Zinc is an essential catalytic or structural element of many proteins, and a signaling messenger that is released by neural activity at many central excitatory synapses. Growing evidence suggests that zinc may also be a key mediator and modulator of the neuronal death associated with transient global ischemia and sustained seizures, as well as perhaps other neurological disease states. Manipulations aimed at reducing extracellular zinc accumulation, or cellular vulnerability to toxic zinc exposure, may provide a novel therapeutic approach toward ameliorating pathological neuronal death in these settings.

Zinc and brain injury

11 . Pertinent experimental data . . . . . . . . . . . . 157 (I) Regeneration in the peripheral nervous system . . . . . . . . 158 (2) Axonal regeneration in the C.N.S. . . . . . . . . . . 158 (a) Wounds of the brain and spinal cord . . . . . . . . . 158 . I59 (3) Neurosecretory axons . . . . . . . . . . . . 160 (4) Monoaminergic fibres . . . . . . . . . . . . 161 ( 5 ) Regeneration through spinal roots . . . . . . . . . . 161 (6) Primary olfactory neurones . . . . . . . . . . . 161 (7) Regeneration of axons into non-neural tissues transplanted into the brain . . . 162 (a) Skin . . . . . . . . . . . . . . . 162 (b) Striated muscle . . . . . . . . . . . . . 162 (c) Smoothmuscle . . . . . . . . . . . . . 162 (d) Other tissues . . . . . . . . . . . . . 163

Hypotheses concerned with axonal regeneration in the mammalian nervous system

The capacity of the olfactory epithelium (OE) for lifelong neurogenesis and regeneration depends on the persistence of neurocompetent stem cells, which self-renew as well as generating all of the cell types found within the nasal epithelium. This Review focuses on the types of stem and progenitor cells in the epithelium and their regulation. Both horizontal basal cells (HBCs) and some among the population of globose basal cells (GBCs) are stem cells, but the two types plays vastly different roles. The GBC population includes the basal cells that proliferate in the uninjured OE and is heterogeneous with respect to transcription factor expression. From upstream in the hierarchy to downstream, GBCs encompass 1) Sox2+ /Pax6+ stem-like cells that are totipotent and self-renew over the long term, 2) Ascl1+ transit-amplifying progenitors with a limited capacity for expansive proliferation, and 3) Neurog1+ /NeuroD1+ immediate precursor cells that make neurons directly. In contrast, the normally quiescent HBCs are activated to multipotency and proliferate when sustentacular cells are killed, but not when only OSNs die, indicating that HBCs are reserve stem cells that respond to severe epithelial injury. The master regulator of HBC activation is the ΔN isoform of the transcription factor p63; eliminating ΔNp63 unleashes HBC multipotency. Notch signaling, via Jagged1 ligand on Sus cells and Notch1 and Notch2 receptors on HBCs, is likely to play a major role in setting the level of p63 expression. Thus, ΔNp63 becomes a potential therapeutic target for reversing the neurogenic exhaustion characteristic of the aged OE. J. Comp. Neurol. 525:1034-1054, 2017. © 2016 Wiley Periodicals, Inc.

/pdf/stem-and-progenitor-cells-of-the-mammalian-olfactory-4ghlhenrno.pdf

Stem and progenitor cells of the mammalian olfactory epithelium: Taking poietic license.

Publisher Summary This chapter reviews the usefulness of the bulbectomy model and gives a detailed account of the neuroanatomical and behavioral effects of bilateral bulbectomy, followed by a synopsis of the neurochemical changes that are associated with the bulbectomy. The usefulness of the model to the neuropharmacologist is evaluated. The olfactory bulbectomy (OBY) syndrome is especially sensitive to the antidepressant drugs. The effects of olfactory bulbectomy on intermale aggression is largely species-dependent because intermale aggression plays different roles and is exhibited to different degrees in various species. In mice and hamsters, intermale aggression finds frequent expression. In these species, recognition of a conspecific male is sufficient to elicit aggressive behavior. The behavioral changes occurring after bilateral bulbectomy can be attributed in part to the animal's inability to adapt to its environment. Indirect evidence for the noradrenaline deficit that occurs in rodents following bulbectomy is obtained from studies in which chronically administered antidepressants had been shown to reverse the behavioral deficits.

Anatomical, physiological, and behavioral aspects of olfactory bulbectomy in the rat.

Producing and interpreting experimental olfactory deficits.

Changes in the olfactory mucosa and the olfactory nerves following intranasal treatment with one per cent zinc sulphate.

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Changes in the olfactory mucosa and the olfactory nerves following intranasal treatment with one per cent zinc sulphate.