Publications by authors named "R S Putnam"

As a field that predominately supports individuals with autism spectrum disorder (ASD), we have an ethical duty as behavior analysts to ensure that the goals we write and interventions we prescribe promote best outcomes across the lifespan. This is critical, given that as it stands now, outcomes in adulthood for individuals with ASD are poor in every area assessed. The can be interpreted to provide support for teaching the right goals, the right way, with respect to inherent rights of those we serve, in order to help affect positive changes in these outcomes.

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In Skinner's chapter titled , he stated, "By giving too much help, we postpone the acquisition of effective behavior and perpetuate the need for help" (Skinner, 1996, p. 63). Through years of living cross-culturally in various African countries, the first author has seen this demonstrated not only in organizations but also as part of the very fabric of society.

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The cellular mechanisms by which LC neurons respond to hypercapnia are usually attributed to an "accelerator" whereby hypercapnic acidosis causes an inhibition of K channels or activation of Na and Ca channels to depolarize CO-sensitive neurons. Nevertheless, it is still unknown if this "accelerator" mechanism could be controlled by a brake phenomenon. Whole-cell patch clamping, fluorescence imaging microscopy and plethysmography were used to study the chemosensitive response of the LC neurons.

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Central chemoreceptors are highly sensitive neurons that respond to changes in pH and CO2 levels. An increase in CO2/H+ typically reflects a rise in the firing rate of these neurons, which stimulates an increase in ventilation. Here, we present an ionic current model that reproduces the basic electrophysiological activity of individual CO2/H+-sensitive neurons from the locus coeruleus (LC).

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Rats reared in hyperoxia hypoventilate in normoxia and exhibit progressive blunting of the hypoxic ventilatory response, changes which are at least partially attributed to abnormal carotid body development. Since the carotid body also responds to changes in arterial CO/pH, we tested the hypothesis that developmental hyperoxia would attenuate the hypercapnic ventilatory response (HCVR) of neonatal rats by blunting peripheral and/or central chemoreceptor responses to hypercapnic challenges. Rats were reared in 21% O (Control) or 60% O (Hyperoxia) until studied at 4, 6-7, or 13-14days of age.

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