Life Style

Author: Lucia Vizziello
Date: 25/09/2012


It’s a widespread scientific knowledge that musical training leads to multiple functional changes in the brain, especially in the sensorimotor cortex. Musical experience, in fact, modifies the structural organization of the musician’s nervous system, through the multisensory stimulation of different cortical areas and their mutual connections. Playing and listening to music transmits visual, auditory and motor information to our brain, which in turn has a specific network for processing it, consisting in the frontotemporoparietal regions

“Playing a musical instrument requires a complex skill set that depends on the brain’s ability to quickly integrate information from multiple senses. It has been well documented that intensive musical training alters brain structure and function within and across multisensory brain regions, supporting the experience-dependent plasticity model. Here, we argue that this experience-dependent PLASTICITY occurs because of the multisensory nature of the brain and may be an important contributing factor to musical learning.”

("The multisensory brain and its ability to learn music, 2012")

Music performance is regarded as complex voluntary sensorimotor behavior that becomes automated during extensive practice with auditory feedback. It involves all motor, somatosensory, and auditory areas of the brain. Because of the life-long plasticity of neuronal connections, practicing a musical instrument results first in a temporary and later in a stable increase in the amount of nerve tissue devoted to various component tasks.


In neuroscience, synaptic plasticity is the ability of the connection, or synapse, between two neurons to change in strength in response to either use or disuse of transmission over synaptic pathways. Plastic change also results from the alteration of the number of receptors located on a synapse. There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters. Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon calcium. Since memories are postulated to be represented by vastly interconnected networks of synapses in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

Biochemical mechanism:

Two molecular mechanisms for synaptic plasticity (researched by the Eric Kandel laboratories) involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca2+ concentration and this has been linked to long term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely displaces the magnesium ions that block NMDA ion channels and allows calcium ions to enter a cell – probably causing LTP, while weaker depolarization only partially displaces the Mg2+ ions, resulting in less Ca2+ entering the post-synaptic neuron and lower intracellular Ca2+ concentrations (which activate protein phosphatases and induce long-term depression, LTD).

These activated protein kinases serve to phosphorylate post-synaptic excitatory receptors (e.g. AMPA receptor), improving cation conduction, and thereby potentiating the synapse. Also, this signals recruitment of additional receptors into the post-synaptic membrane, and stimulates the production of a modified receptor type, thereby facilitating an influx of calcium. This in turn increases post-synaptic excitation by a given pre-synaptic stimulus. This process can be reversed via the activity of protein phosphatases, which act to dephosphorylate these cation channels.
The second mechanism depends on a second messenger cascade regulating gene transcription and changes in the levels of key proteins at synapses such as CaMKII and PKAII. Activation of the second messenger pathway leads to increased levels of CaMKII and PKAII within the dendritic spine. These protein kinases have been linked to growth in dendritic spine volume and LTP processes such as the addition of AMPA receptors to the plasma membrane and phosphorylation of ion channels for enhanced permeability. Localization or compartmentalization of activated proteins occurs in the presence of their given stimulus which creates local effects in the dendritic spine. Calcium influx from NMDA receptors is necessary for the activation of CaMKII. This activation is localized to spines with focal stimulation and is inactivated before spreading to adjacent spines or the shaft, indicating an important mechanism of LTP in that particular changes in protein activation can be localized or compartmentalized to enhance the responsivity of single dendritic spines. Individual dendritic spines are capable of forming unique responses to presynaptic cells. This second mechanism can be triggered by protein phosphorylation but takes longer and lasts longer, providing the mechanism for long-lasting memory storage. The duration of the LTP can be regulated by breakdown of these second messengers. Phosphodiesterase, for example, breaks down the secondary messenger cAMP, which has been implicated in increased AMPA receptor synthesis in the post-synaptic neuron

Long-lasting changes in the efficacy of synaptic connections (long-term potentiation, or LTP) between two neurons can involve the making and breaking of synaptic contacts. Genes such as activin ß-A, which encodes a subunit of activin A, are up-regulated during early stage LTP. The activin molecule modulates the actin dynamics in dentritic spines through the MAP kinase pathway. By changing the F-actin cytoskeletal structure of dendritic spines, spines are lengthened and the chance that they make synaptic contacts with the axonal terminals of the presynaptic cell is increased. The end result is long term maintenance of LTP.

The number of ion channels on the post-synaptic membrane affects the strength of the synapse. Research suggests that the density of receptors on post-synaptic membranes changes, affecting the neuron’s excitability in response to stimuli. In a dynamic process that is maintained in equilibrium, N-methyl D-aspartate receptor (NMDA receptor) and AMPA receptors are added to the membrane by exocytosis and removed by endocytosis. These processes, and by extension the number of receptors on the membrane, can be altered by synaptic activity. Experiments have shown that AMPA receptors are delivered to the synapse through vesicular membrane fusion with the postsynaptic membrane via the protein kinase CaMKII, which is activated by the influx of calcium through NMDA receptors. CaMKII also improves AMPA ionic conductance through phosphorylation. When there is high-frequency NMDA receptor activation, there is an increase in the expression of a protein PSD-95 that increases synaptic capacity for AMPA receptors. This is what leads to a long-term increase in AMPA receptors and thus synaptic strength and plasticity.
If the strength of a synapse is only reinforced by stimulation or weakened by its lack, a positive feedback loop will develop, causing some cells never to fire and some to fire too much. But two regulatory forms of plasticity, called scaling and mataplasticity, also exist to provide negative feedback. Synaptic scaling is a primary mechanism by which a neuron is able to stabilize firing rates up or down.

Synaptic scaling serves to maintain the strengths of synapses relative to each other, lowering amplitudes of small excitatory postsynaptic potentials in response to continual excitation and raising them after prolonged blockage or inhibition. This effect occurs gradually over hours or days, by changing the numbers of NMDA receptors at the synapse (Pérez-Otaño and Ehlers, 2005). Metaplasticity varies the threshold level at which plasticity occurs, allowing integrated responses to synaptic activity spaced over time and preventing saturated states of LTP and LTD. Since LTP and LTD (long-terme depression) rely on the influx of Ca2+ through NMDA channels, metaplasticity may be due to changes in NMDA receptors, altered calcium buffering, altered states of kinases or phosphatases and a priming of protein synthesis machinery. Synaptic scaling is a primary mechanism by which a neuron to be selective to its varying inputs. The neuronal circuitry affected by LTP/LTD and modified by scaling and metaplasticity leads to reverberatory neural circuit development and regulation in a Hebbian manner which is manifested as memory, whereas the changes in neural circuitry, which begin at the level of the synapse, are an integral part in the ability of an organism to learn.
There is also a specificity element of biochemical interactions to create synaptic plasticity, namely the importance of location. Processes occur at microdomains – such as exocytosis of AMPA receptors is spatially regulated by the t-SNARE Stx4. Specificity is also an important aspect of CAMKII signaling involving nanodomain calcium. The spatial gradient of PKA between dendritic spines and shafts is also important for the strength and regulation of synaptic plasticity. It is important to remember that the biochemical mechanisms altering synaptic plasticity occur at the level of individual synapses of a neuron. Since the biochemical mechanisms are confined to these “microdomains,” the resulting synaptic plasticity affects only the specific synapse at which it took place.

("Synaptic plasticity - Wikipedia, the free encyclopedia")

Music Making as a Tool for Promoting Brain Plasticity across the Life Span

Skill learning offers a useful model for studying plasticity because it can be easily manipulated in an experimental setting. In particular, music making (e.g., learning to sing or to play a musical instrument) is an activity that is typically started early in life, while the brain is most sensitive to plastic changes, and is often continued throughout life by musicians. Furthermore, music making involves multiple sensory modalities and motor planning, preparation, and execution systems (Schlaug and others 2010).

("Music making as a tool for promoting brain pl... [Neuroscientist. 2010] - PubMed - NCBI")

The main evidences of this process are the seguent:

1. Learning to play a musical instrument in childhood can result in long-lasting changes in brain organization. The first study that examined neuroanatomical differences between musicians and nonmusicians reported larger anterior corpus callosum in musicians.

("Increased corpus callosum size in musicians. [Neuropsychologia. 1995] - PubMed - NCBI")

Corpus callosum differences in adults (musicians v. nonmusicians) and changes over time in children. The midsagittal slice of an adult musician (A) and nonmusician (B) shows a difference in the size of the anterior and midbody of the corpus callosum (see Schlaug and others 1995a). © The major subdivisions of the corpus callosum and locations of the interhemispheric fibers connecting the motor hand regions on the right and left hemisphere through the corpus callosum according to a scheme used by Hofer and Frahm (2006). Reprinted with permission from Elsevier. (D) Areas of significant difference in relative voxel size over 15 months comparing instrumental (n = 15) versus noninstrumental control children (n = 16) superimposed on an average image of all children (see also Hyde and others 2009). Interestingly, most changes over time were found in the midbody portion of the corpus callosum, representing parts of the corpus callosum that contain primary sensorimotor and premotor fibers.

2. Additional studies have also reported structural differences between musicians and nonmusicians in regions such as the planum temporale, or secondary auditory cortex. A pronounced leftward asymmetry of the planum temporale was linked to the ability to perceive absolute pitch.

3. Intensive musical training can also be associated with an expansion of functional representation of finger or hand maps. In string players, for example, the somatosensory representations of their playing fingers were found to be larger compared to those of nonmusicians

("Representational cortex in musicians. Plast... [Ann N Y Acad Sci. 2001] - PubMed - NCBI")

Brain surface renderings of a typical keyboard and string player. The central sulcus is marked with a white line. The portion of the precentral gyrus containing the configuration similar to that of the inverted Greek letter “omega” is found within the red circles. In the 2 examples, a prominent omega sign can be seen on the left more than the right in the keyboard player and only on the right in the string player. In Bangert and Schlaug (2006), we reported significantly more prominent omega signs in the right hemisphere of string players compared to the right hemisphere of nonmusicians and more prominent omega signs in the left hemisphere of keyboard players compared to the left hemispheres of both nonmusicians and string players. Reproduced from Bangert and Schlaug 2006, with permission of Oxford University Press.

4. Parallels between music and language suggest that musical training may lead to enhanced verbal abilities. Children with language disorders, in particular, may benefit from intensive musical training because of the overlapping responses to music and language stimuli in the brain. For instance, fMRI studies have reported activation of the Broca area during music perception tasks (Koelsch and others 2002).

Changes in the arcuate fasciculus after instrumental music training. The top row shows the right (green and red fibers represent the ventral and dorsal components of the arcuate fasciculus) and left (yellow and pink fibers represent the ventral and dorsal components of the arcuate fasciculus) arcuate fasciculus of an 8-year-old child without instrumental music training scanned twice (A and B) 2 years apart. Bottom row shows the right and left arcuate fasciculus of an 8-year-old child before© and 2 years after (D) instrumental music training involving a string instrument.

5. The effects of intensive training on the aging adult brain have been investigated by a handful of studies. For example, Sluming and others (2002) reported that practicing musicians have greater gray matter volume in the left inferior frontal gyrus compared to that of matched nonmusicians. For the nonmusicians, significant age-related reductions in total brain volumes and in regions such as the dorsolateral prefrontal cortex and the left inferior frontal gyrus were not observed in musicians. Thus, musicians appear to be less susceptible to age-related degenerations in the brain, such as Senile Dementia, presumably as a result of their daily musical activities.

Cerebral activation pattern of a rhythm discrimination task modulated by maturity and experience. Statistical parametric images superimposed onto a surface rendering of a standardized anatomical brain depict significant activations during a rhythmic discrimination task in a group of 5- to 7-year-old musically naïve children, adult nonmusicians, and adult musicians. The children showed prominent superior temporal gyrus activation on both sides. The adult groups show an extended pattern of activation involving polar and posterior planar regions of the superior temporal lobe as well as the parietal lobe (green circles), parts of the frontal lobe, in particular, the inferior frontal gyrus region (blue circles), and the cerebellum. Adult musicians differ from adult nonmusicians by having less activation of the primary auditory cortex but more activation of frontal regions bilaterally, particularly in the inferior frontal gyrus (blue circles). Reproduced from Bangert and Schlaug 2006, with permission of Oxford University Press.

The arcuate fasciculus, an auditory-motor tract, enhanced by music training. (A) The arcuate fasciculus of a healthy 65-year-old instrumental musician and (B) the arcuate fasciculus of a healthy 63-year-old nonmusician, otherwise matched with regard to their handedness, gender, and overall IQ. A comparison between both individuals shows that the musician has a larger arcuate fasciculus on the left as well as the right hemisphere than the nonmusician. Ongoing studies in our laboratory and other laboratories have shown evidence for structural plasticity of the arcuate fasciculus (Schlaug and others 2009) in individuals who undergo instrumental training or therapy using tasks that involve auditory-motor mapping, a task that musicians do throughout their life.

Shared brain resources of a music-motor imagery task and a mental calculation task. The functional magnetic resonance image on the left (A) shows significant activations of an fMRI experiment in which subjects were asked to imagine playing scales and short music phrases with their right hand compared to a visual imagery task of 4 objects. Contrasting motor imagery (MI) with visual imagery (VI) showed bilateral activations in the superior parietal lobe as well as around the intraparietal sulcus (IPS), medial superior precuneus region, premotor region, and the supplementary motor area (SMA). Significant activations are superimposed onto a standardized brain. The functional magnetic resonance images on the right (B) show the activation pattern of a mental subtraction task in which the subtraction task was contrasted with a letter-naming task (Chochon and others 1999). It is interesting to see the similarity in the activation pattern, in particular with regard to the parietal lobe activation. Reprinted from Chochon and others 1999, with permission of MIT Press Journals.

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