Nicotine attenuates spatial learning deficits induced in the rat by perinatal lead exposure

Zhou, Mingfu; Suszkiw, Janusz B.

doi:10.1016/j.brainres.2003.10.068

Cited by 27 publications

(21 citation statements)

References 21 publications

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“…Virtually all of these previous studies utilized considerably higher doses of maternal nicotine treatment (e.g., 6 mg/kg/day) compared with the 2 mg/ kg/day dose used in the present study, which is more comparable to studies reporting beneficial effects of prenatal nicotine administration on adult cognition (e.g., Cutler et al 1996;Levin et al 1996b; see also Zhou and Suszkiw 2004). Interestingly, Slotkin et al (2005) recently reported that prenatal choline administration can ameliorate some of the deleterious effects of high-level prenatal nicotine exposure on brain bio-markers in rhesus monkeys.…”

Section: Learning and Memory 129supporting

confidence: 69%

α7 Nicotinic acetylcholine receptors and temporal memory: Synergistic effects of combining prenatal choline and nicotine on reinforcement-induced resetting of an interval clock

Cheng

Meck²,

Williams³

2006

Learn. Mem.

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We previously showed that prenatal choline supplementation could increase the precision of timing and temporal memory and facilitate simultaneous temporal processing in mature and aged rats. In the present study, we investigated the ability of adult rats to selectively control the reinforcement-induced resetting of an internal clock as a function of prenatal drug treatments designed to affect the ␣7 nicotinic acetylcholine receptor (␣7 nAChR). Male Sprague-Dawley rats were exposed to prenatal choline (CHO), nicotine (NIC), methyllycaconitine (MLA), choline + nicotine (CHO + NIC), choline + nicotine + methyllycaconitine (CHO + NIC + MLA), or a control treatment (CON). Beginning at 4-mo-of-age, rats were trained on a peak-interval timing procedure in which food was available at 10-, 30-, and 90-sec criterion durations. At steady-state performance there were no differences in timing accuracy, precision, or resetting among the CON, MLA, and CHO + NIC + MLA treatments. It was observed that the CHO and NIC treatments produced a small, but significant increase in timing precision, but no change in accuracy or resetting. In contrast, the CHO + NIC prenatal treatment produced a dramatic increase in timing precision and selective control of the resetting mechanism with no change in overall timing accuracy. The synergistic effect of combining prenatal CHO and NIC treatments suggests an organizational change in ␣7 nAChR function that is dependent upon a combination of selective and nonselective nAChR stimulation during early development.

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Section: Learning and Memory 129supporting

confidence: 69%

α7 Nicotinic acetylcholine receptors and temporal memory: Synergistic effects of combining prenatal choline and nicotine on reinforcement-induced resetting of an interval clock

Cheng

Meck²,

Williams³

2006

Learn. Mem.

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“…In animal models, nicotine improves hippocampal performance in aged rats with cognitive impairment or in young rats with cholinergic lesions (Levin, 1993). Furthermore, a recent study found that acute nicotine administration temporarily offsets the cognitive deficits induced by perinatal lead exposure (Zhou and Suszkiw, 2004), so that pharmacotherapeutic approaches to the reversal of neurobehavioral teratogenesis may, in fact, be widely applicable.…”

Section: Discussionmentioning

confidence: 99%

Nicotine Therapy in Adulthood Reverses the Synaptic and Behavioral Deficits Elicited by Prenatal Exposure to Phenobarbital

Beer

Slotkin

Seidler

et al. 2004

Neuropsychopharmacol

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A major objective in identifying the mechanisms underlying neurobehavioral teratogenicity is the possibility of designing therapies that reverse or offset drug-or toxicant-induced neural damage. In our previous studies, we identified deficits in hippocampal muscarinic cholinergic receptor-induced membrane translocation of protein kinase C (PKC)g as the likely mechanism responsible for adverse behavioral effects of prenatal phenobarbital exposure. We therefore explored whether behavioral and synaptic defects could be reversed in adulthood by nicotine administration. Pregnant mice were given milled food containing phenobarbital to achieve a daily dose of 0.5-0.6 g/kg from gestational days 9-18. In adulthood, offspring showed deficits in the Morris maze, a behavior dependent on the integrity of septohippocampal cholinergic synaptic function, along with the loss of the PKCg response. Phenobarbital-exposed and control mice then received nicotine (10 mg/kg/day) for 14 days via osmotic minipumps. Nicotine reversed the behavioral deficits and restored the normal response of hippocampal PKCg to cholinergic receptor stimulation. The effects were regionally specific, as PKCg in the cerebellum was unaffected by either phenobarbital or nicotine; furthermore, in the hippocampus, PKC isoforms unrelated to the behavioral deficits showed no changes. Nicotine administration thus offers a potential therapy for reversing neurobehavioral deficits originating in septohippocampal cholinergic defects elicited by prenatal drug or toxicant exposures.

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“…Zhou and Suskiw (2004) have demonstrated that acute systemic administration of nicotine reversed these deficits in rats.…”

Section: Animal Studiesmentioning

confidence: 96%

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

2005

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Discovery of the behavioral, pharmacological, and anatomic specificity of nicotinic effects on learning, memory, and attention not only aids the understanding of nicotinic involvement in the basis of cognitive function, but also helps in the development of novel nicotinic treatments for cognitive dysfunction. Nicotinic treatments directed at specific receptor subtypes and nicotinic cotreatments with drugs affecting interacting transmitter systems may provide cognitive benefits most relevant to different syndromes of cognitive impairment such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder. Further research is necessary in order to determine the efficacy and safety of nicotinic treatments of these cognitive disorders.

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Nicotine attenuates spatial learning deficits induced in the rat by perinatal lead exposure

Cited by 27 publications

References 21 publications

α7 Nicotinic acetylcholine receptors and temporal memory: Synergistic effects of combining prenatal choline and nicotine on reinforcement-induced resetting of an interval clock

α7 Nicotinic acetylcholine receptors and temporal memory: Synergistic effects of combining prenatal choline and nicotine on reinforcement-induced resetting of an interval clock

Nicotine Therapy in Adulthood Reverses the Synaptic and Behavioral Deficits Elicited by Prenatal Exposure to Phenobarbital

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

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