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T Mutoh

Publications and source records attributed to T Mutoh.

112 records · Page 7Linked to original sources
PubMedDate not supplied

Unglycosylated Trk protein does not co-localize nor associate with ganglioside GM1 in stable clone of PC12 cells overexpressing Trk (PCtrk cells).

Our previous studies have shown that acidic glycosphingolipid, ganglioside GM1 (GM1), is an endogenous regulator of high affinity nerve growth factor receptor, Trk, which is an essential factor for the normal development and differentiation of neuronal cells by forming a complex with Trk. GM1 is also known to be a major constituent of caveola or glycosphingolipid-enriched microdomain (GEM) of the plasma membrane. In order to study the effect of the glycosylation of Trk on the formation of GM1-Trk complex and subcellular distribution of this protein, we generated PC12 cells stably overexpressing Trk (PCtrk). Pretreatment of this stable clones with tunicamycin, a potent inhibitor of N-glycosylation, caused the appearance of unglycosylated Trk core protein. These unglycosylated Trk can hardly respond to its ligand, NGF. Sucrose density gradient analysis revealed that unglycosylated Trk core protein was recovered in high density fractions, whereas most of GM1 is present in low density fractions corresponding to caveola or GEM fractions. Moreover, these unglycosylated Trk proteins lose their ability to form a complex with GM1, although GM1 is present in the same high density fractions. These data strongly suggest that spatial segregation of GM1 from the Trk protein by the inhibition of the glycosylation of Trk might be an important molecular mechanism for the unresponsiveness to NGF. Moreover, the binding site of GM1 in the Trk protein might act as an important determinant for the normal trafficking of the Trk protein within the cells.

Animals↗
PubMedDate not supplied

Respiratory reflexes in response to upper-airway administration of sevoflurane and isoflurane in anesthetized, spontaneously breathing dogs.

OBJECTIVE: To evaluate the respiratory effects occurring during administration of sevoflurane or isoflurane to the upper airway in dogs. STUDY DESIGN: A prospective, randomized study. ANIMALS: Twelve healthy adult beagles (6 males, 6 females). METHODS: At least 2 weeks after undergoing permanent tracheostomy, dogs were premedicated with acepromazine-buprenorphine, and anesthesia was induced with thiopental and maintained with alpha-chloralose. The upper airway was functionally isolated so that the inhalant could be administered to the upper airway while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to the administration of sevoflurane or isoflurane at concentrations of 1.2, 1.8, and 2.4 times the minimal alveolar concentration (MAC) (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of each anesthetic were also recorded following upper-airway administration of lidocaine. RESULTS: Respiratory reflexes elicited by upper-airway administration of each anesthetic were characterized by a dose-dependent increase in expiration time, with a resultant decrease in respiratory minute ventilation and increase in end-tidal PCO2. The magnitude of these responses was greater with isoflurane than with sevoflurane at 1.8 and 2.4 MAC. These reflexes were abolished after lidocaine nebulization into the upper airway. CONCLUSION: Isoflurane induces greater reflex inhibition of breathing than does sevoflurane when the anesthetic is inhaled into the upper airway at concentrations used for mask induction.

Anesthetics, Inhalation↗