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David Barber

Publications and source records attributed to David Barber.

5 recordsLinked to original sources
PubMed2006

Modeling of gene expression pattern alteration by p,p'-DDE and dieldrin in largemouth bass.

In this study, largemouth bass (LMB) were subchronically exposed to p,p'-DDE or dieldrin in their diet to evaluate the effect of exposure on expression of genes involved in reproduction and steroid homeostasis. Using real-time PCR, we detected a different gene expression pattern for each OCP, suggesting that they each affect LMB in a different way. We also detected a different expression pattern among sexes, suggesting that sexes are affected differently by OCPs perhaps reflecting the different adaptive responses of each sex to dysregulation caused by OCP exposure.

Animals↗
PubMed2006

Optimal spike-timing-dependent plasticity for precise action potential firing in supervised learning.

In timing-based neural codes, neurons have to emit action potentials at precise moments in time. We use a supervised learning paradigm to derive a synaptic update rule that optimizes by gradient ascent the likelihood of postsynaptic firing at one or several desired firing times. We find that the optimal strategy of up- and downregulating synaptic efficacies depends on the relative timing between presynaptic spike arrival and desired postsynaptic firing. If the presynaptic spike arrives before the desired postsynaptic spike timing, our optimal learning rule predicts that the synapse should become potentiated. The dependence of the potentiation on spike timing directly reflects the time course of an excitatory postsynaptic potential. However, our approach gives no unique reason for synaptic depression under reversed spike timing. In fact, the presence and amplitude of depression of synaptic efficacies for reversed spike timing depend on how constraints are implemented in the optimization problem. Two different constraints, control of postsynaptic rates and control of temporal locality, are studied. The relation of our results to spike-timing-dependent plasticity and reinforcement learning is discussed.

Action Potentials↗
PubMed2003

Altered expression of transcripts for alpha-tubulin and an unidentified gene in the spinal cord of phenyl saligenin phosphate treated hens (Gallus gallus).

Phenyl saligenin phosphate (PSP) induces a central-peripheral distal axonopathy in domestic fowl that develops 7-21 days after a single exposure. Neurotoxic esterase (NTE) is the initial molecular target for this neurotoxicity. PSP has to covalently bind to NTE and chemically "age" for induction of axonopathy. It was hypothesized that exposure to PSP results in early changes in spinal cord gene expression that do not occur with phenylmethylsulfonyl fluoride, a non-neuropathic compound that also inhibits NTE, or DMSO controls. Targeted display was used to screen approximately 15,000 gel bands. Three candidate genes were identified, but only the transcript designated P1 showed decreased expression following PSP exposure (2 mg/kg i.m.) in subsequent Northern blot and in situ hybridization experiments in samples taken <48 h after exposure. Additional experiments revealed that a approximately 2.5 kb alpha-tubulin transcript had decreased expression at 12-48 h after PSP exposure, with maximum change at 48 h (33%, p = 0.0479). A approximately 4.5 kb alpha-tubulin transcript had increased expression at 12 h (38%, p = 0.0125) and decreased expression at 48 h (28%, p = 0.0576). In situ hybridization on spinal cord revealed neuronal expression of P1 and alpha-tubulin transcripts. Decreased expression of transcripts for P1 and alpha-tubulin was present at 12 and 48 h, respectively. This decrease occurred in all neurons, not just those whose axons degenerate. Results suggest that (1) in PSP-induced OPIDN (organophosphorus-induced delayed neurotoxicity) some gene transcript expression changes are associated with initiation of axonopathy, and (2) PSP modulates spinal cord gene expression in neuronal types that do not undergo axonal degeneration.

Animals↗