Olfactory bulb dopamine neurons survive deafferentation-induced loss of tyrosine hydroxylase

Baker, Harriet; Kawano, Teruaki; Albert, Vivian R.; T, Joh; Dj, Reis; Margolis, Frank L.

doi:10.1016/0306-4522(84)90047-2

Cited by 109 publications

(67 citation statements)

References 34 publications

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“…To address this issue directly, we combined radiolabeled ligand binding with a unilateral destruction of the ORNs in the nasal cavity. Destruction of ORNs results in degeneration of ORN axons and terminals in the bulb (Ehrlich et al, 1990) without loss of JG cells (Baker et al, 1984). This treatment drastically reduced spiperone binding in the outer bulb layers and suggests that many D2-like receptors in the glomerular layer are located on ORN terminals.…”

Section: Mature Olfactory Receptor Neurons Express D2 Darsmentioning

confidence: 98%

“…However, D2 receptors on JG cells may down-regulate in response to deafferentation. It is well established that tyrosine hydroxylase, the rate-limiting enzyme in the production of DA, is down-regulated in JG cells after deafferentation (Baker et al, 1983(Baker et al, , 1984Baker, 1990;Stone et al, 1991). It remains to be determined whether JG D2 receptor expression is regulated by deafferentation.…”

Section: Mature Olfactory Receptor Neurons Express D2 Darsmentioning

confidence: 98%

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Olfactory receptor neurons express D2 dopamine receptors

et al. 1999

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Section: Mature Olfactory Receptor Neurons Express D2 Darsmentioning

confidence: 98%

Section: Mature Olfactory Receptor Neurons Express D2 Darsmentioning

confidence: 98%

Olfactory receptor neurons express D2 dopamine receptors

et al. 1999

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“…Furthermore, MOB dopamine expression is regulated by afferent input. For example, olfactory nerve transection, naris closure, or olfactory epithelial damage, either neonatally or in adults, resulted in decreased levels of TH immunoreactivity and gene expression (Baker, 1990;Baker et al, 1984Baker et al, , 1989Baker et al, , 1993Kosaka et al, 1987;Cho et al, 1996).…”

Section: Comparison With Effects Of Decreased Afferent Inputmentioning

confidence: 99%

Olfactory bulb development is altered in small-eye (Sey) mice

1998

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Small-eye (Sey) is a spontaneous, semidominant murine mutation that results from a point mutation in the Pax-6 gene. Both the eyes and the olfactory system fail to develop in homozygotes and these animals die neonatally. Heterozygotes (Sey/+) have different degrees of eye abnormalities including decreased lens size and cataracts. In the present study, we examined whether one mutated allele of Pax-6 also affects olfactory system development. By 42 days of age, main olfactory bulb volume was significantly decreased in Sey/+ animals compared with wild-type littermates, and this effect was even more dramatic in 70-day-old animals. In contrast, there was no effect on accessory olfactory bulb, olfactory epithelial, or vomeronasal organ development at any age in Sey/+ animals, demonstrating the specificity of the effect. In the main olfactory bulb, the largest differences in laminar volume were found in the glomerular and granule cell layers. These layers contain the olfactory bulb interneurons, and a subpopulation of these cells were found to be Pax-6 immunoreactive. Examination of the neurochemical consequences of this mutation showed that the number of both tyrosine hydroxylase (TH)- and gamma-aminobutyric acid (GABA)-immunoreactive profiles were dramatically decreased in Sey/+ animals as compared with controls. In contrast, neither calretinin nor calbindin immunoreactivity was affected by this mutation. Dual-labeling immunohistochemistry showed that nearly all TH-immunoreactive cells and a subpopulation of GABA-immunoreactive cells coexpressed Pax-6. However, calretinin- and calbindin-immunoreactive cells were not Pax-6 immunopositive. These data indicate that two normal alleles of Pax-6 are required for normal olfactory bulb development and, as part of this effect, this gene may be involved in the development of specific neurotransmitter systems.

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“…72 It is unknown whether damage to the olfactory neuroepithelium per se can induce, in either humans or rodents, elements of the complex cascade of brain changes observed after bulbectomy. Axotomy or ZnSO 4 irrigation of the olfactory neuroepithelium does lead to a 33 to 75% decrease of bulb weight in rats after a month, [73][74][75] largely reflecting degenerative changes within the glomerular and external plexiform layers of the bulb. In humans, decreased olfactory bulb volumes determined using magnetic resonance imaging have been reported secondary to age, 76 head trauma, 77 upper respiratory infections that induce epithelial damage, 78 and schizophrenia.…”

Section: Centrifugal Afferent Innervation Comes From the Horizontal Lmentioning

confidence: 99%

The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

Doty

2008

Annals of Neurology

348

279

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Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formative stages of Alzheimer's and Parkinson's diseases, together with evidence that xenobiotics, some epidemiologically linked to these diseases, can readily enter the brain via the olfactory mucosa, have led to the hypothesis that Alzheimer's and Parkinson's diseases may be caused or catalyzed by agents that enter the brain via this route. Evidence for and against this concept, the “olfactory vector hypothesis,” is addressed in this review. Ann Neurol 2008;63:7–15

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Olfactory bulb dopamine neurons survive deafferentation-induced loss of tyrosine hydroxylase

Cited by 109 publications

References 34 publications

Olfactory receptor neurons express D2 dopamine receptors

Olfactory receptor neurons express D2 dopamine receptors

Olfactory bulb development is altered in small-eye (Sey) mice

The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

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