Neural-cell adhesion molecules (N-CAMs) are members of the immunoglobulin superfamily mediating homo- and heterophilic cell-cell interactions. N-CAM exists in various isoforms which are generated by alternative splicing. During embryonic development, N-CAMs are expressed in derivatives of all three germ layers, whereas in the adult animal they are predominantly present in neural tissue. Processes like neurulation, axonal outgrowth, histogenesis of the retina and development of the olfactory system are correlated with the regulated expression of N-CAMs. We show here that N-CAM-deficient mice generated by gene targeting appear healthy and fertile, but adult mutants show a 10% reduction in overall brain weight and a 36% decline in size of the olfactory bulb. N-CAM deficiency coincides with almost total loss of protein-bound alpha-(2,8)-linked polysialic acid, a carbohydrate structure thought to be correlated with neural development and plasticity. The animals showed deficits in spatial learning when tested in the Morris water maze, whereas activity and motor abilities appeared normal.

Inactivation of the N-CAM gene in mice results in size reduction of the olfactory bulb and deficits in spatial learning.

Brain plasticity refers to the brainis ability to change structure and function Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity These anatomical changes are correlated with behavioral differences between subjects with and without the changes Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning

/pdf/brain-plasticity-and-behavior-eh85uqto8k.pdf

Brain plasticity and behavior

/pdf/growth-hormone-deficiency-in-adulthood-and-the-effects-of-2rhyqdqxkb.pdf

Growth Hormone Deficiency in Adulthood and the Effects of Growth Hormone Replacement: A Review

Brain plasticity refers to the brain's ability to change structure and function. Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans. It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity. These anatomical changes are correlated with behavioral differences between subjects with and without the changes. Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology. We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning.

/pdf/brain-plasticity-and-behavior-3512cjh0ly.pdf

Brain plasticity and behavior.

The classical observations of the skin as a target for melanotropins have been complemented by the discovery of their actual production at the local level. In fact, all of the elements controlling the activity of the hypothalamus-pituitary-adrenal axis are expressed in the skin including CRH, urocortin, and POMC, with its products ACTH, α-MSH, and β-endorphin. Demonstration of the corresponding receptors in the same cells suggests para- or autocrine mechanisms of action. These findings, together with the demonstration of cutaneous production of numerous other hormones including vitamin D3, PTH-related protein (PTHrP), catecholamines, and acetylcholine that share regulation by environmental stressors such as UV light, underlie a role for these agents in the skin response to stress. The endocrine mediators with their receptors are organized into dermal and epidermal units that allow precise control of their activity in a field-restricted manner. The skin neuroendocrine system communicates with itself and wi...

Neuroendocrinology of the skin.

Acromegaly is characterized by coarsening of facial features, acanthosis nigricans, hypertrichosis and oily skin. To determine the site through which GH exerts these effects, we have used immunohistochemistry to localize the GH receptor/binding protein (BP) in rat, rabbit and human skin. Three monoclonal antibodies (MAb 1, 43, 263) were immunoreactive in identical locations, whereas no immunoreactivity was evident when control monoclonal antibodies (MAb 50.8 and MAb 7 (rat] were used. Skin from neonatal and adult animals was used to determine whether GH receptor/BP expression was developmentally regulated. Immunoreactivity of the GH receptor/BP in the three species was consistently localized in the stratum basale and stratum spinosum. Intermittent staining was observed in the stratum granulosum. Scattered basal epidermal cells often displayed more intense immunoreactivity. This distribution was observed at all maturational stages examined. Intense GH receptor/BP immunoreactivity was observed in all histological layers of the lower one-third of hair follicles and in hair matrix cells of the dermal papillae. Immunoreactivity was also detected in the outer epithelial root sheath of the upper two-thirds of hair follicles, in sebaceous glands and in fibroblasts of the connective tissue sheath surrounding the follicle. GH receptor/BP immunoreactivity was also present in the secretory duct and myoepithelial cells of human eccrine sweat glands. Fibroblasts, Schwann cells of peripheral nerve fascicles, skeletal muscle cells and adipocytes of the dermis were also immunoreactive as were medial smooth muscle and endothelial cells of arteries. These results provide evidence that GH acts locally on the epidermis and epidermal appendages concordant with our recent localization of GH receptor/BP to epithelial cell types of the gastrointestinal and reproductive systems.

Localization of the Growth-Hormone Receptor-Binding Protein in Skin

It is generally accepted that the olfactory system is unique among the senses since the olfactory receptor cells, which are primary neurons, are thought to have a limited life span. Implicit in the current literature is the notion that these receptor cells are born, live and die by some “inherent clock” which, in mammals, lead to neuronal death after about 30 days (Moulton 1974; Graziadei and Monti Graziadei 1979). The turnover of receptor cells and their “programmed” replacement from a basally located progenitor cell compartment is thought to continue throughout the life of an animal and at a constant rate. This concept has gradually developed since Nagahara (1940) first reported the appearance of mitotic activity in the olfactory epithelium proprium of adult mice. Mitosis of basally located progenitor cells and repair of experimentally destroyed sensory cells was subsequently confirmed in a variety of other species (Lams 1940; Schultz 1941, 1960; Smith 1951; Bimes and Planel 1952; Westerman and von Baumgarten 1964; Andres 1965; Thornhill 1970; Craziadei and Metcalf 1971; Craziadei and Dehan 1973; Moulton 1974; Graziadei 1973; Breipohl and Ohyama 1981; Simmons et al. 1981; Matulionis 1982). Recent investigations on cell proliferation, cell death and repair by Hinds et al. (1984), Balboni and Vannelli (1982), Matulionis (1982) and our own group (Breipohl 1982b; Breipohl et al. 1985 a,b; 1986) lead to some doubt about a constant turnover of olfactory receptor cells throughout life.

Neurogenesis in the Vertebrate Main Olfactory Epithelium

Ontogeny of olfaction

Growth hormone receptors expression in the proliferating rat mammary gland.

Changes in granule cells of the ferret olfactory bulb associated with imprinting on prey odours.

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