Synaptic plasticity in the direct feedback pathway of the electrosensory lateral line lobe of Apteronotus leptorhynchus.

• Main Author: Wang, Daliang.
• Other Authors: Maler, Leonard
• Format: Thesis
• Language: unknown
• Published: University of Ottawa (Canada) 1997
• Subjects: Biology; Neuroscience; DML
• Online Access: http://hdl.handle.net/10393/4176; https://doi.org/10.20381/ruor-13619

The electrosensory lateral line lobe (ELL) of Apteronotus Leptorhynchus is a good model for study of structure-function correlations. The ELL is a rhombencephalic laminated structure and pyramidal cells, the major projection neurons, have their somata in the pyramidal cell layer; their somatic dendrites in the same layer receive inhibitory input from interneurons; their basal dendrites extending to the deep neuropil layer receive input from primary afferents; the pyramidal cell apical dendrites go up to the molecular layer where direct feedback pathway from the nucleus preeminentialis dorsalis (Pd) contact the proximal part of the dendrites in the ventral molecular layer (VML) and an indirect feedback pathway from the Pd through the eminentia granularis posterior (EGP) form synapses with the distal part of the dendrites in the dorsal molecular layer (DML). The direct feedback pathway is involved in regulation of the pyramidal cell responses. However, the neurotransmitter utilized in this pathway is not known and the synaptic plasticity remains unexplored. Immunocytochemical techniques at both light and electron microscope levels and electrophysiology combined with pharmacological interventions have been employed to address these issues. Immunocytochemistry showed that the primary afferent fibers to ELL, pyramidal cell and both feedback pathways to the VML and DML of ELL used glutamate as a neurotransmitter. Pharmaco-electrophysiological results demonstrate that at the direct feedback fiber-pyramidal cell synapses in VML there was a posttetanic potentiation (PTP), which is blocked by $\rm Ca\sp{2+}$-calmodulin dependent protein kinase II (CaMKII) antagonist KN-62 applied focally in VML. Postsynaptic application of KN-62 or CaMKII inhibitory peptide did not block PTP in VML indicating that KN-62 blockade of PTP in VML may be presynaptic. There was also a PTP at the indirect feedback fiber-pyramidal synapses in DML but it was not sensitive to KN-62; Although it has been shown that protein phosphorylation contributes to PTP in some preparations, protein phosphatase antagonists calyculin A and FK-520 failed to enhance PTP in VML. I have also shown that long-term changes (long-term potentiation, LTP and long-term depression, LTD) were not inducible by tetanic stimulation of TSF, even at different stimulation frequencies. They could not be induced even with GABA antagonism. When the tetanization of TSF was paired with postsynaptic hyperpolarization a potentiated excitatory response was induced in VML that lasted for about 15 min while the tetanization paired with depolarization did not produce any significant changes in response. It is concluded that PTP regulation in different sets of synapses is different. In the direct feedback fiber-pyramidal cell synapse PTP is regulated by CaMKII while at the indirect feedback pathway-pyramidal synapse in DML PTP is not; long-term plasticity may not be induced even in glutamatergic synapses with NMDA receptors indicating that long-term changes may require other key factor(s); a novel synaptic plasticity exists in the direct feedback pathway and may regulate sensory processing.