LRIPs from LEC produced strong inhibitory postsynaptic potentials in a large fraction of CA1 interneurons located in the region of the EC inputs. Although pharmacogenetic silencing of LRIPs in hippocampus did not prevent CFC or NOR memory, it caused mice to show an inappropriate fear response to a neutral context and a diminished ability to distinguish a novel object from a familiar object. Calcium imaging revealed that the LRIP axons and presynaptic terminals responded to various sensory stimuli. Moreover, pairing such signals with appetitive or aversive stimuli increased LRIP activity, consistent with a role of the LRIPs in memory specificity. Intracellular recordings demonstrated that the LRIPs powerfully suppressed the activity of a subclass of cholecystokinin-expressing interneurons (CCK INs). These interneurons were normally strongly excited by the CA3 inputs, which results in pronounced feedforward inhibition (FFI) of CA1 pyramidal neuron dendrites.

Causal terminology is often introduced in the interpretation of encoding and decoding models trained on neuroimaging data. In this article, we investigate which causal statements are warranted and which ones are not supported by empirical evidence. We argue that the distinction between encoding and decoding models is not sufficient for this purpose: relevant features in encoding and decoding models carry a different meaning in stimulus- and in response-based experimental paradigms. We show that only encoding models in the stimulus-based setting support unambiguous causal interpretations. By combining encoding and decoding models trained on the same data, however, we obtain insights into causal relations beyond those that are implied by each individual model type. We illustrate the empirical relevance of our theoretical findings on EEG data recorded during a visuo-motor learning task.