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K Lankford

Publications and source records attributed to K Lankford.

4 recordsLinked to original sources

Nerve growth cone motility.

Although many issues remain unresolved, the past year has witnessed a number of advances in our understanding of the inter-relationships between extracellular influences, cell phenotype, growth associated proteins, second messengers, and cytoskeletal components in the control of neurite outgrowth and growth cone behavior. Some of the early events associated with process initiation have been tentatively identified, and more is known about the assembly and stabilization of the microtubular framework of growing neurites. The mechanical forces involved in neurite extension have begun to be quantified, and interactions between the actin and microtubule systems are being further characterized. The current data more strongly support a functional role for GAP-43 in control of motility. The data also tend to support a central role for cytoplasmic calcium in mediating the actions of many growth-regulating influences, and strongly implicate changes in actin filament stability as mediating the behavioral effects of calcium.

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A transient embryonic dopamine receptor inhibits growth cone motility and neurite outgrowth in a subset of avian retina neurons.

To investigate the possible developmental significance of a transient dopamine receptor in the avian central nervous system, we examined the effects of dopamine on the morphology and motility of cultured retina neurons. Neurite arborization was significantly reduced by chronic dopamine stimulation. Using continuous video microscope monitoring, we observed that a subset of neurons responded to short-term dopamine with decreased filopodial activity and retracted neurites. The effects of dopamine could be blocked or reversed by haloperidol or SCH23390 and forskolin produced a response similar to dopamine, indicating the morphological changes were mediated by D1-receptor stimulation of adenylate cyclase.

Animals↗