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Thomas W. Abrams

Researcher at University of Maryland, Baltimore

Publications -  29
Citations -  2519

Thomas W. Abrams is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Aplysia & Adenylyl cyclase. The author has an hindex of 18, co-authored 28 publications receiving 2282 citations. Previous affiliations of Thomas W. Abrams include Weizmann Institute of Science & Columbia University.

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Two endogenous neuropeptides modulate the gill and siphon withdrawal reflex in Aplysia by presynaptic facilitation involving cAMP-dependent closure of a serotonin-sensitive potassium channel.

TL;DR: It appears that several transmitters can converge to produce presynaptic facilitation in the sensory neurons of the defensive withdrawal reflex, and all of the transmitters studied here, the SCPs and serotonin, act via an identical molecular cascade.
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Biochemical studies of stimulus convergence during classical conditioning in Aplysia: dual regulation of adenylate cyclase by Ca2+/calmodulin and transmitter

TL;DR: The dependence of cyclase activation on the temporal pattern of Ca2+ and transmitter addition is explored and it is suggested that the dually regulated adenylate cyclase might underlie the temporal requirements for effective classical conditioning in this system.
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A test of Hebb's postulate at identified synapses which mediate classical conditioning in Aplysia

TL;DR: It is found that the mechanism postulated by Hebb is neither necessary nor sufficient to produce the associative change in synaptic strength that underlies conditioning in Aplysia, and impulse activity in the presynaptic cell must be paired with facilitatory input, supporting the hypothesis that the temporal specificity of classical conditioning in
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cAMP modulates multiple K+ currents, increasing spike duration and excitability in Aplysia sensory neurons

TL;DR: It is found that cAMP plays a major role in the spike-broadening effects of facilitatory transmitter; however, broadening requires higher levels of activation of the cAMP-dependent kinase than does increasing excitability.