Can Cell Therapy Restore Hearing Loss?

Post by Anastasia Sares

The takeaway

In an experimental cell therapy treatment, researchers transplanted young, immature auditory cells from the ears of newborn mice into older mice whose hearing had been damaged. These cells, surrounded by a new environment, matured and repaired the hearing of the older mice. 

What's the science?

Deep in the inner ear are cells called hair cells that are responsible for taking sound from the environment and turning it into electrical signals to be sent to the brain. These cells are attached to a membrane in the ear that vibrates with incoming sounds, and the movement of this membrane causes the cells to fire. However, as we age, hair cells experience significant wear and tear, and they are sensitive to insults like loud noise exposure, infections, and head trauma. There are even certain classes of drugs that can cause hair cells to die off as a side effect. Hair cells generally do not regenerate in adults, so when they die, it causes an irreversible loss in hearing. While there are some solutions for hair cell loss, such as cochlear implants, these all come with their own drawbacks.

Cell therapy is a kind of medical treatment that involves taking cells from one organism and transplanting them into another (or from one organ/tissue to another within the same organism). It includes treatments like bone marrow transplants and stem cell therapy. When trying to apply this kind of therapy to hearing loss, there are several challenges: will the transplanted cells develop into functioning hair cells? Will the procedure be too invasive and cause additional damage to the inner ear? Will the procedure result in significantly better hearing in the end?

This week in Neuroscience, Liu and colleagues showed that cells can be successfully transplanted into the inner ear and restore hearing function in mice that have drug-induced hearing loss.

How did they do it?

The authors first induced hearing loss in a group of adult mice by administering an antibiotic known to cause hair cell death (kanamycin). Then, relying on previous research, they extracted a very specific type of cell from the inner ears of newborn mice and grew these cells in a gel matrix, where the cells clumped together to form small “organoids” that were ready to become hair cells. They then injected these cells into the left inner ear of each adult mouse (with the right ear serving as a control).

To measure the mice’s hearing, the authors used the auditory brainstem response, which records electrical activity from the brainstem to measure how well the early auditory system responds to sound. They made these measurements before hearing loss, after hearing loss, and after cell therapy.

What did they find?

The authors confirmed that hair cells had died and that the adult mice’s hearing was severely impaired after being exposed to kanamycin. After cell therapy, hair cells survived the transplant and did not cause any additional hearing loss in the mice. The new cells were able to repopulate the inner ear, and hearing thresholds recovered substantially (though not completely) following the cell therapy.

What's the impact?

This study shows that it is possible to restore the function of hair cells and significantly improve hearing using cell therapy. Cell therapy may be a viable way to address the previously irreversible problem of hearing loss that affects millions of people worldwide.

Access the original scientific publication here.

Brain Rhythms Translate Empathy Into Prosocial Behavior

Post by Amanda Engstrom 

The takeaway

Orexin neurons in the anterior cingulate cortex generate theta oscillations that transform empathic perception into prosocial behavior, revealing a precise circuit linking emotional understanding to helpful behavior.

What's the science?

Empathy allows animals to perceive and share others’ emotional states and drives prosocial behaviors, which are essential for societal cohesion and well-being. In mice, empathy has been associated with changes in theta oscillations (slow, repeating electrical patterns that coordinate communication between brain regions) in the anterior cingulate cortex (ACC). The ACC has been suggested to be a “central hub” for empathy and prosocial behaviors, projecting into multiple brain regions involved in these complex behaviors. 

The neuropeptide orexin regulates arousal, stress, and emotional processing and promotes theta oscillations. However, it remains unclear what upstream circuits modulate these oscillations and how they influence empathy and prosocial behaviors. This week in Science, Kim and colleagues examine how orexin modulates ACC theta oscillations and their relationship to prosocial behaviors. 

How did they do it?

The authors evaluated empathy’s effects on prosocial behavior using an observational fear-conditioning paradigm (one mouse watches another receive a foot shock) combined with a consolation assay measuring allogrooming (the observer mouse grooming the foot-shocked mouse). They tested two paradigms: an experience-dependent observer (EXP), which had previously received a foot shock, and a naïve observer with no prior fear experience. They measured vicarious freezing (the observer mouse freezes at the tone when the experimental mouse receives the foot shock) and allogrooming in both groups and evaluated the impact of consolation on the shocked mouse using an open-field test. To dissect the neuronal mechanisms involved in these behaviors, the authors recorded ACC theta oscillations (5–7 Hz) during behavior. They conducted fiber photometry recordings using a genetically encoded orexin sensor (OxLight1), and using optogenetics, they inhibited ACC-projecting orexigenic circuits in observing mice only during the observation period when the experimental mouse received a foot shock. 

What did they find?

Both naïve and EXP observers exhibited vicarious freezing during observation and increased allogrooming after foot shock reunion. However, EXP mice displayed stronger vicarious freezing and more allogrooming compared to naïve mice. Self-grooming increased after observing the foot shock, but did not differ between groups. Notably, emphatic-like behaviors required visual attention - an observer mouse looking away during the foot shock showed no effects. Additionally, the authors found that the increased allogrooming by EXP observers resulted in less anxiety-like behavior in the mice that received the foot shock. Together, these data suggest that shared experiences enhance prosocial behaviors but don’t alter self-directed care.

To dissect the mechanism behind these behaviors, the authors show that both naïve and EXP observers have increased 5- to 7- Hz theta oscillations in the ACC while mice are observing the foot shock and during allogrooming (i.e. empathy and prosocial behavior), but not self-grooming. Concordantly, there was a selective increase in orexin activity at the same time, but only in EXP mice, suggesting that orexin-dependent increases require shared experience rather than observation alone. Inhibiting orexin input to the ACC specifically during the observation period reduced theta power and allogrooming in EXP mice and had no effect in naïve mice. These findings suggest that orexinergic inputs drive ACC theta oscillations to modulate affective empathy and prosocial action when there is shared experience.

What's the impact?

This study found that orexin-dependent increases in ACC theta oscillations link affective empathy to prosocial comforting behaviors. It demonstrates that social behavior relies on specific neuromodulatory rhythms to translate emotional experience into action. Elucidation of this upstream mechanism can provide potential targets for treating disorders that lead to empathy deficits. 

Access the original scientific publication here.

Practice Does Not Always Make Perfect: How Reward Timing Impacts Learning

Post by Annika Matthiesen 

The takeaway

This study challenges the idea that we learn faster just by repeating something more often. Instead, it shows that learning depends on timing, and even when rewarded events are spaced far apart, overall learning progresses at the same pace with fewer experiences.

What's the science?

Most theories of reward learning in neuroscience argue that the learning rate is a flexible parameter with no fixed rule, and that dopamine signals whether something is better or worse than expected. However, psychology has shown that learning can improve when experiences are spread out over time, though no clear biological rule has been established.

This week in Nature Neuroscience, Burke and colleagues sought to understand how learning rates vary under different conditions.

How did they do it?

The authors trained several groups of mice to associate a sound cue with a drop of sugar water, varying the waiting period in between trials by tenfold. They measured learning by tracking anticipatory licking and monitored dopamine release in the nucleus accumbens, a key reward-related brain region, using a dopamine-sensitive virus and an implanted lens. Comparing across groups, they identified a relationship between reward spacing and learning and used mathematical models to predict both behavior and dopamine response. To test their mathematical model, they also tracked learning using partial reinforcement, giving rewards on only some trials to increase the time between rewards, keeping cue frequency the same. In addition, they examined reward omission trials, where an expected reward was withheld, to test whether dopamine signals changed when rewards were unexpectedly absent.

What did they find?

The researchers found that learning rate depends on the time between rewards, not just how often a cue and reward are paired. When rewards were spaced farther apart, animals learned more from each reward and needed fewer trials to form the association. However, the proposed mathematical learning rate prediction model did not fully hold at the most extreme condition, where rewards were separated by a very long interval. Even so, the researchers showed that the timing rule held under partial reinforcement, where rewards were delivered only some of the time, further confirming that learning scales with the interval between rewards. Additionally, dopamine signals followed the same pattern as behavior, and the emergence of dopamine responses to reward omission occurred much later than cue responses, challenging traditional reinforcement learning models. Overall, the findings reveal a fundamental timing-based rule that governs how the brain updates associations during reward learning.

What's the impact?

This study is the first to show that learning rate follows rules based on the time between cue–reward experiences, rather than simply increasing with repetition. In simpler terms, learning depends not just on practice, but on how that practice is timed. Practice alone does not make perfect, and carefully spaced timing may be key to more effective learning, reshaping how we think about education and habit formation.

Access the original scientific publication here.