Publications by authors named "Robert Waldeck"

Usually nicotinic receptors in the central nervous system only influence the strength of a signal between neurons. At a few critical connections, for instance some of those involved in the flight response, nicotinic receptors not only modulate the signal, they actually determine whether a signal is conveyed or not. We show at one of the few such connections accessible for study, up to three different nicotinic receptor subtypes mediate the signal.

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The workshop "Introduction to FUN Electrophysiology Labs" was organized by Patsy Dickinson (Bowdoin College), Steve Hauptman (Bowdoin College), Bruce Johnson (Cornell University), and Carol Ann Paul (Wellesley College). It took place July 27-30 2006 at Bowdoin College. There were fifteen participants, most of whom were junior faculty at college and universities around the country.

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Our investigation concerns the connection between the telencephalon and the startle response, mediated by reticulospinal neurons. Before surgery fish respond to the startle stimulus in 95% of the trials and 66% of the time with complete full turns. Following telencephalon removal fish respond in only 50% of the trials but make complete full turns only 7% of the time.

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We have previously reported that short-term (48-72 h) exposure to the GABA-modulatory steroid 3alpha-OH-5alpha-pregnan-20-one (3alpha,5alpha-THP) increases expression of the alpha4 subunit of the GABA(A) receptor (GABAR) in the hippocampus of adult rats. This change in subunit composition was accompanied by altered pharmacology and an increase in general excitability associated with acceleration of the decay time constant (tau) for GABA-gated current of pyramidal cells acutely isolated from CA1 hippocampus similar to what we have reported following withdrawal from the steroid after chronic long-term administration. Because GABAR can be localized to either synaptic or extrasynaptic sites, we tested the hypothesis that this change in receptor kinetics is mediated by synaptic GABAR.

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Hereditary canine spinal muscular atrophy (HCSMA) is an autosomal dominant degenerative disorder of motor neurons. In homozygous animals, motor units produce decreased force output and fail during repetitive activity. Previous studies suggest that decreased efficacy of neuromuscular transmission underlies these abnormalities.

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