to (+)-methamphetamine (Meth) results in long-term behavioural abnormalities but its developmental mechanisms are unknown. In a series of experiments, rats were treated from post-natal days (PD) 11–20 (stage that approximates human development from the second to third trimester) with Meth or saline and assessed using locomotor activity as the readout following pharmacological challenge doses with dopamine, serotonin and glutamate agonists or antagonists during adulthood. Exposure to Meth early in life resulted in an exaggerated adult locomotor hyperactivity response to the dopamine D1 agonist SKF-82958 at multiple doses, a high dose only under-response activating effect of the D2 agonist quinpirole, and an exaggerated under-response to the activating effect of the N-methyl-d-aspartic acid (NMDA) receptor antagonist, MK-801. No change in locomotor response was seen following challenge with the 5-HT releaser p-chloroamphetamine or the 5-HT2/3 receptor agonist, quipazine. These are the first data to show that PD 11-20 Meth exposure induces long-lasting alterations to dopamine D1, D2 and glutamate NMDA receptor function and may suggest how developmental Meth exposure leads to many of its long-term adverse effects.

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Long-term effects of methamphetamine exposure on cognitive function and muscarinic acetylcholine receptor levels in mice

Cited by 39 publications

References 106 publications

Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice

Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice

Long-Term Effects of Early Adolescent Methamphetamine Exposure on Depression-Like Behavior and the Hypothalamic Vasopressin System in Mice

Neonatal (+)-methamphetamine exposure in rats alters adult locomotor responses to dopamine D1 and D2 agonists and to a glutamate NMDA receptor antagonist, but not to serotonin agonists

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