Fig. 15.

Models for PTK and PKC interactions in the production of learning-produced changes in Hermissenda type B cell excitability. In the parallel/independent model (left), light leads to increases in intracellular calcium within B cells, whereas rotation leads to neurotransmitter (e.g., serotonin [5-HT] and γ-aminobutyric acid) stimulation of G-protein–triggered signal-transduction pathways, including those that result in membrane phospholipid hydrolysis and the production of IP₃ and diacylglycerol (DAG). In this model, pairing specificity arises from the requirements for kinase activation (temporally contiguous increase in both intracellular calcium ion concentration, [Ca²⁺]_i, and DAG are necessary for PKC activation) and the differential ability of each sensory stimulus to stimulate [Ca²⁺]_i and DAG increases. Although IP₃ would be produced by rotational stimulation and thereby lead to [Ca²⁺]_i increases (in addition to DAG), we suggest that the [Ca²⁺]_i increases produced are normally below the threshold needed for PKC activation. Thus repeated exposures to rotational stimulation in the absence of paired light presentations would be insufficient to induce PKC-mediated changes in B cell excitability. Similarly, in the case of PTK activation, we assume that for a calcium-dependent, nonreceptor-type PTK (e.g., PYK2), light-induced [Ca²⁺]_i increases may be insufficient to activate the kinase unless rotation also adds to [Ca²⁺]_i increases. Alternatively, the PTK(s) activated during conditioning may be receptor-type PTKs, dependent on both rotation-mediated stimulation and light-induced [Ca²⁺]_i increases within B cells for their activation. In a second class of models (serial/interdependent, right), PTKs and PKCs interact and affect one another (see discussion). One possible interaction between PTKs and PKC in type B photoreceptors might involve PTK participation in activation of PLC-γ and subsequent activation of PKC by DAG and IP₃. Our data are most consistent with the parallel/independent model (left).