Serotonin and cAMP Mediate Plastic Changes in Swimming Activity of Hirudo m

Abstract

The mechanisms of some short-term non-associative learning processes, such as habituation and sensitization (or dishabituation) have been analyzed in detail in the defensive withdrawal reflex of the gill and the siphon of Aplysia. It has been shown that behavioral sensitization results from heterosynaptic facilitation of transmitter output on the mechanosensory neurons of the abdominal ganglion that innervate the gill and the siphon. The facilitation of synaptic output between sensory and motor neuron is mediated by two sets of neurons so far identified as the L28 and L29 cells which take contacts with terminal branches of sensory neurons. Serotonin as well as peptide transmitters (small cardioactive peptides SCPa and SCPb) or other unknown transmitters converge to produce synaptic facilitation in the sensory neurons via different receptors triggering a common molecular chain of events to produce the same modulatory effect. The transmitter released activates an adenylate cyclase which increases the intracellular level of cAMP (Brunelli et al. 1976). This enhancement leads to a cAMP-dependent protein phosphorilation through a protein kinase activation which induces a suppression of a specific K⁺ current. The block of K⁺ current is thought to cause broadening of the presynaptic action potential and therefore a prolonged influx of Ca⁺⁺ in the presynaptic terminal which potentiates the transmitter release (Kandel and Schwartz 1982).