Who gets to play? Investigating equity in musical instrument instruction in Scottish primary schools

There is a widely held view that learning to play a musical instrument is a valuable experience for all children in terms of their personal growth and development. Although there is no statutory obligation for instrumental music provision in Scottish primary schools, there are well-established Instrumental Music Services in Local Education Authorities that have been developed to provide this facility for pupils. This article presents the findings of a study that was aimed at investigating the extent to which the opportunity to undertake instrumental instruction in Scottish primary schools is equitable. The study employed a mixed-methods approach. Data were gathered from 21 Scottish primary schools, a total pupil population of 5122 pupils of whom 323 pupils were receiving instrumental instruction. The analysis involved an investigation of the academic profile of this group, the representation of children with additional support needs (ASN) and the nature of their ASN. A qualitative analysis of policy and guideline documents and interviews with Heads of Instrumental Services, headteachers and instrumental instructors served to explain and illuminate the quantitative data. The findings showed that particular groups of children with ASN were significantly under-represented and offer explanations of the processes by which this occurs.

Molecular mechanisms controlling synaptic recruitment of GluA4 subunit-containing AMPAreceptors

Synaptic recruitment of AMPA receptors (AMPARs) represents a key postsynaptic mechanism driving functional development and maturation of glutamatergic synapses. At immature hippocampal synapses, PKA-driven synaptic insertion of GluA4 is the predominant mechanism for synaptic reinforcement. However, the physiological significance and molecular determinants of this developmentally restricted form of plasticity are not known. Here we show that PKA activation leads to insertion of GluA4 to synaptic sites with initially weak or silent AMPAR-mediated transmission. This effect depends on a novel mechanism involving the extreme C-terminal end of GluA4, which interacts with the membrane proximal region of the C-terminal domain to control GluA4 trafficking. In the absence of GluA4, strengthening of AMPAR-mediated transmission during postnatal development was significantly delayed. These data suggest that the GluA4-mediated activation of silent synapses is a critical mechanism facilitating the functional maturation of glutamatergic circuitry during the critical period of experience-dependent fine-tuning.