Dopaminergic modulation of spinal neurons in the lamprey: Network, cellular, and synaptic effects
Abstract
It has previously been shown that dopamine is present in cell bodies and processes in the lamprey spinal cord and that dopamine modulates fictive swimming (Neurosci. Lett., 166:23-26, 1994). To further investigate the actions of dopamine, the effects of dopaminergic agents were studied at several levels: in intact swimming lamprey, and on network, cellular, and synaptic properties in the isolated spinal cord. The experiments were done on adult sea lampreys (Petromyzon marinus) and adult silver lamprey (Ichthyomyzon unicuspis). Standard electrophysiological techniques were used for intra- and extracellular recordings. Video kinematic studies were performed using a Hi-8 video camera and analyzed using NIH ColorImage 1.32 software. Injection of the dopamine agonist apomorphine into intact adult sea lampreys decreased the cycle period of swimming, an effect similar to that of low concentrations ($<$10$\mu$M) of dopamine during fictive swimming. The D2 dopamine receptor antagonist sulpiride was able to completely block the effects of dopamine on fictive swimming while the D1 dopamine receptor antagonist SCH-23390 did not. Dopamine reduced the late after-spike hyperpolarization in motoneurons (MN), primary sensory dorsal cells (DC), stretch receptor edge cells (EC), and giant interneurons (GI) and increased the firing frequencies of MNs, ECs, and GIs in response to current injection. Calcium action potentials in MNs, DCs, and GIs, were reduced by dopamine, suggesting that reduced Ca$\sp{++}$ influx may lead to decreased activation of the Ca$\sp{++}$ activated K$\sp+$ current responsible for the late AHP. Poly- and monosynaptic inhibitory postsynaptic potentials in MNs elicited by stimulation of crossed axons were also reduced by dopamine. These results suggest that dopamine may modulate fictive swimming in lamprey via a D2 receptor, by altering Ca$\sp{++}$ influx, leading to changes in both the firing properties and synaptic strengths of spinal neurons. (Supported by NIH NS-28369 and MH-49581).
This paper has been withdrawn.