Exploring Neural Adaptations to Visual Stimuli
Aida Davila and Adam Kohn
(see article e2257232025)
Humans adapt to changing external environments and stimuli via adaptations that occur in sensory neurons. But how inputs to these neurons from external stimuli are distributed across the brain to support neuronal adaptation and sensory processing is not clear. Davila and Kohn explored sensory adaptation in this issue by probing how different sensory stimuli change visual cortex responses in macaque monkeys. They first assessed how neuronal activity in the visual cortex (V1) and area V2 changes with exposure to different textures. Both regions were responsive to textures, but V2 neurons were more sensitive. To explore whether the type of stimulus alters neuronal adaptations in these brain regions, the authors compared textures with random noise images. Again, responses occurred in both brain regions, but V2 neurons were less responsive to noise than texture images and adaptations were weaker with noise images in V2. These findings shed light on how image properties influence neural adaptations and may have broader implications for other sensory systems.
Representative image of a unilateral viral injection site in the VTA. Rabies-mediated monosynaptic labeling was used to map VTA neuron circuitry. See Jo et al. for more information.
Circuit-Level Insight on Symptoms of Withdrawal
Adrienne Y. Jo, Yihan Xie, Lisa M. Wooldridge, Sophie A. Rogers, Blake A. Kimmey et al.
(see article e1154242025)
The urge to find relief from unpleasant emotional states, or negative affect, associated with opioid withdrawal makes it difficult to abstain from opioid use. Identifying molecular treatment targets to diminish negative affect during withdrawal may prolong abstinence and effectively treat opioid addiction. But research on the circuits and mechanisms that underlie opioid withdrawal-induced negative affect is lacking. In this issue, Jo et al. explored whether a neuron population that contributes to opioid dependence undergoes maladaptive changes that drive unpleasant emotional states during withdrawal. Prolonged activation of μ-opioid receptor-expressing neurons in the ventral tegmental area (VTAMOR) of mice during opioid exposure altered how these neurons were structurally connected to other circuits. This led to altered reward processing and unpleasant emotional states. After inducing withdrawal following chronic opioid use, the researchers further revealed that VTAMOR neurons mediate social deficits associated with opioid withdrawal. Thus, it may be that long-term opioid use alters the connectivity of VTAMOR neuron circuits, which leads to negative affect and social deficits associated with withdrawal. According to the authors, by pointing to circuits with molecular targets that may alleviate the negative symptoms hindering abstinence, this work may inform treatment development.
Footnotes
This Week in The Journal was written by Paige McKeon
