The membrane potential of cat hippocampal neurons recorded in vivo displays four different reaction-mechanisms to iontophoretically applied transmitter agonists.

Intracellular recordings were obtained in vivo from cat hippocampal pyramidal cells and cells in deeper layers of the hippocampal formation. Five transmitter agonists were applied to these cells by microiontophoresis. Glutamate caused depolarizations with fast onset and decay, fastest reaction times being within hundreds of msec of the beginning and the of the application. These depolarizations were accompanied by a decrease of the apparent input resistance (AIR) and an increase of the mean firing rate. Carbachol, a cholinergic agonist, caused depolarizations with slow onset and decay, reaction times were in the range of tens of seconds. The depolarizations were also accompanied by an increase in the mean firing rate. These effects are thought to be muscarinic. gamma-Aminobutyric acid elicited fast hyperpolarizations, a decrease of the AIR, mean firing rate and occasionally of the amplitude of action potentials (APs). Dopamine and norepinephrine hyperpolarized the membrane potential relatively fast, reaction times being within seconds, and reduced the mean firing rate, but this was accompanied by a marked increase of the AIR, of the size of the remaining APs and fimbria-evoked EPSPs. Inhibitory slow depolarizations of the type seen in an earlier study with dopamine in the caudate were not seen on pyramidal cells and only very rarely on non-identified cells of the deeper layers. These results indicate a partially tissue-specific effect of dopamine compared to that on caudate cells.