Biomedical subjects

Daniel N Weber

Publications and source records attributed to Daniel N Weber.

3 recordsLinked to original sources

PubMed2005

Waterborne lead exposure affects brain endocannabinoid content in male but not female fathead minnows (Pimephales promelas).

There are several similarities between the behavioral and neurochemical effects of lead (Pb2+) and the cannabinoids. Both Pb2+ exposure and cannabinoid treatment decrease exploratory behavior. Pb2+-induced hyperactivity has been observed in rats and fish. By comparison, cannabinoids increase locomotor activity at higher doses in rats. Moreover, Pb2+ exposure produces learning and memory impairments as do the cannabinoids. Many of the behavioral effects of Pb2+ are thought to be due, in part, to the ability of Pb2+ to either inhibit or mimic the actions of calcium (Ca2+). At low concentrations, Pb2+ enhances basal release of neurotransmitter from presynaptic terminals by increasing intracellular free Ca2+ concentrations. Pb2+ also decreases evoked neurotransmitter release due to blockade of voltage-gated Ca2+ channels. Interestingly, the endocannabinoids (eCBs) including N-arachidonylethanolamine (AEA) and 2-arachidonylglycerol (2-AG) are synthesized in response to increases in intracellular Ca2+ and activate the CB1 receptor that inhibits voltage-gated Ca2+ channels. We tested the hypothesis that waterborne Pb2+ exposure significantly affects whole-brain eCB content in adult male and female fathead minnows (Pimephales promelas). Waterborne Pb2+ exposure (1.0 ppm) resulted in a time-dependent accumulation of Pb2+ in bone in both males and females. Brain AEA and 2-AG content were significantly greater in females compared to males. Pb2+ exposure increased brain AEA content in males at 7 and 14 days of exposure and increased brain 2-AG content at 14 days. Pb2+ exposure had no effect on either brain AEA or 2-AG content in females at any of the time points examined. As eCBs serve as activity-dependent retrograde inhibitors of neurotransmitter release, the increase in brain eCB content would accentuate Pb2+-induced decreases in evoked neurotransmitter release in male but not female fathead minnows.

Animals↗

PubMed2003

Effects of dietary lead and/or dimercaptosuccinic acid exposure on regional serotonin and serotonin metabolite content in rainbow trout (Oncorhynchus mykiss).

The lead (Pb) chelator, meso-2,3-dimercaptosuccinic acid (DMSA) may be effective in reversing some of the adverse effects of Pb exposure. Pb-induced behavioral deficits observed in fish are due to disruptions in the integrative functioning of the medulla, cerebellum, and optic tectum. Pb exposure increased serotonin (5-HT) content in all three brain regions without an effect on 5-hydroxy-3-indoleacetic acid (5-HIAA). Pb exposure followed by no Pb in the diet increased 5-HT and 5-HIAA content in all three brain regions. The replacement of dietary Pb with DMSA had no effect on 5-HT and increased 5-HIAA content. DMSA increased 5-HIAA content in all three brain regions and increased 5-HT content only the optic tectum. Treatment with DMSA may be more effective than removal of Pb from the diet in reversing Pb-induced alterations in 5-HT.

Animals↗

PubMedDate not supplied

Ethanol effects on the developing zebrafish: neurobehavior and skeletal morphogenesis.

Exposure to ethanol during development can lead to a constellation of congenital anomalies, resulting in prenatal and postnatal failure to thrive, central nervous system (CNS) deficits, and a number of patterning defects that lead to defects in the cardiovascular system, facial structures, and limbs. The cellular, biochemical, and molecular mechanisms by which ethanol exerts its developmental toxicity and the genes that influence sensitivity to developmental ethanol exposure have yet to be discovered, despite being one of the more common nongenetic causes of birth defects. The zebrafish undergoes much the same patterning and morphogenesis as other vertebrate embryos do--including humans--that are distinct and cannot be studied in invertebrates. Developmental processes in zebrafish are affected by ethanol exposure in a dose-dependent manner, resulting in learning and memory deficits, cell death in the CNS, skeletal dysmorphogenesis, and alterations in startle reflex responses. Interestingly, significant ethanol effects on learning and behavioral endpoints occurred at concentrations well below those that induced cell death in the CNS. This work provides the foundation for identifying genes and pathways involved in developmental alcohol toxicity in vertebrates, leading to a more complete mechanistic understanding of fetal alcohol disorders in humans.

Alcohol-Induced Disorders, Nervous System↗