Transneuronal regulation of tyrosine hydroxylase expression in olfactory bulb of mouse and rat

Baker, Harriet; Kawano, Teruaki; Margolis, F. L.; T, Joh

doi:10.1523/jneurosci.03-01-00069.1983

Cited by 288 publications

(230 citation statements)

References 4 publications

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“…1C) at 21 and 28 d after lesion (F (2,17) ϭ 12.95; p Ͻ 0.0001). This finding indicates that olfactory deafferentation lasts at least 1 month and supports previous observations made from distinct methods to induce olfactory deafferentation (Baker et al, 1983;Mandairon et al, 2006;Bastien-Dionne et al, 2010;Parrish-Aungst et al, 2011).…”

Section: Effectiveness Of the Olfactory Lesionsupporting

confidence: 91%

“…1C). TH, the rate-limiting enzyme in the catecholamine synthesis, is expressed only in dopaminergic periglomerular (PG) neurons through an activity-dependent manner (Baker et al, 1983;Kiyokage et al, 2010;Kosaka and Kosaka, 2011). We found a drastic decrease in the TH immunoreactivity in lesioned mice compared with controls ( Fig.…”

Section: Effectiveness Of the Olfactory Lesionmentioning

confidence: 72%

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Early Activation of Microglia Triggers Long-Lasting Impairment of Adult Neurogenesis in the Olfactory Bulb

Lazarini

Gabellec²,

Torquet³

et al. 2012

J. Neurosci.

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Microglia, the innate immune cells of the brain, engulf and eliminate cellular debris during brain injury and disease. Recent observations have extended their roles to the healthy brain, but the functional impact of activated microglia on neural plasticity has so far been elusive. To explore this issue, we investigated the role of microglia in the function of the adult olfactory bulb network in which both sensory afferents and local microcircuits are continuously molded by the arrival of adult-born neurons. We show here that the adult olfactory bulb hosts a large population of resident microglial cells. Deafferentation of the olfactory bulb resulted in a transient activation of microglia and a concomitant reduction of adult olfactory bulb neurogenesis. One day after sensory deafferentation, microglial cells proliferate in the olfactory bulb, and their numbers peaked at day 3, and reversed at day 7 after lesion. Similar lesions performed on immunodeficient mice demonstrate that the both innate and adaptive lymphocyte responses are dispensable for the lesion-induced microglial proliferation and activation. In contrast, when mice were treated with an antiinflammatory drug to prevent microglial activation, olfactory deafferentation did not reduce adult neurogenesis, showing that activated microglial cells per se, and not the lack of sensory experience, relates to the survival of adult-born neurons. We conclude that the status of the resident microglia in the olfactory bulb is an important factor directly regulating the survival of immature adult-born neurons.

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Section: Effectiveness Of the Olfactory Lesionsupporting

confidence: 91%

Section: Effectiveness Of the Olfactory Lesionmentioning

confidence: 72%

Early Activation of Microglia Triggers Long-Lasting Impairment of Adult Neurogenesis in the Olfactory Bulb

Lazarini

Gabellec²,

Torquet³

et al. 2012

J. Neurosci.

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“…It might be surprising that the decrease in A:D synapses is not accompanied by a reduction in TH expression and activity (17,38). TH expression in the glomerular layer is decreased when odorant-induced activity is eliminated with naris occlusion (39) or OSN elimination (40). However, the age-related decrease in glomerular synapses may result in more subtle changes in activity that would be unlikely to affect TH expression.…”

Section: Are Morphological Changes In the Ob Related To Alterations Inmentioning

confidence: 99%

Age-induced disruption of selective olfactory bulb synaptic circuits

Richard

Taylor²,

Greer³

2010

Proc. Natl. Acad. Sci. U.S.A.

121

125

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Little is known about how normal aging affects the brain. Recent evidence suggests that neuronal loss is not ubiquitous in aging neocortex. Instead, subtle and still controversial, region-and layerspecific alterations of neuron morphology and synapses are reported during aging, leading to the notion that discrete changes in neural circuitry may underlie age-related cognitive deficits. Although deficits in sensory function suggest that primary sensory cortices are affected by aging, our understanding of the age-related cellular and molecular changes is sparse. To assess the effect of aging on the organization of olfactory bulb (OB) circuitry, we carried out quantitative morphometric analyses in the mouse OB at 2, 6, 12, 18, and 24 mo. Our data establish that the volumes of the major OB layers do not change during aging. Parallel to this, we are unique in demonstrating that the stereotypic glomerular convergence of M72-GFP OSN axons in the OB is preserved during aging. We then provide unique evidence of the stability of projection neurons and interneurons subpopulations in the aging mouse OB, arguing against the notion of an age-dependent widespread loss of neurons. Finally, we show ultrastructurally a significant layer-specific loss of synapses; synaptic density is reduced in the glomerular layer but not the external plexiform layer, leading to an imbalance in OB circuitry. These results suggest that reduction of afferent synaptic input and local modulatory circuit synapses in OB glomeruli may contribute to specific age-related alterations of the olfactory function.aging | axodendritic synapses | dendrodendritic synapses | mitral cells A ge-related neurodegenerative diseases, such as Parkinson and Alzheimer's, involve localized or widespread neuronal loss, but little is known about the changes occurring in the brain during normal aging. A growing consensus argues against widespread neuronal loss and atrophy during aging (1, 2). Rather, subtle region-and layer-specific alterations of neuronal morphology and synaptic connections are reported in the neocortex and hippocampus, where they may contribute to age-related cognitive deficits.The laminar organization of olfactory bulb (OB) neurons and synapses provides a simplified cortical model in which we can probe principles of neuronal and synaptic organization during aging. Sensory functions are affected by aging, including alterations in olfactory acuity, discrimination, and memory (3-12). The OB is the first central relay in the pathway processing odor information: it receives afferent input from olfactory sensory neurons (OSNs) located in the olfactory epithelium (OE) and is responsible for detecting odors in the nasal cavity. OSN axons synapse on mitral/tufted cell dendrites in OB glomerular neuropils. OB local interneurons modulate the activity of mitral/tufted cells, contributing to odor signal integration, before propagation to the piriform cortex. Projections from the OE to the OB are organized in an odor receptor (OR) map; each subpopulation of OSNs expressin...

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“…This is consistent with regulation of TH protein levels above or below immunohistochemically detectable levels without addition or subtraction of neurons. (3) Many studies have reported activitydependent changes in TH gene and protein expression within cells over a timescale of several hours [17][18][19][20][21][22][23] , and the same has been reported in midbrain 4 .…”

Section: Environmental Manipulationsmentioning

confidence: 78%

Environmental Modulations of the Number of Midbrain Dopamine Neurons in Adult Mice

Tomas

Prijanto

Burrows

et al. 2015

JoVE

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Long-lasting changes in the brain or 'brain plasticity' underlie adaptive behavior and brain repair following disease or injury. Furthermore, interactions with our environment can induce brain plasticity. Increasingly, research is trying to identify which environments stimulate brain plasticity beneficial for treating brain and behavioral disorders. Two environmental manipulations are described which increase or decrease the number of tyrosine hydroxylase immunopositive (TH+, the rate-limiting enzyme in dopamine (DA) synthesis) neurons in the adult mouse midbrain. The first comprises pairing male and female mice together continuously for 1 week, which increases midbrain TH+ neurons by approximately 12% in males, but decreases midbrain TH+ neurons by approximately 12% in females. The second comprises housing mice continuously for 2 weeks in 'enriched environments' (EE) containing running wheels, toys, ropes, nesting material, etc., which increases midbrain TH+ neurons by approximately 14% in males. Additionally, a protocol is described for concurrently infusing drugs directly into the midbrain during these environmental manipulations to help identify mechanisms underlying environmentally-induced brain plasticity. For example, EEinduction of more midbrain TH+ neurons is abolished by concurrent blockade of synaptic input onto midbrain neurons. Together, these data indicate that information about the environment is relayed via synaptic input to midbrain neurons to switch on or off expression of 'DA' genes. Thus, appropriate environmental stimulation, or drug targeting of the underlying mechanisms, might be helpful for treating brain and behavioral disorders associated with imbalances in midbrain DA (e.g. Parkinson's disease, attention deficit and hyperactivity disorder, schizophrenia, and drug addiction). Video LinkThe video component of this article can be found at

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Transneuronal regulation of tyrosine hydroxylase expression in olfactory bulb of mouse and rat

Cited by 288 publications

References 4 publications

Early Activation of Microglia Triggers Long-Lasting Impairment of Adult Neurogenesis in the Olfactory Bulb

Early Activation of Microglia Triggers Long-Lasting Impairment of Adult Neurogenesis in the Olfactory Bulb

Age-induced disruption of selective olfactory bulb synaptic circuits

Environmental Modulations of the Number of Midbrain Dopamine Neurons in Adult Mice

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