Quantitative pharmacohistochemistry of acetylcholinesterase in neostriatum of inbred strains of mice

Iacopino, Carmela; Altavista, Maria Concetta; Gozzo, Stefano; Albanese, Alberto

doi:10.1016/0006-8993(86)90439-7

Cited by 11 publications

(4 citation statements)

References 20 publications

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“…For instance, compared to C57 mice, DBA mice have increased striatal acetylcholine esterase density and activity (Iacopino et al, 1986). This difference in enzymatic activity may result in greater acetylcholine levels during burst stimulations in C57 mice, and thus increase C57 mouse susceptibility to nAChR desensitization (Giniatullin et al, 2005; Threlfell et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Because the inhibitory effects of ethanol and nAChR-modulation of dopamine release are both frequency-dependent, we examined nAChR involvement in the dopamine-decreasing effects of ethanol. C57 and DBA mice express a number of differences in cholinergic systems, including enzymatic activity and nAChR sensitivity to ethanol (Iacopino et al, 1986; Butt et al, 2003; Symons et al, 2010). Therefore, in an attempt to investigate potential mechanisms of ethanol’s effects on dopamine release in the two mouse strains, we investigated whether nAChR blockade would reduce ethanol-mediated inhibition of dopamine release under high frequency conditions.…”

Section: Introductionmentioning

confidence: 99%

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Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

et al. 2015

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The mesolimbic dopamine system, originating in the ventral tegmental area (VTA) and projecting to the nucleus accumbens (NAc), has been heavily implicated in the reinforcing effects of ethanol. Recent slice voltammetry studies have shown that ethanol inhibits dopamine release selectively during highfrequency activity that elicits phasic dopamine release shown to be important for learning and reinforcement. Presently, we examined ethanol inhibition of electrically evoked NAc dopamine in two mouse strains with divergent dopamine responses to ethanol, C57BL/6 (C57) and DBA/2J (DBA) mice. Previous electrophysiology and microdialysis studies have demonstrated greater ethanol induced VTA dopaminergic firing and NAc dopamine elevations in DBA compared to C57 mice. Additionally, DBA mice have greater ethanol responses in dopamine-related behaviors, including hyperlocomotion and conditioned place preference. Currently, we demonstrate greater sensitivity of ethanol inhibition of NAc dopamine signaling in C57 compared to DBA mice. The reduced sensitivity to ethanol inhibition in DBA mice may contribute to the overall greater ethanol-induced dopamine signaling and related behaviors observed in this strain. NAc cholinergic activity is known to potently modulate terminal dopamine release. Additionally, ethanol is known to interact with multiple aspects of nicotinic acetylcholine receptor activity. Therefore, we examined ethanol-mediated inhibition of dopamine release at two ethanol concentrations (80 and 160mM) during bath application of the non-selective nicotinic receptor antagonist mecamylamine, as well as compounds selective for the β2- (DhβE) and α6- (α-conotoxin MII [H9A; L15A]) subunit-containing receptors. Mecamylamine and DhβE decreased dopamine release and reduced ethanol's inhibitory effects on dopamine in both DBA and C57 mice. Further, α-conotoxin also reduced the dopamine release and the dopamine-inhibiting effects of ethanol at the 80mM, but not 160mM, concentration. These data suggest that ethanol is acting in part through nicotinic acetylcholine receptors, or downstream effectors, to reduce dopamine release during high-frequency activity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

et al. 2015

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“…The gene coding for the a 2 subunit is in a region on proximal chromosome 14 with markers associated with a cluster of METH-related phenotypes (discussed below). There is also substantial biochemical and histochemical evidence suggesting that B6 and D2 mice differ with respect to cholinergic activity (Ebel et al, 1973;Durkin et al, 1977) and cell density (Albanese et al, 1985;Iacopino et al, 1986;Schwab et al, 1990). Furthermore, the genetic variability in cholinergic cell number in the striatum was shown by Dains (1995) to be correlated with neuroleptic-induced catalepsy in the mouse, suggesting an interaction between acetylcholine and dopamine in the production of striatally mediated motor behavior.…”

Section: Candidate Neurotransmitter Modulationmentioning

confidence: 99%

Quantitative Trait Loci Affecting Methamphetamine Responses in BXD Recombinant Inbred Mouse Strains

et al. 1997

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Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.

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“…The pharmacohistochemical treatment of Butcher and Bilezikjian [12] was used for the demonstration of AChE activity in neu ronal cell bodies [6]. The animals received an injection of diisopropylfluorophosphate (DFP, 3.5 mg/kg i.m., dissolved in peanut oil).…”

Section: Ache Histochemistrymentioning

confidence: 99%

Regional Cholinergic Differences in the Brain of DBA/2 and C57BL/6 Mice: A Morphological Study during Ontogeny

Schwab

Brückner

Castellano

et al. 1990

Dement Geriatr Cogn Disord

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C57BL/6 and DBA/2 mice present a number of behavioral and neurobiological differences and react in opposite ways to cholinergic drugs. A morphological study during ontogony of brain cholinergic organization of these strains was therefore performed by using acetylcholinesterase pharmacohistochemistry and choline acetyltransferase immunohistochemistry. Cross-sectional areas and rostrocaudal measures of selected brain regions were analyzed. C57 mice were characterized by a lower cholinergic density. This deficit was most pronounced in the striatum, the nucleus basalis of Meynert and the nucleus of the diagonal band of Broca. The observed strain differences were shown to be age-related by using mice aged 20–110 postnatal days. The differentially expressed cholinergic deficit in C57 mice may lead to an approach of the degenerative patterns of cholinergic systems in humans.

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Quantitative pharmacohistochemistry of acetylcholinesterase in neostriatum of inbred strains of mice

Cited by 11 publications

References 20 publications

Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

Quantitative Trait Loci Affecting Methamphetamine Responses in BXD Recombinant Inbred Mouse Strains

Regional Cholinergic Differences in the Brain of DBA/2 and C57BL/6 Mice: A Morphological Study during Ontogeny

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