is no longer possible, even in the face of an intensive and synchronized release of ACh (C). Although nicotine mimics the action of ACh at the receptors, it cannot duplicate the time course of intrasynaptic agonist concentration required for appropriate high-frequency ganglionic activation. The concentration of nicotine in the synaptic cleft can neither build up as rapidly as that of ACh released from nerve terminals nor can nicotine be eliminated from the synaptic cleft as quickly as ACh.
For about four decades now, a course in receptor pharmacology has been given at University College
London for undergraduate students in their final year of study for the Bachelor of Science degree
in pharmacology. More recently, the course has also been taken by students reading for the Bachelor
of Science degree in medicinal chemistry. The students following the course have relied for their
reading upon a variety of sources, including original papers, reviews, and various textbooks, but
no single text brought together the material included in the course.
Fatty acids can stimulate the secretory activity of insulin-producing beta-cells. At elevated concentrations, they can also be toxic to isolated beta-cells. This toxicity varies inversely with the cellular ability to accumulate
neutral lipids in the cytoplasm. To further examine whether cytoprotection
can be achieved by decreasing cytoplasmic levels of free acyl moieties, we
investigated whether palmitate toxicity is also lowered by stimulating its
Fluorescence ratio imaging indicates that immobilized,
aspirin-treated platelets, loaded with Fura-2, respond to
inositol 1,4,5-trisphosphate- (InsP3)-generating agonists
such as thrombin by high-frequency, irregular rises in
i with spikes that vary in peak level and
peak-to-peak interval. This differs from the regular [Ca
oscillations observed inother, larger cells.