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GABAergic and dopaminergic influences in the cortex have been found to be inhibitory and predominantly inhibitory, respectively. Activation of GABAB receptors produces slow IPSPs with long duration while postsynaptic activation of GABAA receptors evokes fast IPSPs with an increase in Cl- conductance. GABAB-mediated slow (late) IPSPs accompanied by an increase in K+ conductance build up very slowly and continue to develop for more than 500 ms in cat cerebral cortical neurons. Suppression of cortical IPSPs by GABAB antagonists is suggested to be involved in postsynaptic events. Our study, however, elucidated that GABAB receptor antagonists CGP35348 and phaclofen shortened the transcallosal response latency of cat motor cortical neurons predominantly presynaptically. Shortening of the latency by postsynaptic mechanism was also observed in some neurons. On the other hand, iontophoretic dopamine (DA) application reduced the action potentials. The complex DAergic modulation is known to be mediated by D1 and D2 receptors positively and negatively coupled to adenylate cyclase, respectively. The inhibitory effect of DA on EPSCs via both D1 and D2 receptors has already been reported. Recently, the presence of DA receptor in presynaptic terminals has been suggested. However, our experiments elucidated that D1 antagonists SCH23390 (SCH) and D2 antagonists sulpiride (SUL) and haloperidol (HAL) facilitated the transcallosal activity on cat motor neurons by blocking the suppressive effect of DA but did not change the response latency.

Achatin-I, a neuropeptide isolated from the ganglia of Achatina fulica Ferussac, was proposed as an excitatory neurotransmitter and neuromodulator for A. fulica neurons (Kamatani et al. 1989; Kim et al. 1991; Liu and Takeuchi 1993). This peptide induced an inward current (Iin) on the giant neuron type, periodically oscillating neuron (PON). This Iin was found to be Na2+-dependent and is mediated by the cyclic AMP-PKA and calmodulin systems (Kim et al. 1991; Emaduddin et al. 1996). It was also found that some histamine H1 receptor antagonists inhibited this Iin (Santos et al. 1995). This paper, which is a part of studies on the characterization of Iin induced by achatin-I on PON, describes the suppressing effects of some H1 receptor antagonists and their analogues on this current. Their structure-activity relationship was also elucidated.