The expression of behavioural adaptive responses to stress is proposed to reflect an important evolutionary principle by which individuals are able to maintain stable behaviour or display behaviour that meets environmental demands as a function of their available internal resources. The degree to which individuals can meet the continuing challenge between stressors and available internal resources depends on a complex interplay among environmental load, experience, and cognitive capacity. The organism's ability to display situation-appropriate responses and downregulate stress is argued to reflect processes of adaptation. These processes of adaptation actively contribute to resilience and psychological well-being by enabling the organism to deal better with comparable stressful situations in the future (McEwen Reference McEwen1998). In fact, Kalisch et al. propose that a cognitive positive appraisal style serves as a protecting factor against the damaging effects of stress and promotes resilience and well-being.

The degree to which an individual can adopt a cognitive positive appraisal style is arguably determined by the flexibility of the central nervous system for maintaining internal bodily homeostasis. In particular, the dynamic range of changes as a result of context-related demands is known as brain plasticity, and it provides a neurobiological basis for the individual's ability to generate, select, and execute situation-appropriate behavioural (coping) strategies. More specifically, the up- and downregulation of cortical excitability levels reflect an important aspect of brain plasticity that is considered fundamental to humans' ability to adapt and anticipate to their surroundings on the basis of experience (Lourenco & Casey Reference Lourenco and Casey2013). Long-term potentiation and long-term depression, also known as input- and synapse-specific Hebbian plasticity, have been identified as basic neurobiological principles by which cortical excitability and synaptic signal transmission can be respectively enhanced or reduced (Barrionuevo et al. Reference Barrionuevo, Schottler and Lynch1980; Lømo Reference Lømo1966; Pascual-Leone et al. 1998).

The modulation of neuronal excitability levels arguably depends on an intricate balance between excitatory (glutamatergic) and inhibitory (GABAergic) circuits (Lui & Lachamp Reference Lui and Lachamp2006). In general, increased cortical excitability has been linked to greater plasticity and being beneficial to adaptive behaviour, whereas enhanced inhibition of cortical excitability levels has been associated with impaired plasticity and behavioural impairments (Johnston Reference Johnston2009). Importantly, however, the regulation of the balance between inhibitory and excitatory systems keeps neural circuits within a functional range (Whitt et al. Reference Whitt, Petrus and Lee2013). This regulatory process is called homeostatic plasticity and satisfies two necessary conditions for successful adaptation, namely stability and variability, and prevents states of excessive neuronal hypo- and hyperexcitability (Bienenstock et al. Reference Bienenstock, Cooper and Munro1982; Quartarone et al. Reference Quartarone, Siebner and Rothwell2006).

A typical example of an organism's adaptive response to stress is the fight–flight response, which, among many other physiological reactions, includes activation of the hypothalamus-pituitary-adrenal cortex (HPA) axis and the release of the hormone cortisol. Several studies have found that cortisol negatively affects brain plasticity by influencing the inhibitory system (Milani et al. Reference Milani, Piu, Popa, Della Volpe, Bonifazi, Rossi and Mazzocchio2010; Sale et al. Reference Sale, Ridding and Nordstrom2008). In a paired associative stimulation (PAS) study in which peripheral nerve stimulation is combined with transcranial magnetic stimulation of the cerebral cortex to elevate neural excitability levels, it was shown that the administration of cortisol in healthy volunteers interferes with PAS-induced increases in cortical excitability (Sale et al. Reference Sale, Ridding and Nordstrom2008). The observed reductions in cortical excitability were interpreted as effects caused by increased inhibitory activity, which, at first glance, seems at odds with more-recent findings showing that cortisol administration increases cortical excitability levels (Milani et al. Reference Milani, Piu, Popa, Della Volpe, Bonifazi, Rossi and Mazzocchio2010). In the latter study, cortisol administration reduced intracortical inhibition and was interpreted as a cortisol-driven decrease in GABAergic activity (Milani et al. Reference Milani, Piu, Popa, Della Volpe, Bonifazi, Rossi and Mazzocchio2010).

This paradoxical finding can be explained by homeostatic plasticity: Cortisol administration increases cortical excitability, but when combined with another excitatory intervention, such as PAS, the effects of cortisol become inhibitory to prevent cortical hyperexcitability (cf. Siebner et al. Reference Siebner, Lang, Rizzo, Nitsche, Paulus, Lemon and Rothwell2004). Furthermore, it is possible that cortisol promotes brain plasticity acutely but has a disruptive effect when circulating levels are chronically elevated. How these temporal effects exactly translate to the behavioural domain remains an open question. Nonetheless, in agreement with Kalisch et al., homeostatic plasticity plays an important role for keeping the brain in a functional range in response to stress. Homeostatic plasticity thus provides a protective physiological mechanism, which promotes psychological resilience by allowing a certain amount of variability on top of stability.

Because abnormalities of inhibitory circuits and cortical plasticity have been repeatedly demonstrated in patients with depression (Bajbouj et al. Reference Bajbouj, Lisanby, Lang, Danker-Hopfe, Heuser and Neu2006; Player et al. Reference Player, Taylor, Weickert, Alonzo, Sachdev, Martin, Mitchell and Loo2013), impaired homeostatic plasticity in response to stress can provide an account, at least in part, for the relation between lowered psychological resilience and presence of depressive symptoms. More indirect support comes from a study showing a positive association between neuroticism and reduced intracortical inhibition in healthy volunteers (Wassermann Reference Wassermann, Greenberg, Nguyen and Murphy2001). These reductions may hint at an imbalance between inhibitory and excitatory circuits and provide a neurobiological basis for suboptimal coping strategies due to cortical hyperexcitability. That neuroticism is characterized by a lack of cognitive positive appraisal style and a susceptibility to experiencing anxiety and depression concurs with the inverse relation between neuroticism and psychological resilience (Campbell-Sills et al. Reference Campbell-Sills, Cohan and Stein2006). Moreover, in stressful conditions, neurotic individuals tend to display a limited amount of coping strategies or reside in stereotypical responses that were successful on prior occasions (Parkes Reference Parkes1986). As brain plasticity in healthy individuals is a mechanism for initiating a more dynamical range of situation-appropriate coping behaviours, such maladaptive behavioural response patterns arguably are due to aberrant brain plasticity.

In this commentary, we have introduced homeostatic plasticity as a candidate neurobiological mechanism to explain the psychological effects of cognitive positive appraisal style on well-being. Suboptimal forms of homeostatic plasticity are argued to more easily lead to a dysfunctional imbalance between the inhibitory and excitatory cortical circuits that undermines behavioural flexibility and lowers psychological resilience. In addition to complementing the model of Kalisch and colleagues, homeostatic plasticity may further help set the physiological boundaries for studying the psychological mechanisms of resilience.