Chemical deafferentation of the olfactory bulb: Plasticity of the levels of tyrosine hydroxylase, dopamine and norepinephrine

Nadi, N. S.; Head, Richard; Grillo, Mary; Hempstead, J.; Grannot-Reisfeld, N.; Margolis, Frank L.

doi:10.1016/0006-8993(81)90241-9

Cited by 164 publications

(109 citation statements)

References 39 publications

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“…Here, we pharmacologically isolated the intrinsic properties of primary sensory synapses (baseline release of transmitter and activation ionotropic glutamate receptors) by using sulpiride to block D 2 receptors and CGP55845 to block GABA B receptors. Future investigations should focus on interactions between sensory experience, plasticity at OSN synapses, and several key neuromodulators known to affect glomerular physiology, particularly mGluRs (De Saint Jan and Westbrook, 2005;Yuan and Knopfel, 2006;De Saint Jan and Westbrook, 2007), dopamine (Guthrie et al, 1991;Wilson and Sullivan, 1995;Cho et al, 1996;Berkowicz and Trombley, 2000;Ennis et al, 2001), norepinephrine (Nadi et al, 1981;Wilson and Leon, 1988b;Brennan et al, 1990;Brinon et al, 2001), and serotonin (Hardy et al, 2005;Gomez et al, 2007). For example, does odor experience induce differential modulation of D 2 receptor isoforms at OSN synapses?…”

Section: Discussionmentioning

confidence: 99%

Experience-Dependent Modification of Primary Sensory Synapses in the Mammalian Olfactory Bulb

et al. 2007

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Experience-dependent changes in neural circuits have traditionally been investigated several synapses downstream of sensory input. Whether experience can alter the strength of primary sensory synapses remains mostly unknown. To address this issue, we investigated the consequences of odor deprivation on synapses made by olfactory sensory axons in the olfactory bulb of rats. Odor deprivation triggered an increase in the probability of glutamate release from olfactory sensory neuron synapses. Deprivation also increased the amplitude of quantal synaptic currents mediated by AMPA-and NMDA-type glutamate receptors, as well as the abundance of these receptors in the glomerular region. Our results demonstrate that sensory experience is capable of modulating synaptic strength at the earliest stages of information transfer between the environment and an organism. Such compensatory experience-dependent changes may represent a mechanism of sensory gain control.

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Section: Discussionmentioning

confidence: 99%

Experience-Dependent Modification of Primary Sensory Synapses in the Mammalian Olfactory Bulb

et al. 2007

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“…(Baker et al, 1999;Cho et al, 1996;Nadi et al, 1981). Th expression was detected around the olfactory glomeruli of O/E3 GFP/GFP animals, but its expression in dorsal OB was greatly attenuated due to the absence of olfactory glomeruli and reduction of ORN axons in this region (Fig.…”

Section: Phenotype Of O/e2-deficient Micementioning

confidence: 92%

Genetic disruptions ofO/E2andO/E3genes reveal involvement in olfactory receptor neuron projection

et al. 2004

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The mammalian Olf1/EBF (O/E) family of repeated helix-loop-helix (rHLH)transcription factors has been implicated in olfactory system gene regulation,nervous system development and B-cell differentiation. Ebf(O/E1) mutant animals showed defects in B-cell lineage and brain regions where it is the only O/E family member expressed, but the olfactory epithelium appeared unaffected and olfactory marker expression was grossly normal in these animals. In order to further study the mammalian O/E proteins,we disrupted O/E2 and O/E3 genes in mouse and placed tau-lacZ and tau-GFP reporter genes under the control of the respective endogenous O/E promoters. Mice mutant for each of these genes display reduced viability and other gene-specific phenotypes. Interestingly, both O/E2 and O/E3 knockout mice as well as O/E2/O/E3 double heterozygous animals share a common phenotype:olfactory neurons (ORN) fail to project to dorsal olfactory bulb. We suggest that a decreased dose of O/E protein may alter expression of O/E target genes and underlie the ORN projection defect.

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“…Levels of tyrosine hydroxylase, the rate limiting enzyme in biosynthesis of catecholamine neurotransmitters, decrease to 20᎐30% of control levels in the OB within 10 days following Triton X-100 irrigation of the nasal cavity, and then recover to control values over the course of the next 40 days. 66 Since tyrosine hydroxylase appears to be present only in neuronal processes intrinsic to the bulb, this suggests that synaptic function in the OB responds to loss of afferent input, even if cell numbers do not. 66 Using the naris occlusion model with juvenile rodents, significant changes are seen in the OB.…”

Section: Olfactory Bulbmentioning

confidence: 99%

“…66 Since tyrosine hydroxylase appears to be present only in neuronal processes intrinsic to the bulb, this suggests that synaptic function in the OB responds to loss of afferent input, even if cell numbers do not. 66 Using the naris occlusion model with juvenile rodents, significant changes are seen in the OB. When Ž .…”

Section: Olfactory Bulbmentioning

confidence: 99%

Neuronal regeneration: Lessons from the olfactory system

Murray

Calof

1999

Seminars in Cell & Developmental Biology

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Chemical deafferentation of the olfactory bulb: Plasticity of the levels of tyrosine hydroxylase, dopamine and norepinephrine

Cited by 164 publications

References 39 publications

Experience-Dependent Modification of Primary Sensory Synapses in the Mammalian Olfactory Bulb

Experience-Dependent Modification of Primary Sensory Synapses in the Mammalian Olfactory Bulb

Genetic disruptions ofO/E2andO/E3genes reveal involvement in olfactory receptor neuron projection

Neuronal regeneration: Lessons from the olfactory system

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