Introduction A variety of homeostatic

Introduction A variety of homeostatic processes in the brain ensure optimal balances in key factors such as excitation/inhibition (E/I) balance, and neurotransmitter balance (Turrigiano, 2011). In contrast to some well-studied local cellular and molecular homeostatic mechanisms that can restore local adaptive balance, we know considerably less about the whole brain and neural systems level adaptive processes, and even less about their compensatory responses in the face of altered signal processing at the synapse. This gap in our knowledge may be critical given that common developmental disorders, such as autism and ADHD, are known to result from both intrinsic and environmental factors; in other words, the way a particular brain adapts during ontogeny to its individual social and physical environment. Furthermore, the way an environment is sampled and perceived early in life itself depends on the specific properties of the brain processing it. Thus, the “effective environment” experienced by some infants may be different simply due to their own particular neural processing limitations. In a recent paper we speculated that the diagnostic behavioral symptoms of autism are the result of processes of early life serine protease inhibitor in response to atypical neural signal processing, potentially at the synapse (Johnson et al., 2015). This sub-optimal quality signal processing may be caused by genetic or environmental effects, sensory limitations, or most often by combinations of factors. Nevertheless, the adaptive response of the developmental trajectory of the human brain will be similar, and the end result of this trajectory, we argued, is the autism diagnostic behavioral phenotype. From this perspective, the coherence of the clinical syndrome originates in the brain’s unitary response to different kinds of altered synaptic processing, possibly reflected in signal-to-noise ratio. We proposed that a series of compensatory and adaptive processes trigger an alternative trajectory of subsequent development, resulting in the majority of the behavioral phenotype associated with an autism diagnosis. By analogy, a single systemic adaptive response such as elevated body temperature (fever) can be triggered by many different causal factors (bacterial, viral, etc.). According to this view, autism should not be described as a disorder of neurodevelopment ; but rather as a perfectly ordered developmental response in the face of an unusual starting state.
Whole brain adaptation Processes in the brain can be observed at multiple levels of organization from molecular to cellular to large-scale systems. Within neuroscience, processes of adaptation have generally been studied at molecular and cellular levels, with less focus on how large-scale neural pathways and systems can compensate for either focal or diffuse disturbances. Two reasons for focusing on this ‘whole brain’ level of description of the nervous system are: (1) to fully understand processes of ontogenetic adaptation we need to consider the whole brain, where evidence shows that distant neural systems and regions can adjust to compensate for poor functioning or damage elsewhere, and (2) common developmental disorders are associated with widespread changes in the functioning of large-scale neural networks, even though these often have multiple different underlying molecular and cellular correlates (Johnson, 2015). Thus, in linking the brain to clinical diagnostic behaviors in developmental psychopathology we need to bridge our understanding with models of whole brain systems function and dysfunction. In parallel, while the concept of adaptation has had multiple definitions within developmental cognitive neuroscience, these have generally been taken to refer to neural processes or behaviors that are shaped by recurrent problems that faced ancestral populations (e.g., see Bjorklund, 2015). My use of the term is as applied to the restoration of a homeostatic balance after a perturbation in individual development; in other words, ontogenetic rather than phylogenetic adaptation.