Feed‐forward dendritic inhibition in rat hippocampal pyramidal cells studied in vitro

Abstract

Intracellular recordings from CA1 pyramidal cells in the rat hippocampal slice preparation were used to study the neuronal pathways involved in hippocampal synaptic inhibition. When direct comparisons are made in a single pyramidal cell, orthodromic stimulation delivered to stratum (s.) radiatum in normal recording conditions is found to be more effective then antidromic stimulation in producing inhibitory post-synaptic potentials (ipsp). Orthodromic ipsp in normal conditions appear to be complex, multiphasic events, whereas antidromic ipsp are relatively simple. The orthodromic ipsp involves both a GABA-mediated dendritic component and a non-GABA-mediated component neither of which is activated by antidromic stimulation. Barbiturates induce a late depolarizing phase of the orthodromic response, a depolarizing ipsp, which is mediated by GABA. The depolarizing ipsp is not produced by antidromic stimulation. Injections of tetrodotoxin and bicuculline methiodide localized to either somatic or apical dendritic regions reveal that the depolarizing ipsp is produced by GABA released from neuronal elements in the dendritic field which acts on pyramidal cell dendrites. The depolarizing ipsp is strongly temperature-dependent and increases in amplitude and duration progressively as slices are cooled from 37-22.degree. C. Depolarizing ipsp can be produced by orthodromic stimulation is s. oriens as well as in s. radiatum. In each case the depolarizing ipsp appear localized to the dendrites in the field stimulated. The depolarizing ipsp evident in the presence of barbiturates is caused by the same synaptic release of GABA which in normal conditions produces hyperpolarizing dendritic ipsp. Numerous comparisons between orthodromic and antidromic stimulation indicate that dendritic ipsp are activated by feed-forward pathways.