Hippocampal-evoked feedforward inhibition in the nucleus accumbens

Samantha L. Scudder, Corey Baimel, Emma E. Macdonald, Adam G. Carter

Research output: Contribution to journalArticlepeer-review


The nucleus accumbens (NAc) is critical for motivated behavior and is rewired following exposure to drugs of abuse. Medium spiny neurons (MSNs) in the NAc express either D1 or D2 receptors and project to distinct downstream targets. Differential activation of these MSNs depends on both excitation from long-range inputs and inhibition via the local circuit. Assessing how long-range excitatory inputs engage inhibitory circuitry is therefore important for understanding NAc function. Here, we use slice electrophysiology and optogenetics to study ventral hippocampal (vHPC)-evoked feedforward inhibition in the NAc of male and female mice. We find that vHPC-evoked excitation is stronger at D1+ than D1-MSNs, whereas inhibition is unbiased at the two cell types. vHPC inputs contact both parvalbumin-positive (PV+) and somatostatin-positive (SOM+) interneurons, but PV+ cells are preferentially activated. Moreover, suppressing PV+ interneurons indicates they are primarily responsible for vHPC-evoked inhibition. Finally, repeated cocaine exposure alters the excitation of D1+ and D1-MSNs, without concomitant changes to inhibition, shifting the excitation/inhibition balance. Together, our results highlight the contributions of multiple interneuron populations to feedforward inhibition in the NAc. Moreover, they demonstrate that inhibition provides a stable backdrop on which drug-evoked changes to excitation occur within this circuit.

Original languageEnglish (US)
Pages (from-to)9091-9104
Number of pages14
JournalJournal of Neuroscience
Issue number42
StatePublished - Oct 17 2018


  • Cocaine
  • Feedforward inhibition
  • Interneuron
  • Medium spiny neuron
  • Nucleus accumbens
  • Synaptic transmission

ASJC Scopus subject areas

  • General Neuroscience


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