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Regional alterations of brain biogenic amines and GABA/glutamate levels in rats following chronic lead exposure during neonatal development.

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TLDR
The differences observed in the neurotoxic effects of lead in the different regions for each of the transmitters (NA, DA, 5HT) supports the interesting conclusion that the vulnerability of the axon terminals of any given type is dependent on some regional factors, although the projections of the different areas originate from an apparently similar category of neurons in the brain stem.
Abstract
Wistar rat pups were administered either a high dose of lead acetate (400 μg lead/g body weight/day) or a low dose (100 μg lead/g body weight/day) by gastric intubation, from 2 days through 60 days of age. The rats on both these doses exhibited statistically significant decreases in body and brain weights throughout the lead treatment period. A group of rats on high dose was also rehabilitated by discontinuing the lead from 60 days of age. In these rats, at 160 days of age, the body weight but not the brain weight recovered to normal levels. During the lead intake, the rats on high dose revealed significant elevations in the levels of noradrenaline (NA) in the hippocampus (HI), cerebellum (CE), hypothalamus (HY), brainstem (BS), and accumbens-striatum (SA). The elevated levels in all the above regions except in the HY persisted even after rehabilitation. The dopamine (DA) levels changed significantly in opposite directions in HY (elevation) and BS (reduction) during the lead treatment, and the HY recovered after rehabilitation. Under lead, the serotonin (5HT) levels were elevated significantly in the HI, BS and MC (motor cortex), while after rehabilitation the abnormality persisted only in the MC. Low dose lead treatment was also effective on the same areas of brain. In the low dose group, estimation of the levels of GABA and glutamate were also done, and a significant decrease of GABA in CE and glutamate in MC was observed. The differences observed in the neurotoxic effects (none or significant) of lead in the different regions for each of the transmitters (NA, DA, 5HT) supports the interesting conclusion that the vulnerability of the axon terminals of any given type is dependent on some regional factors, although the projections of the different regions originate from an apparently similar category of neurons in the brain stem.

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Dopaminergic and serotoninergic deficiencies in young adult rats prenatally exposed to the bacterial lipopolysaccharide.

TL;DR: Prenatal LPS exposure as a model of PD since DA and 5-HT changes similar to those seen in PD patients are validated and also suggest that prenatal LPS might be a risk factor for other diseases including mood disorders.
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Regional Alterations in the Levels of Brain Biogenic Amines, Glutamate, GABA, and GAD Activity Due to Chronic Consumption of Inorganic Arsenic in Developing and Adult Rats

TL;DR: This study aimed to assess changes in glutamic acid decarboxylase (GAD) activity and in levels of glutamate and gamma-aminobutyric acid(GABA) as these amino acids are not only involved in carbohydrate metabolism but also in neurotransmitter pools.
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Developmental lead exposure in rats: is a behavioral sequel extended at F2 generation?

TL;DR: It appears that developmental lead exposure may cause behavioral effects during the developmental stage of the F1 generation, which remains throughout the animal's adult life as a sequel, regardless of lead accumulation, and is extended to the F2 generation of rats.
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Neurochemical and Neurobehavioral Effects of Low Lead Exposure on the Developing Brain

TL;DR: Low blood levels of lead cannot be considered “safe” or “acceptable” as it causes neurotransmitter alterations in the developing brain which may cause neurobehavioral defects like hyperactivity and other cognitive disorders.
Journal ArticleDOI

Mercuric chloride-induced alterations of levels of noradrenaline, dopamine, serotonin and acetylcholine esterase activity in different regions of rat brain during postnatal development

TL;DR: The changes occurring in the brain at this level of oral mercuric chloride intake seem to reflect adaptive neural mechanisms rather than pathological damage.
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TL;DR: It is revealed that norepinephrine and dopamine are specifically localized in complex systems of neurons in the brain, a finding which lends support to the hypothesis that both amines may be neurotransmitters in the central nervous system.
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TL;DR: Brain, NE, DA, and 5-HT can be assayed simultaneously from discrete samples by this method, which is based upon the alumina method described by Anton and Sayre, utilizing acid extraction of tissues and a single solvent step.
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Drug and neurotransmitter receptors in the brain

TL;DR: Biochemical investigation of receptors for neurotransmitters and drugs in the brain has been one of the most active areas of molecular neuroscience during the past decade and provided useful probes for drug discovery programs.
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