Peripheral Markers of Serotonergic and Noradrenergic Function in Post-Pubertal, Caucasian Males with Autistic Disorder

Croonenberghs, Jan; Delmeire, Laure; Verkerk, Robert; Lin, Aihua; Meskal, Anisa; Neels, Hugo; Planken, Marc van der; Deboutte, Dirk; Pison, Greet; Maes, Michaël

doi:10.1016/s0893-133x(99)00131-1

Cited by 64 publications

(37 citation statements)

References 59 publications

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“…None of the endogenous transmitters acetylcholine, noradrenaline, DA, serotonin, glycine and histamine were detected by the antibodies generated from the IP18-KLH immunization. Not even at the highest concentration of competitor (10 m M ), which exceeds the physiological levels 10 4 - to 10 7 -fold [35, 36, 37], were the transmitters recognized by the IP18-KLH-generated antibodies.…”

Section: Discussionmentioning

confidence: 99%

Active Immunization against Nicotine Suppresses Nicotine-Induced Dopamine Release in the Rat Nucleus accumbens Shell

Villiers

Lindblom²,

Kalayanov³

et al. 2002

Respiration

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Background: Tobacco smoking is the largest preventable cause of morbidity and premature mortality in the world. Although its medical consequences are well documented, 20–50% of the population even in developed countries remain tobacco smokers. The drugs presently used in smoking cessation have limited efficiency and, therefore, there is a need for alternative and improved treatments. One novel approach in this regard may be provided by immunization against nicotine. Objective: The present study in male Wistar rats investigated if active immunization with a novel nicotine immunogen, IP18-KLH, may generate nicotine-selective antibodies and, furthermore, whether this treatment might prevent nicotine from exerting its stimulating effect on the mesolimbic, dopaminergic reward system in the brain. Methods: Enzyme-linked immunosorbent assay (ELISA) was used to determine the titer of nicotine antibodies in plasma after immunization with IP18-KLH in Freund’s adjuvant. Competitive ELISA was used to assess the selectivity of the antibodies. Finally, we used in vivo voltammetry to investigate whether active immunization with IP18-KLH could prevent nicotine-induced dopamine release in the shell of nucleus accumbens (NAC_shell). Results: The present study shows that active immunization with IP18-KLH generates antibodies that are highly selective for nicotine. Furthermore, immunization with IP18-KLH prevented the nicotine-induced increase in dopamine release in the NAC_shell, a biochemical correlate to the rewarding properties of nicotine. Conclusions: Active immunization with IP18-KLH prevents a central effect of nicotine that is considered critical for the induction of nicotine dependence. Consequently, active immunization may provide long-term protection against initiation of tobacco dependence, an effect that may prove particularly advantageous in relapse prevention.

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Section: Discussionmentioning

confidence: 99%

Active Immunization against Nicotine Suppresses Nicotine-Induced Dopamine Release in the Rat Nucleus accumbens Shell

Villiers

Lindblom²,

Kalayanov³

et al. 2002

Respiration

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“…20 Interesingly, plasma concentrations of tryptophan are significantly decreased in autistics, compared to unaffected controls. 7,21 More research into the relationship between tryptophan and free 5-HT plasma levels, platelet 5-HT content, and specific markers of immune function will be required to address this issue.…”

mentioning

confidence: 99%

Serotonin transporter gene promoter variants do not explain the hyperserotoninemia in autistic children

et al. 2002

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Autism is a biologically-heterogeneous disease. Distinct subgroups of autistic patients may be marked by intermediate phenotypes, such as elevated serotonin (5-HT) blood levels, potentially associated with different underlying disease mechanisms. This could lead to inconsistent genetic association results, such as those of prior studies on serotonin transporter (5-HTT) gene promoter variants and autistic disorder. Contributions of 5-HTT gene promoter alleles to 5-HT blood levels were thus investigated in 134 autistic patients and 291 first-degree relatives. Mean 5-HT blood levels are 11% higher in autistic patients carrying the L/L genotype, compared to patients with the S/S or S/L genotype; this trend is not observed in first-degree relatives. The probability of inheriting L or S alleles is significantly enhanced in patients with 5-HT blood levels above or below the mean, respectively (P Ͻ 0.05), but quantitative TDT analyses yield a non-significant trend (P = 0.10), as this polymorphism explains only 2.5% of the variance in 5-HT blood levels of autistic patients. In conclusion, 5-HTT gene promoter variants seemingly exert a small effect on 5-HT blood levels in autistic children, which largely does not account for hyperserotoninemia. Nonetheless, the inconsistent outcome of prior association studies could partly stem from a selection bias of hyper-or hypo-serotoninemic probands.

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“…A range of neurochemical studies have attempted to examine excretion of urinary NA and / or adrenaline (A) in individuals with autism compared with controls and have yielded inconsistent findings. Three studies found higher levels of NA and/or A in autism compared to controls Herault et al 1993;Martineau et al 1994), while four studies found no differences (Launay et al 1987;Martineau et al 1992;Minderaa et al 1994;Croonenberghs et al 2000). Therefore as outlined in Table 2, the range of neurotransmitter abnormalities that have been shown to occur in autism provide a rationale for the use of CAM products that are claim to normalise neurotransmitter levels and function such as: high dose pyridoxine and magnesium, metabolites and co-factors of the transmethylation and trans-sulphuration cycles (see Figure 1), vitamin C, zinc and secretin.…”

Section: Noradrenalinementioning

confidence: 94%

“…Many studies (Young et al 1978;Garnier et al 1986;Launay et al 1987;Minderaa et al 1987;Barthelemy et al 1988;Garreau et al 1988;Barthelemy et al 1989;Minderaa et al 1989;Martineau et al 1991;Martineau et al 1992;Herault et al 1993;Martineau et al 1994;Minderaa et al 1994;Herault et al 1996;Croonenberghs et al 2000;Mulder et al 2009) have focused on neurotransmitter abnormalities in individuals with autism. Abnormalities in various neurotransmitters have been implicated in the development of autism, including serotonin (5-hydroxytryptamine, 5-HT), dopamine (DA), noradrenaline (NA), gamma-aminobutryic acid, glutamate and neuropeptides.…”

Section: Normalise Neurotransmitters and Neurotransmitter Metabolitesmentioning

confidence: 99%

Complementary Medicine Products Used in Autism - Evidence for Rationale

Semple¹,

Hewton²,

Paterson³

et al. 2011

Autism Spectrum Disorders - From Genes to Environment

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Peripheral Markers of Serotonergic and Noradrenergic Function in Post-Pubertal, Caucasian Males with Autistic Disorder

Cited by 64 publications

References 59 publications

Active Immunization against Nicotine Suppresses Nicotine-Induced Dopamine Release in the Rat Nucleus accumbens Shell

Active Immunization against Nicotine Suppresses Nicotine-Induced Dopamine Release in the Rat Nucleus accumbens Shell

Serotonin transporter gene promoter variants do not explain the hyperserotoninemia in autistic children

Complementary Medicine Products Used in Autism - Evidence for Rationale

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