Montreal Children's Hospital

About: Montreal Children's Hospital is a healthcare organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Population & Poison control. The organization has 3842 authors who have published 4816 publications receiving 200198 citations.

Dietary and genetic compromise in folate availability reduces acetylcholine, cognitive performance and increases aggression: Critical role of S-adenosyl methionine

Abstract: Folate deficiency has been associated with age-related neurodegeneration. One direct consequence of folate deficiency is a decline in the major methyl donor, S-adenosyl methionine (SAM). We demonstrate herein that pro-oxidant stress and dietary folate deficiency decreased levels of acetylcholine and impaired cognitive performance to various degrees in normal adult mice (9-12 months of age, adult mice heterozygously lacking 5',10'-methylene tetrahydrofolate reductase, homozygously lacking apolipoprotein E, or expressing human ApoE2, E3 or E4, and aged (2-2.5 year old) normal mice. Dietary supplementation with SAM in the absence of folate restored acetylcholine levels and cognitive performance to respective levels observed in the presence of folate. Increased aggressive behavior was observed among some but not all genotypes when maintained on the deficient diet, and was eliminated in all cases supplementation with SAM. Folate deficiency decreased levels of choline and N-methyl nicotinamide, while dietary supplementation with SAM increased methylation of nicotinamide to generate N-methyl nicotinamide and restored choline levels within brain tissue. Since N-methyl nicotinamide inhibits choline transport out of the central nervous system, and choline is utilized as an alternative methyl donor, these latter findings suggest that SAM may maintain acetylcholine levels in part by maintaining availability of choline. These findings suggest that dietary supplementation with SAM represents a useful therapeutic approach for age-related neurodegeneration which may augment pharmacological approaches to maintain acetylcholine levels, in particular during dietary or genetic compromise in folate usage.

Resilience and vulnerability in long term outcome of attention deficit hyperactive disorder.

Abstract: Follow-up studies of children with attention deficit hyperactive disorder show that they continue to have problems with restlessness, over-activity, impulsive behaviour and inattention, often resul...

Combined autoradiographic and immunohistochemical evidence for an association of somatostatin binding sites with growth hormone-releasing factor-containing nerve cell bodies in the rat arcuate nucleus.

Abstract: The regulation of growth hormone secretion depends upon the complex interplay between two hypothalamic hypophysiotropic factors: growth hormone-releasing factor and somatotropin release inhibiting factor or somatostatin. Interactions between these two neurohormones appear to be exerted both distally, at the level of pituitary somatotropes, and proximally, within the hypothalamus. In an attempt to detect a possible anatomical substrate for central interactions between the two neurohormones, we compared the autoradiographic distribution of specifically labeled somatostatin binding sites with the immunohistochemical distribution of growth hormone-releasing factor-containing neurons in the hypothalamus of adult rats. Somatostatin binding sites were labeled in vitro by incubating serial brain sections with [(125)l]TyrO-DTrp8-somatostatin. Growth hormone-releasing factor-immunoreactive neurons were visualized in a second set of animals, using an antiserum raised against synthetic rat growth hormone-releasing factor (1-29) NH(2). In light microscopic autoradiograms of sections incubated with [(125)l]somatostatin the label was found to be concentrated over small, round or oval neuronal perikarya clustered within the ventrolateral aspect of the arcuate nucleus. The topographic distribution of these [(125)l]somatostatin-labeled cells was similar to that of growth hormone-releasing factor-immunoreactive neurons detected within the same region. Moreover, the number of [(125)l]somatostatin-labeled cells was found to vary in parallel with that of growth hormone-releasing factor-immunoreactive neurons throughout the rostro-caudal extent of the arcuate nucleus (coefficient of correlation r = 0.80). These results suggest that somatostatin binding sites may be directly associated with the perikarya of arcuate growth hormone-releasing factor neurons. Such an association would provide an anatomical substrate for a direct regulation of growth hormone-releasing factor secretion by somatostatin at the hypothalamic level.