Opioids and behavior: genetic aspects

Frischknecht, Hans-Rudolf; Siegfried, Bert; Waser, Peter G.

doi:10.1007/bf01958921

Cited by 66 publications

(10 citation statements)

References 92 publications

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“…Although the inbred strains were chosen for study because of their differences in hippocampal a-bungarotoxin binding, there are many other differences between the strains. In particular, OBA mice, the most deviant strain on both the sensory gating measures and a-bungarotoxin binding, exhibit decreased catecholamine turnover (Kempf et al 1974), increased numbers of forebrain cholinergic neurons (Albanese et al 1985), increased acetylcholinesterase activity (Mandel et al 1974), increased response to opiates (Frischknecht et al 1988), and decreased protein kinase activity (Wehner et al 1990). Given the current understanding of the neurobiology of the hippocampus, none of these differences are likely to account for the differences in auditory response observed in this study.…”

Section: Discussionmentioning

confidence: 99%

Genetic Correlation of Inhibitory Gating of Hippocampal Auditory Evoked Response and α-Bungarotoxin-Binding Nicotinic Cholinergic Receptors in Inbred Mouse Strains

Stevens

Freedman

Collins

et al. 1996

Neuropsychopharmacology

202

190

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One function of the hippocampus is to ascertain the novelty of incoming sensations and encode significant new information into memory. The regulation of response to repeated stimuli may prevent overloading of this function by redundant sensory input. Recent pharmacological studies implicate the role of alpha-bungarotoxin-sensitive nicotinic cholinergic receptors in the inhibition of hippocampal response to repeated auditory stimuli. The number of hippocampal alpha-bungarotoxin-sensitive receptors has a major genetic determinant, as demonstrated by a significant variance between different inbred mouse strains. The purpose of the present study was to determine whether there was a related genetic correlation for the gating of auditory response. Nine inbred mouse strains, representing a continuum of hippocampal alpha-bungarotoxin binding, were tested for the electrophysiological response to repeated auditory stimulation, followed by whole hippocampus membrane alpha-bungarotoxin binding studies. Several parameters of the auditory evoked response showed significant genetic variance over the nine strains, and a significant correlation was found between hippocampal alpha-bungarotoxin binding and both the amplitude of the initial evoked response and its inhibition to repeated auditory stimuli. There was no correlation of the auditory evoked response with high-affinity nicotine binding. These data further support the hypothesis that alpha-bungarotoxin-sensitive nicotinic receptors are involved in the regulation of hippocampal response to repeated auditory stimuli and suggest that this function is genetically controlled.

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Section: Discussionmentioning

confidence: 99%

Genetic Correlation of Inhibitory Gating of Hippocampal Auditory Evoked Response and α-Bungarotoxin-Binding Nicotinic Cholinergic Receptors in Inbred Mouse Strains

Stevens

Freedman

Collins

et al. 1996

Neuropsychopharmacology

202

190

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“…Previous studies in mice have demonstrated that genetic factors significantly influence the ability of opioids to induce behavioral modifications (Eidelberg et al, 1975;Brase et al, 1977;Frishknecht et al, 1988;Shuster, 1989;Belknap and O'Toole, 1991;Crabbe et al, 1994;Mogil et al, 1996) and that mice of various inbred or outbred strains may differ in sensitivity to behavioral effects of morphine Shuster et al, 1975;Brase et al, 1977;Horowitz et al, 1977). In this regard, over the last two decades DBA/2J and C57BL/6J have been the most studied.…”

Section: Introductionmentioning

confidence: 99%

Dopamine and serotonin release in dorsal striatum and nucleus accumbens is differentially modulated by morphine in DBA/2J and C57BL/6J mice

Fadda

Scherma

Fresu

et al. 2005

Synapse

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Numerous studies have demonstrated that genetic factors significantly influence opioid ability to induce behavioral modification in mice. This differential sensitivity has been extensively studied, particularly in the DBA/2J and C57BL/6J strains. In the present study, using the "in vivo" microdialysis technique in these strains, we investigated the effect of morphine administration on the extracellular levels of dopamine (DA), serotonin (5-HT), and their metabolites in the nucleus accumbens and dorsal striatum--areas thought to be involved in morphine-induced locomotor hyperactivity. In the nucleus accumbens, morphine (20 mg/kg) significantly increased extracellular levels of DA in both strains. However, in dorsal striatum the morphine-induced increase of extracellular DA was lower in DBA/2J mice than in C57BL/6J. Moreover, morphine significantly stimulated 5-HT and 5-hydroxyindolacetic acid (5-HIAA) release both in nucleus accumbens and dorsal striatum of C57BL/6J mice, whereas it decreased 5-HT release without modifying 5-HIAA levels in DBA/2J mice. These results suggest that the different behavioral and biochemical responses to acute morphine described in these two strains could be mediated by different sensitivity of both the dopaminergic and the serotonergic systems.

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“…However, these mostly represent individual 'one-off' studies with little attempt being made to follow up the genetic basis or even the biochemical significance of such observations. Many of the studies relating to opioids and opioid receptors have been reviewed by Frischknecht et al 37, and it is clear that a large proportion of papers involve a simple comparison of two strains (frequently C57BL/6 and DBA/2) which differ in behaviour, with an attempt to relate this to a biochemical difference. This can often be misleading (see below).…”

Section: Genetic Variation In Neurotoxicitymentioning

confidence: 99%

Genetic factors in neurotoxicology and neuropharmacology: A critical evaluation of the use of genetics as a research tool

Festing

1991

Experientia

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Animals have evolved a detoxication system to enable them to survive in a hostile chemical environment in which foods contain many non-nutrient chemicals. Detoxication depends on enzymes which are often genetically polymorphic. As a result, inter-individual variation is common, and in humans several Mendelian loci have been identified. However, most variation in response is probably due to the action of several genes. Genetic variation in response to the neurotoxin MPTP and to chemically and physically-induced seizures is reviewed. In the former case, differences between pigmented and white mouse strains have been noted which are consistent with the hypothesis that humans are more sensitive than mice or rats because of the presence of melanin in human brains. However, variation in sensitivity probably also depends on other genes. In the case of audiogenic seizures, a single locus has been identified and mapped, but its relationship with seizures induced by other agents is not clear. Genetic variation in response to alcohol is also discussed. The failure of most toxicologists to consider genetic variation as a potentially confounding variable, and as a powerful research tool, is discussed critically in relation to non-repeatability of research on the neurotoxic effects of lead, and in relation to the genetic variation in MPTP, seizures, and alcohol response already noted. It seems clear that genetic methods provide a powerful research tool which is largely being ignored by toxicologists.

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Opioids and behavior: genetic aspects

Cited by 66 publications

References 92 publications

Genetic Correlation of Inhibitory Gating of Hippocampal Auditory Evoked Response and α-Bungarotoxin-Binding Nicotinic Cholinergic Receptors in Inbred Mouse Strains

Genetic Correlation of Inhibitory Gating of Hippocampal Auditory Evoked Response and α-Bungarotoxin-Binding Nicotinic Cholinergic Receptors in Inbred Mouse Strains

Dopamine and serotonin release in dorsal striatum and nucleus accumbens is differentially modulated by morphine in DBA/2J and C57BL/6J mice

Genetic factors in neurotoxicology and neuropharmacology: A critical evaluation of the use of genetics as a research tool

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