NT4/5 Mutant Mice Have Deficiency in Gustatory Papillae and Taste Bud Formation

Liebl, Daniel J.; Mbiene, Joseph Pascal; Parada, Luis F.

doi:10.1006/dbio.1999.9385

Cited by 66 publications

(56 citation statements)

References 43 publications

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“…In comparison to the overall cell size distribution in these ganglia (e.g. Liebl et al, 1999), this means that the sample of DRG neurons defined by the presence of YFP is slightly biased toward larger cells.…”

Section: Bdnf and Trkb Fl Content Of Regenerating Axonsmentioning

confidence: 99%

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

et al. 2006

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Electrical stimulation of cut peripheral nerves at the time of their surgical repair results in an enhancement of axon regeneration. Regeneration of axons through nerve allografts was used to evaluate whether this effect is due to an augmentation of cell autonomous neurotrophin signaling in the axons or signaling from neurotrophins produced in the surrounding environment. In the thy-1-YFP-H mouse, a single one hour application of electrical stimulation at the time of surgical repair of the cut common fibular nerve results in a significant increase in the proportion of YFP+ dorsal root ganglion neurons that were also immunoreactive for BDNF or trkB as well as an increase in the length of regenerating axons through allografts from wild type litter mates, both one and two weeks later. Axon growth through allografts from neurotrophin-4/5 knockout mice or grafts made acellular by repeated cycles of freezing and thawing is normally very poor, but electrical stimulation results in a growth of axons through these grafts which is similar to that observed through grafts from wild type mice after electrical stimulation. When cut nerves in NT-4/5 knockout mice were electrically stimulated, no enhancement of axon regeneration was found. Electrical stimulation thus produces a potent enhancement of the regeneration of axons in cut peripheral nerves which is independent of neurotrophin production by cells in their surrounding environment but is dependent on stimulation of trkB and its ligands in the regenerating axons themselves.

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Section: Bdnf and Trkb Fl Content Of Regenerating Axonsmentioning

confidence: 99%

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

et al. 2006

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“…Loss of BDNF also produces a selective depletion of Neuropeptide Y (NPY) and parvalbumin expression in the cortex with no change in the total number of interneurons, implicating BDNF in GABAergic interneuron function and peptide expression (Jones et al, 1994). Interestingly, NT-4 deficient mice show no gross neurological abnormalities (Conover et al, 1995) but, like BDNF deficient mice, show deficiencies in gustatory papillae and taste bud formation (Liebl et al, 1999). Impaired development of gustatory systems may in turn regulate appetitive behaviors in BNDF deficient mice (reviewed by Krimm, 2007).…”

Section: A Brief History Of Bdnfmentioning

confidence: 99%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

128

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Brain Derived Neurotrophic Factor (BDNF) has emerged as a regulator of development, plasticity and, recently, addiction. Decreased neurotrophic activity may be involved in ethanol-induced neurodegeneration in the adult brain and in the etiology of alcohol-related neurodevelopmental disorders. This can occur through decreased expression of BDNF or through inability of the receptor to transduce signals in the presence of ethanol. In contrast, recent studies implicate region-specific up-regulation of BDNF and associated signaling pathways in anxiety, addiction and homeostasis after ethanol exposure. Anxiety and depression are precipitating factors for substance abuse and these disorders also involve region-specific changes in BDNF in both pathogenesis and response to pharmacotherapy. Polymorphisms in the genes coding for BDNF and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of alcoholism. This review summarizes historical and pre-clinical data on BDNF and TrkB as it relates to ethanol toxicity and addiction. Many unresolved questions about region-specific changes in BDNF expression and the precise role of BDNF in neuropsychiatric disorders and addiction remain to be elucidated. Resolution of these questions will require significant integration of the literature on addiction and comorbid psychiatric disorders that contribute to the development of alcoholism.

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“…Consequently, fungiform and circumvallate taste buds are lost in BDNF null mice (Nosrat et al, 1997;Zhang et al, 1997;Cooper and Oakley, 1998;Mistretta et al, 1999). Fungiform papillae are also lost in NT4 À/À mice, but circumvallate papilla are normal (Liebl et al, 1999). In addition, mice that overexpress BDNF or NT4 in the lingual epithelium have twice the number of geniculate neurons normally observed in adults (Krimm et al, 2001).…”

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confidence: 99%

Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood

Krimm

2006

Anat. Rec.

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Brain-derived neurotrophic factor and neurotrophin-4 are required for normal taste bud development. Although these neurotrophins normally function via the tyrosine kinase receptor, trkB, they also bind to the panneurotrophin receptor, p75. The goal of the present study was to determine whether the p75 receptor is required for the development or maintenance of a full complement of adult taste buds. Mice with p75 null mutations lose 34% of their circumvallate taste buds, 36% of their fungiform papillae, and 26% of their fungiform taste buds by adulthood. The reduction of taste buds in the adult circumvallate papilla was similar to that observed previously at postnatal day 7 (Fan et al. Brain Res Dev Brain Res 2004;150:23-39). Taken together, these findings indicate that the p75 receptor is critical for the development of a full complement of taste buds, but is not required for maintenance of circumvallate taste buds in adulthood. Immunolabeling for p75 was not observed in taste buds, indicating that p75 signaling influences taste bud number indirectly. Geniculate ganglion neurons, which provides innervation to fungiform taste buds, express the p75 receptor. Mice with p75 null mutations also have fewer neurons in the geniculate ganglion. Together, these results suggest that the p75 receptor is important for the survival of geniculate neurons and geniculate neuron survival is required for the development of a full complement of taste buds by adulthood.

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NT4/5 Mutant Mice Have Deficiency in Gustatory Papillae and Taste Bud Formation

Cited by 66 publications

References 43 publications

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

Ethanol–BDNF interactions: Still more questions than answers

Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood

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