Rather than just a relay station to detect smells, the olfactory bulb (OB) may dynamically modulate odor processing according to experience (Wu, Yu, and Komiyama, 2020). In fact, all layers in the feedforward neural circuit of the OB show some plasticity level. Olfactory conditioning increases the number of activated glomerulus (Abraham et al., 2014) and their size (Jones et al., 2008). Passive and recurrent experience with the same odor reduces mitral cell (MC) activity over time, and this plasticity is odor-specific and recoverable (Kato et al., 2012). Odor discrimination can be modulated up and down by the respective activation and inactivation of granule cells (GC) (Gschwend et al., 2015), the primary source of lateral inhibition in the OB (Shepherd et al., 2007).

An additional component of OB’s plasticity is the continuous resource of adult-born periglomerular (PG) and GC (Lemasson, Saghatelyan and Lledo, 2005; Brann and Firestein, 2014). Young adult-born PG cells refine their connectivity and response accordingly to experienced odors (Livneh and Mizrahi, 2012). The odor discrimination (Breton-Provencher et al., 2009) and memory (Alonso et al., 2012) are affected by adult-born GCs plasticity. After the olfactory experience, these same cells direct their apical spines to MC, which in turn attracts GC by releasing brain-derived neurotrophic factor (BDNF) (Breton-Provencher et al., 2016).

BDNF is produced from the proteolytic cleavage of pro-BDNF (Nagappan et al., 2009, Nagappan, et al., 2009, Pang, et al., 2016). However, in neuronal cells, both proteins are biologically active. Their release is triggered by the membrane depolarization (Kuczewski et al., 2009) in a ratio determined by physiological conditions (Nagappan et al., 2009, Nagappan, et al., 2009). Pro-BDNF dictates neuronal fate through activation of neurotrophin receptor (p75NTR) (Bamji et al., 1998), while BDNF regulates plasticity, in general improving synaptic transmission through TrkB (tropomyosin-related kinase B) receptor activation (Tyler e Pozzo-Miller, 2001; Rauti et al., 2020).

OB may be a promising target for BDNF actions. BDNF strengthens synapses in the OB (Estévez, Defterali and Vicario, 2022), increases the excitability of MC (Mast and Fadool, 2012) and modulates olfaction-dependent behaviors (Ricci et al., 2018; Hern, Pimentel-farfan and Peña-ortega, 2022). For instance, transgenic mice with decreased BDNF production do not spontaneously discriminate between odorants (Bath et al., 2008) and inhibition of TrkB receptors into the OB impaired the consolidation of odor-rewarded associative memory (Tong et al., 2018).

One type of memory particularly involved with OB functioning is the hippocampus-dependent social recognition memory (SRM) (Pena, et al., 2014, Lüscher Dias et al., 2016, Salimi et al., 2022), which enables the identification of conspecifics by their olfactory signature (Noack et al., 2010). SRM processing strongly relies on neurogenesis and plasticity in the OB (Pena, et al., 2014, Almeida-Santos et al., 2019, Guarnieri et al., 2020). Therefore, in the present study, we tested the hypothesis that SRM is modulated by BDNF-dependent signaling in the OB.