Altered gating of K<sub>v</sub>1.4 in the nucleus accumbens suppresses motivation for reward.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31487241.
- Also identified by DOI 10.7554/eLife.47870 and PMC identifier 6728144.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Deficient motivation contributes to numerous psychiatric disorders, including withdrawal from drug use, depression, schizophrenia, and others. Nucleus accumbens (NAc) has been implicated in motivated behavior, but it remains unclear whether motivational drive is linked to discrete neurobiological mechanisms within the NAc. To examine this, we profiled cohorts of Sprague-Dawley rats in a test of motivation to consume sucrose. We found that substantial variability in willingness to exert effort for reward was not associated with operant responding under low-effort conditions or stress levels. Instead, effort-based motivation was mirrored by a divergent NAc shell transcriptome with differential regulation at potassium and dopamine signaling genes. Functionally, motivation was inversely related to excitability of NAc principal neurons. Furthermore, neuronal and behavioral outputs associated with low motivation were linked to faster inactivation of a voltage-gated potassium channel, K<sub>v</sub>1.4. These results raise the prospect of targeting K<sub>v</sub>1.4 gating in psychiatric conditions associated with motivational dysfunction.
Medical subject headings
- Kv1.4 Potassium Channel
- Motivation
- Neurons
- Nucleus Accumbens
- Reward