How to increase brain plasticity for language learning

Tue Jun 27 2023

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REOPENING CRITICAL PERIODS

A continuing question is whether the age-related changes in phonetic perception involve a full loss of sensitivity. Those consonant contrasts that show the most robust evidence of perceptual attunement in infancy—such as the English /r/-/l/ and the Hindi /d/-/D/—are the same ones that show the most resistance to training in adulthood. With systematic training, however, significant improvement on discrimination of nonnative contrasts can be induced (e.g., Bradlow et al. 1997, Lively et al. 1994, McCandliss et al. 2002), particularly when feedback is provided (Lively et al. 1994) or the training progresses from the easiest to the most difficult tokens (Ingvalson et al. 2012). Although training seldom leads to improvements to the level of native speakers (e.g., Bradlow et al. 1997), there are large individual differences in performance following training (McCandliss et al. 2002), with one predictor of success the thickness of white matter tracts in Heschl's gyrus in the left hemisphere (Golestani et al. 2007).

Animal models now indicate that the mature brain is intrinsically plastic and actively stabilized by a variety of brake-like factors in adult life (see Table 1). As a result, it is possible to reopen CP levels of plasticity by judicious lifting of these brakes. Two potent pathways by which to do this involve focused attention and epigenetics (turning on or off genes), both of which can reestablish the E-I balance necessary for opening plasticity (see sidebar for further details). In the past, we would have explained the improvements in nonnative speech perception in adults as evidence that the CP had never fully closed and/or that there was thus some residual plasticity. Today we can investigate an equally plausible explanation: The training regimens that are most effective work by activating biological processes that remove molecular brakes.

The action of neuromodulators (such as the serotonin and nicotinic acetylcholine receptor signaling onto particular GABA neurons) acutely regulates E-I balance (Lee et al. 2010), effectively disinhibiting the local circuitry to enable adult learning (Brown et al. 2012, Donato et al. 2013, Letzkus et al. 2011). In adult barn owls, active hunting can extend CP plasticity (Bergan et al. 2005). Video games are particularly potent in engaging attentional mechanisms, which can be leveraged for enhanced learning (Bavelier & Davidson 2013). Highly engaging learning situations similarly may be more effective in improving speech perception in adults.

Stimulation of the basal forebrain or vagus nerve raises neuromodulatory tone to produce CP plasticity in adult A1 (Engineer et al. 2011, Kilgard & Merzenich 1998) sufficient to correct a rodent model of tinnitus. In V1, the Lynx1 protein was further identified as a brake-like factor that actively suppresses adult plasticity (see sidebar) (Morishita et al. 2010). Genetic removal of Lynx1 or acetylcholinesterase inhibitor treatment of adult wild-type animals restores CP plasticity, enabling recovery from amblyopia in adulthood. Likewise, phase 2 clinical trials with SRIs are proceeding for the treatment of amblyopia, as these drugs were found to rescue amblyopia in a rodent model by acutely perturbing E-I balance, perhaps epigenetically (Maya Vetencourt et al. 2008, 2011). Interestingly, contemplative practices to focus attention may also achieve plasticity enhancement noninvasively by engaging neuromodulatory systems (Slagter et al. 2011) as well as by producing epigenetic changes (Kaliman et al. 2014). This is another area for future study.

Epigenetic signatures such as DNA methylation, histone acetylation, and phosphorylation accompany the closure of CPs (Putignano et al. 2007). Thus, treating adult rodents with HDAC inhibitors such as valproic acid alters preference to paired acoustic stimuli (Yang et al. 2012) or reopens plasticity and rescues amblyopia in V1 (Silingardi et al. 2010). The same valproic acid treatment of healthy young adult humans enables the acquisition of absolute pitch, again when trained concurrently (Gervain et al. 2013). Elimination of inhibitory synapses is a major component of adult visual plasticity (Takesian & Hensch 2013, van Versendaal et al. 2012).

As noted at the beginning of this review, language is one of the few complex cognitive systems for which CPs exist. This may have implications for when and whether training of speech sound discrimination can improve language use. To date, the improvements reported at the level of speech sound (phonetic) discrimination seldom generalize to new syllables or new speakers (Ingvalson et al. 2011). Moreover, even when nonnative phonetic sensitivities improve with training, deficits still exist in how well the retrained categories facilitate the recognition of words in continuous speech (e.g., Pallier et al. 1997). In animal model work, prolonged sensory deprivation (such as dark rearing or white noise in adulthood) has been shown to change the E-I balance and reopen plasticity (Duffy & Mitchell 2013, He et al. 2006, Zhou et al. 2011). It remains to be determined whether comparable manipulations would similarly reopen CPs in language acquisition, but it is a theoretical possibility. Moreover, since input at all levels of the language system—not just phonetic perception—would be removed, perhaps higher-level use of speech perception sensitivities would also improve.

CONCLUSIONS AND FUTURE DIRECTIONS

In summary, infants begin life with a set of perceptual biases, learning mechanisms, and neural systems that orients them to language, provides an initial foundation for categorization, and allows them to learn the properties of the native language. Infants become attuned to these properties in a sequential fashion, beginning with the most global prosodic characteristics of the native language and eventually reaching to detailed phonetic analysis. In at least some cases, the timing of attunement appears to be under maturational control, suggesting the operation of a critical or sensitive period. The perceptual attunement to native language characteristics supports acquisition of the relevant structures, for example, of cues to word order or of word-meaning mappings. Moreover, attunement of the properties at each tier enables more focused attention to the next level of specificity.

It is often claimed that because there is lifetime plasticity, CPs are moot—but that misses the point. There are biologically verifiable CPs beyond which the brain works hard to maintain stability. By understanding the processes that function to maintain stability (molecular brakes), we may figure out how to remove those brakes and reopen plasticity. The opening and closing of a CP is like opening and then locking a door. Once a key is turned or a combination set, the door is locked. However, if one has the key or knows the combination, the door can be unlocked. The exciting work in neurobiology over the past 15 years has shed light on how that unlocking is done (Takesian & Hensch 2013).

New advances have brought within reach a more objective mechanistic definition of CP timing as a consequence of maturational state. Future directions include the combination of animal models with human work, as illustrated above. For example, despite the long-postulated parallels of birdsong and human language acquisition (Doupe & Kuhl 1999), only recently has mechanistic work been done with respect to CPs (Balmer et al. 2009). In the barn owl system, incremental training is effective in producing cumulative large changes in auditory maps (Linkenhoker & Knudsen 2002).

In addition, one can now carefully examine human populations with molecular markers in mind (see Table 1). Methods borrowed from experimental neuroscience, such as serendipitous pharmacology or epigenetic profiling, can be applied to track the trajectory of human language acquisition. Notably, many mental illnesses that include language impairment—such as schizophrenia and autism—are of neurodevelopmental origin and share defects in the triggers and brakes that normally regulate CP timing (Gogolla et al. 2009, Insel 2010, Rubenstein & Merzenich 2003). Interventions to restore CP mistiming are starting to yield promising therapeutic strategies in animal models (Gogolla et al. 2014).

In summary, in this article we have reviewed recent work on CPs in speech perception development within the mechanistic framework of understanding how sensory CPs work at a biological level. We are hopeful that by bringing new insights from neuroscience to one of the longest-standing debates in the language acquisition field, we can move beyond old strictures to better position scientists and clinicians across fields to gain a deeper understanding of how language development unfolds and to implement more effective interventions when development goes awry.