Soft robotics: a bioinspired evolution in robotics.

Maltreatment-related childhood adversity is the leading preventable risk factor for mental illness and substance abuse. Although the association between maltreatment and psychopathology is compelling, there is a pressing need to understand how maltreatment increases the risk of psychiatric disorders. Emerging evidence suggests that maltreatment alters trajectories of brain development to affect sensory systems, network architecture and circuits involved in threat detection, emotional regulation and reward anticipation. This Review explores whether these alterations reflect toxic effects of early-life stress or potentially adaptive modifications, the relationship between psychopathology and brain changes, and the distinction between resilience, susceptibility and compensation.

The effects of childhood maltreatment on brain structure, function and connectivity

Adolescence as a Sensitive Period of Brain Development

Mapping of Brain Activity by Automated Volume Analysis of Immediate Early Genes

Autism is a complex neurodevelopmental condition, and little is known about its neurobiology Much of autism research has focused on the social, communication and cognitive difficulties associated with the condition However, the recent revision of the diagnostic criteria for autism has brought another key domain of autistic experience into focus: sensory processing Here, we review the properties of sensory processing in autism and discuss recent computational and neurobiological insights arising from attention to these behaviours We argue that sensory traits have important implications for the development of animal and computational models of the condition Finally, we consider how difficulties in sensory processing may relate to the other domains of behaviour that characterize autism

Sensory perception in autism

The potency of the environment to shape brain function changes dramatically across the lifespan. Neural circuits exhibit profound plasticity during early life and are later stabilized. A focus on the cellular and molecular bases of these developmental trajectories has begun to unravel mechanisms, which control the onset and closure of such critical periods. Two important concepts have emerged from the study of critical periods in the visual cortex: (1) excitatory-inhibitory circuit balance is a trigger; and (2) molecular "brakes" limit adult plasticity. The onset of the critical period is determined by the maturation of specific GABA circuits. Targeting these circuits using pharmacological or genetic approaches can trigger premature onset or induce a delay. These manipulations are so powerful that animals of identical chronological age may be at the peak, before, or past their plastic window. Thus, critical period timing per se is plastic. Conversely, one of the outcomes of normal development is to stabilize the neural networks initially sculpted by experience. Rather than being passively lost, the brain's intrinsic potential for plasticity is actively dampened. This is demonstrated by the late expression of brake-like factors, which reversibly limit excessive circuit rewiring beyond a critical period. Interestingly, many of these plasticity regulators are found in the extracellular milieu. Understanding why so many regulators exist, how they interact and, ultimately, how to lift them in noninvasive ways may hold the key to novel therapies and lifelong learning.

Balancing Plasticity/Stability Across Brain Development

Sensory Integration in Mouse Insular Cortex Reflects GABA Circuit Maturation

Cortical sensory maps are remodeled during early life to adapt to the surrounding environment. Both sensory and contextual signals are important for induction of this plasticity, but how these signals converge to sculpt developing thalamocortical circuits remains largely unknown. Here we show that layer 1 (L1) of primary auditory cortex (A1) is a key hub where neuromodulatory and topographically organized thalamic inputs meet to tune the cortical layers below. Inhibitory interneurons in L1 send narrowly descending projections to differentially modulate thalamic drive to pyramidal and parvalbumin-expressing (PV) cells in L4, creating brief windows of intracolumnar activation. Silencing of L1 (but not VIP-expressing) cells abolishes map plasticity during the tonotopic critical period. Developmental transitions in nicotinic acetylcholine receptor (nAChR) sensitivity in these cells caused by Lynx1 protein can be overridden to extend critical-period closure. Notably, thalamocortical maps in L1 are themselves stable, and serve as a scaffold for cortical plasticity throughout life.

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Inhibitory circuit gating of auditory critical-period plasticity.

All-Optical Electrophysiology Reveals the Role of Lateral Inhibition in Sensory Processing in Cortical Layer 1.

Inhibitory neurotransmission is a critical determinant of neuronal network gain and dynamic range, suggesting that network properties are shaped by activity during development. A previous study demonstrated that sensorineural hearing loss (SNHL) in gerbils leads to smaller inhibitory potentials in L2/3 pyramidal neurons in the thalamorecipient auditory cortex, ACx. Here, we explored the mechanisms that account for proper maturation of γ-amino butyric acid (GABA)ergic transmission. SNHL was induced at postnatal day (P) 10, and whole-cell voltage-clamp recordings were obtained from layer 2/3 pyramidal neurons in thalamocortical slices at P16–19. SNHL led to an increase in the frequency of GABAzine-sensitive (antagonist) spontaneous (s) and miniature (m) inhibitory postsynaptic currents (IPSCs), accompanied by diminished amplitudes and longer durations. Consistent with this, the amplitudes of minimum-evoked IPSCs were also reduced while their durations were longer. The α1- and β2/3 subunit–specific agonists zolpidem and loreclezole increased control but not SNHL sIPSC durations. To test whether SNHL affected the maturation of GABAergic transmission, sIPSCs were recorded at P10. These sIPSCs resembled the long SNHL sIPSCs. Furthermore, zolpidem and loreclezole were ineffective in increasing their durations. Together, these data strongly suggest that the presynaptic release properties and expression of key postsynaptic GABAA receptor subunits are coregulated by hearing.

Anne E. Takesian

Papers

Balancing Plasticity/Stability Across Brain Development

Sensory Integration in Mouse Insular Cortex Reflects GABA Circuit Maturation

Inhibitory circuit gating of auditory critical-period plasticity.

All-Optical Electrophysiology Reveals the Role of Lateral Inhibition in Sensory Processing in Cortical Layer 1.

Hearing Loss Prevents the Maturation of GABAergic Transmission in the Auditory Cortex