The effects of maternal ethanol exposure on neurotransmission and second messenger systems: a quantitative autoradiographic study in the rat brain

Nio, Eiko; Kogure, Kyuya; Yae, Tetsuji; Oda, Hiroshi

doi:10.1016/0165-3806(91)90189-p

Cited by 41 publications

(22 citation statements)

References 41 publications

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“…The finding agrees with earlier observations in the murine cerebellum (Smith, 1987). No effect was found in adult rats exposed to ethanol in utero with respect to forskolin binding sites (Nio et al, 1991). Findings reported in the literature thus suggest the second messenger generating systems coupled to muscarinic receptors to be altered in rodent brain after ethanol exposure (Kuriyama and Ohkum, 1990) but further studies are needed.…”

supporting

confidence: 88%

“…In young control animals carbachol inhibited forskolin-stimulated adenylate cyclase activity but this effect was not observed in young ethanol-treated rats (Pietrzak et al, 1990 b). Nio et al (1991) recently reported a reduction in inositol phosphate (IP3) receptors in several brain regions including cerebellum of adult rats maternal ethanol exposured. The finding agrees with earlier observations in the murine cerebellum (Smith, 1987).…”

mentioning

confidence: 99%

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Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

Nordberg

Wahlström

1992

J. Neural Transmission

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The aim of this review is to summarize the effects of acute and chronic treatment with barbiturates, ethanol and benzodiazepines on cholinergic mechanisms in the brains of experimental animals. A single dose of each of these substances reduces the turnover of ACh in the brain. Long-term treatment has the opposite effect; complicated interactions including decreased content of ACh are induced. Barbiturates have been shown to bind stereospecifically to muscarinic and nicotinic receptors in the brain, but this has not been observed for ethanol or the benzodiazepines. The effects on the cholinergic system are affected by the length of treatment and choice of treatment regimen. No effect on cholinergic parameters, such as muscarinic receptors, in the brain is observed on withdrawal of ethanol or barbiturate treatment when the animals are still tolerant towards the substances. The increase in the number of muscarinic receptors observed in several brain regions on withdrawal is seen as a sign of cholinergic supersensitivity. The number of receptors returns to normal when abstinence convulsions have occurred. The assumption of a cholinergic influence is supported by the finding that atropine, given as a single dose on the day of withdrawal of barbital, can prevent the muscarinic receptor changes. Furthermore, long-term barbital or ethanol treatment can induce permanent persistent changes in the cholinergic system in the brain. Cognitive defects and a significant permanent reduction in the content of ACh can be measured in rats which have had long-term barbital treatment. Similarly, a reduced number of muscarinic receptors has been measured in different brain regions of chronic alcoholics. Accumulating data support the role of the cholinergic system in expressing symptoms of physical dependence on barbiturates, ethanol and benzodiazepines as well as in the permanent long-term effects observed after end of treatment.

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supporting

confidence: 88%

mentioning

confidence: 99%

Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

Nordberg

Wahlström

1992

J. Neural Transmission

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“…With this rodent binge alcohol model, prenatal EtOH exposure has been shown to result in a reduction in the number, size, and dendritic outgrowth of VTA dopamine neurons (Shen et al 1999;Shetty et al 1993;Szot et al 1999), as well as decreases in tyrosine hydroxylase messenger RNA (mRNA; the rate-limiting enzyme in dopamine biosynthetic pathway) and dopamine transporter mRNA (Szot et al 1999). Prenatal EtOH also produces a reduction in dopamine receptor binding sites and dopamine turnover in the striatum and cortex of both genders Lucchi et al 1983;Nio et al 1991). Finally, the EtOH metabolite, acetaldehyde enhances chronic nicotine intake via daily 3-h nose-poke sessions in adolescent, but not adult, rats (Belluzzi et al 2005).…”

Section: Discussionmentioning

confidence: 98%

Combined exposure to nicotine and ethanol throughout full gestation results in enhanced acquisition of nicotine self-administration in young adult rat offspring

Matta

Elberger

2007

Psychopharmacology

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“…Ethanol reduces the IP 3 -binding capacity without affecting the affinity for IP 3 [144] . Exposure of pregnant rats to ethanol also results in a decreased IP 3 R expression in the cerebellum and other regions of the brain of the offspring [124]. The decrease in cerebellar IP 3 R expression can be caused by a decrease in mRNA encoding IP 3 R1 [155], a decrease in translation of IP 3 R mRNA to functional protein, or an increased proteolysis of IP 3 Rs [147].…”

Section: Ethanolmentioning

confidence: 97%

Pharmacology of inositol trisphosphate receptors

Bultynck

Sienaert

Parys

et al. 2003

Pflugers Arch - Eur J Physiol

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In almost all cells, cytosolic Ca(2+) is a crucial intracellular messenger, regulating many cellular processes. In non-excitable as well as in some excitable cells, Ca(2+) release from the intracellular stores into the cytoplasm is primarily initiated by the second messenger inositol 1,4,5-trisphosphate (IP(3)), which interacts with the IP(3) receptor (IP(3)R), a tetrameric intracellular Ca(2+)-release channel. This review focuses on the pharmacological modulation of the various functionally important sub-domains of the IP(3)R, including the IP(3)-binding domain, calmodulin-binding sites, adenine nucleotide-binding sites and the sites for interaction for FK506-binding proteins and other regulators. We will particularly focus on the pharmacological tools that interfere with these domains and discuss their relative specificity for the IP(3)R, thereby indicating their potential usefulness for unraveling the complex functional regulation of the IP(3)R.

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The effects of maternal ethanol exposure on neurotransmission and second messenger systems: a quantitative autoradiographic study in the rat brain

Cited by 41 publications

References 41 publications

Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

Combined exposure to nicotine and ethanol throughout full gestation results in enhanced acquisition of nicotine self-administration in young adult rat offspring

Pharmacology of inositol trisphosphate receptors

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