Cross-Cultural Adaptation, Reliability and Validity of the Short Version of the Parenting Styles and Dimensions Questionnaire (PSDQ) for Spanish Populations.

The development of the mammalian brain is a highly orchestrated process, governed by the interplay of extrinsic signalling cues and intrinsic genetic programs that shape neural circuits and establish precise connectivity patterns [–]. Among these signalling cues, neurotrophins —particularly brain-derived neurotrophic factor (BDNF)— are master regulators of neuronal differentiation, survival, and connectivity maturation across brain regions [–]. BDNF exerts its effects via tropomyosin-receptor kinase B (TrkB), activating the mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and phospholipase C-gamma (PLCγ) pathways []. These cascades target nuclear and cytoskeletal elements, driving gene expression and structural remodelling, essential for excitatory and inhibitory neuron maturation. This balance is critical for circuit functionality []. Disruptions in this equilibrium are implicated in neurodevelopmental and psychiatric disorders []. BDNF’s influence spans development, from neurogenesis [, ] to synaptic refinement in adolescence and adulthood []. In cortical and hippocampal glutamatergic neurons, BDNF enhances spine formation and synaptic plasticity by upregulating cytoskeletal proteins (MAP2, PSD-95) and immediate-early genes (IEGs; e.g., , ) [, ]. In GABAergic neurons, including cortical interneurons and striatal medium spiny neurons (MSNs), BDNF regulates dendritic arborization and inhibitory synapse formation [, , ]. The striatum, where GABAergic MSNs constitute more than 90% of the neuronal population, is a main hub integrating corticostriatal inputs for motor, reward, and habit functions. This brain area relies on BDNF, mainly secreted from corticostriatal projections, for proper MSNs branching and dendritic spine formation [–]. In vitro and genetic deletion studies revealed differential BDNF dependency: glutamatergic pyramidal neurons show no changes in their dendrites [], while GABAergic populations—especially MSNs—exhibit pronounced impairments in dendritic complexity and growth [, –], suggesting region- and cell-specific signalling modulation. BDNF also modulates activity-dependent Methyl-CpG-binding protein 2 (MeCP2) phosphorylation [], which is a key regulator of the development of several brain areas [, ], including the striatum []. However, the signalling pathways mediating MeCP2 phosphorylation may differ between brain areas: in the cortex and hippocampus, it relies on calcium/calmodulin-dependent protein kinases (CaMKs) [, ], whereas in the striatum, the BDNF-dependent pathway controlling MeCP2 activation remains unexplored. Interestingly, MAPK/ERK alterations, linked to anxiety and addiction [, ], are also related to autism spectrum disorders (ASDs) and Rett Syndrome [, , ], neurodevelopmental disorders associated with both BDNF and MeCP2 dysfunction [, ].