The intricate connectivity patterns of neural circuits support a wide repertoire of communication processes and functional interactions. Here we systematically investigate how neural signaling is constrained by anatomical connectivity in the mesoscale Drosophila (fruit fly) brain network. We use a spreading model that describes how local perturbations, such as external stimuli, trigger global signaling cascades that spread through the network. Through a series of simple biological scenarios we demonstrate that anatomical embedding potentiates sensory-motor integration. We find that signal spreading is faster from nodes associated with sensory transduction (sensors) to nodes associated with motor output (effectors). Signal propagation was accelerated if sensor nodes were activated simultaneously, suggesting a topologically mediated synergy among sensors. In addition, the organization of the network increases the likelihood of convergence of multiple cascades towards effector nodes, thereby facilitating integration prior to motor output. Moreover, effector nodes tend to coactivate more frequently than other pairs of nodes, suggesting an anatomically enhanced coordination of motor output. Altogether, our results show that the organization of the mesoscale Drosophila connectome imparts privileged, behaviorally relevant communication patterns among sensors and effectors, shaping their capacity to collectively integrate information.

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Deficits in auditory nerve (AN) function for older adults reduce afferent input to the cortex. The extent to which the cortex in older adults adapts to this loss of afferent input and the mechanisms underlying this adaptation are not well understood. We took a neural systems approach measuring AN and cortical evoked responses within 50 older and 27 younger human adults (59 female) to estimate central gain or increased cortical activity despite reduced AN activity. Relative to younger adults, older adults' AN response amplitudes were smaller, but cortical responses were not. We used the relationship between AN and cortical response amplitudes in younger adults to predict cortical response amplitudes for older adults from their AN responses. Central gain in older adults was thus defined as the difference between their observed cortical responses and those predicted from the parameter estimates of younger adults. In older adults, decreased afferent input contributed to lower cortical GABA levels, greater central gain, and poorer speech recognition in noise (SIN). These effects on SIN occur in addition to, and independent from, effects attributed to elevated hearing thresholds. Our results are consistent with animal models of central gain and suggest that reduced AN afferent input in some older adults may result in changes in cortical encoding and inhibitory neurotransmission, which contribute to reduced SIN. An advancement in our understanding of the changes that occur throughout the auditory system in response to the gradual loss of input with increasing age may provide potential therapeutic targets for intervention.

There is great interest in developing non‐invasive approaches for studying cortical plasticity in humans. High‐frequency presentation of auditory and visual stimuli, or sensory tetanisation, can induce long‐term‐potentiation‐like (LTP‐like) changes in cortical activity. However, contrasting effects across studies suggest that sensory tetanisation may be unreliable. We review these contrasting effects, conduct our own study of auditory and visual tetanisation, and perform meta‐analyses to determine the average effect of sensory tetanisation across studies. We measured auditory‐evoked amplitude changes in a group of younger (18–29 years of age) and older (55–83 years of age) adults following tetanisation to 1 and 4 kHz tone bursts and following a slow‐presentation control. We also measured visual‐evoked amplitude changes following tetanisation to horizontal and vertical sign gradients. Auditory and visual response amplitudes decreased following tetanisation, consistent with some studies but contrasting with others finding amplitude increases (i.e. LTP‐like changes). Older adults exhibited more modest auditory‐evoked amplitude decreases, but visual‐evoked amplitude decreases like those of younger adults. Changes in response amplitude were not specific to tetanised stimuli. Importantly, slow presentation of auditory tone bursts produced response amplitude changes approximating those observed following tetanisation in younger adults. Meta‐analyses of visual and auditory tetanisation studies found that the overall effect of sensory tetanisation was not significant across studies or study sites. The results suggest that sensory tetanisation may not produce reliable changes in cortical responses and more work is needed to determine the validity of sensory tetanisation as a method for inducing human cortical plasticity in vivo.

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