Activity-dependent synaptic plasticity regulates the flow of information in neuronal networks and has important implications for the expression of behavior. We find a functional role for short-term synaptic enhancement (STE) such as facilitation, augmentation, and post-tetanic potentiation at central synapses in the sea slug Aplysia californica. Consummatory feeding in Aplysia such as rhythmic biting is controlled by command-like cerebral-buccal interneurons (CBIs) that drive rhythmic motor output in the buccal ganglia. CBI interneuron-2 (CBI-2) makes monosynaptic connections onto buccal neurons, including premotor neurons B31/32 and B34 and motor neurons B61/62. Stimulating CBI-2 at a physiological firing frequency of 10 Hz for 30 sec causes these synapses to increase their EPSP amplitude by approximately 200%. This STE persists for nearly 2 min, during which time there is an increased cycle frequency of rhythmic ingestion buccal motor programs (iBMPs) elicited by CBI-2. This increase does not occur if the contralateral CBI-2 is trained and the test is performed with the ipsilateral CBI-2; therefore, the effect on motor programs only occurs in CBI-2 pathways in which STE is elicited. Furthermore, we find that STE elicited at CBI-2 buccal synapses permits iBMPs to be initiated at lower firing frequencies. Thus, STE of CBI-2 synapses appears to contribute to the initiation or modulation, or both, of buccal motor programs for rhythmic ingestion in Aplysia.
No takes yet. Share an insight, caveat, or question.
Sńchez et al. (2000) studied this question.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: