The capability for regulation of insulin secretion by somatostatin in purified pancreatic islet B cells during aging

Pancreatic islet B cells from Sprague--Dawley and Fisher 344 rats aged 3-27 months were separated from A and D cells by centrifugation over a linear percoll density gradient, and incubated in vitro with various concentrations of glucose and somatostatin. Elevation of glucose concentration in the incubation medium from 2.6 to 16.7 mM provokes an insulin secretory response that is independent of rat donor age. Inhibition of the insulin secretory response by somatostatin is independent of rat donor age beyond 12 months. These data indicate that the impaired regulation of insulin secretion during aging observed previously in vivo and in vitro in intact islets may not be intrinsic to the B cells, but instead reflect changes in islet paracrine regulatory mechanisms that relate to the quality and/or quantity of endogenous somatostatin and/or glucagon.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26358/1/0000445.pd

Spiral Ganglion Neurons Are Protected from Degeneration byGDNF Gene Therapy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42436/1/10162-1-4-315_00010315.pd

CNTF promotes the survival of neonatal rat corticospinal neurons in vitro

Corticospinal neurons were identified in cell cultures of neonatal rat cortex by immunostaining of cholera toxin B subunit (CTB), retrogradely transported from the cervical part of the spinal cord. The CTB-immunoreactive neurons were larger than the neurons in the overall (unstained) neuronal population and represented a small fraction of it (average of 0.3%) after 6 hours in vitro. The number of both total and CTB-labeled neurons declined progressively with time in culture. The neuronal death was, however, markedly faster in the CTB-labeled neuronal population than in the overall neuronal population. Ciliiary neurotrophic factor (CNTF) promoted the survival of CTB-positive corticospinal neurons in a dose-dependent manner; with CNTF, the death rate of the CTB-labeled neurons became identical to that of the over-all population

Potential regulation by trophic factors of low-affinity NGF receptors in spinal motor neurons

Developing spinal motor neurons (SMN) express low-affinity nerve growth factor receptors (LNGFR) but not high-affinity transducing NGF receptors. Moreover, SMN are not supported by NGF in vitro. In the normal adult rat most SMN are not LNGFR immunoreactive (LNGFR-IR), but they transiently reexpress LNGFR (though not the high-affinity receptor) after peripheral nerve injury. With a cut lesion of the sciatic nerve (when only a neuroma forms), the number of LNGFR-IR SMN at L4–L6 rapidly increases to a maximum between day 1 and 7 and returns to baseline levels by day 30. After a crush lesion (accompanied by regeneration to the muscle), LNGFR-IR SMN appear in about the same numbers, but they start to disappear 1 week later. We speculate that the similar appearance and differential decline of LNGFR-IR seen after the two types of lesions are regulated by the availability of a common signal such as ciliary neurotrophic factor. The adult SMN model provides a good opportunity to investigate the reexpression of LNGFR after peripheral nerve injury, and more generally, the unknown role and regulation of LNGFR