Trifid Mandibular Condyle: Case Report and Current Review of the Literature.

Trifid mandibular condyle (TMC) is a rare anatomical variation characterized by the duplication of the mandibular condyle. The aim of this study is to report a new case of a 26-year-old female patient with a left TMC and to review the current existing literature on TMC, the relevant cases, etiology, symptoms and different treatment modalities. The database engines PubMed, EMBASE, Scopus, Web of science, Scientific Electronic Library Online, Cochrane and CINAHL were searched for TMC cases from inception until April of 2022. Only 13 previous cases of TMC were found. Although it is a rare anatomical entity, TMC is increasingly being detected due to more advanced imaging techniques, especially computed tomography (CT), cone beam CT (CBCT) and magnetic resonance imaging (MRI) emerging in the field of dentistry. The etiology and pathogenesis of TMC and its relationship with TMD are still unclear. Further studies and follow-up may help to better understand this anatomic variant and possible interactions with local pathologies.

Activation of EphB2 Forward Signaling Enhances Memory Consolidation.

EphB2 is involved in enhancing synaptic transmission and gene expression. To explore the roles of EphB2 in memory formation and enhancement, we used a photoactivatable EphB2 (optoEphB2) to activate EphB2 forward signaling in pyramidal neurons in lateral amygdala (LA). Photoactivation of optoEphB2 during fear conditioning, but not minutes afterward, enhanced long-term, but not short-term, auditory fear conditioning. Photoactivation of optoEphB2 during fear conditioning led to activation of the cAMP/Ca2+ responsive element binding (CREB) protein. Application of light to a kinase-dead optoEphB2 in LA did not lead to enhancement of long-term fear conditioning memory or to activation of CREB. Long-term, but not short-term, auditory fear conditioning memory was impaired in mice lacking EphB2 forward signaling (EphB2lacZ/lacZ). Activation of optoEphB2 in LA of EphB2lacZ/lacZ mice enhanced long-term fear conditioning memory. The present findings show that the level of EphB2 forward signaling activity during learning determines the strength of long-term memory consolidation.

The roles of Eph receptors in contextual fear conditioning memory formation.

Eph receptors regulate glutamate receptors functions, neuronal morphology and synaptic plasticity, cellular events believed to be involved in memory formation. In this study we aim to explore the roles of Eph receptors in learning and memory. Toward that end, we examined the roles of EphB2 and EphA4 receptors, key regulators of synaptic functions, in fear conditioning memory formation. We show that mice lacking EphB2 (EphB2(-/-)) are impaired in short- and long-term contextual fear conditioning memory. Mice that express a carboxy-terminally truncated form of EphB2 that lacks forward signaling, instead of the full EphB2, are impaired in long-term, but not short-term, contextual fear conditioning memory. Long-term contextual fear conditioning memory is attenuated in CaMKII-cre;EphA4(lx/-) mice where EphA4 is removed from all pyramidal neurons of the forebrain. Mutant mice with targeted kinase-dead EphA4 (EphA4(KD)) exhibit intact long-term contextual fear conditioning memory showing that EphA4 kinase-mediated forward signaling is not needed for contextual fear memory formation. The ability to form long-term conditioned taste aversion (CTA) memory is not impaired in the EphB2(-/-) and CaMKII-cre;EphA4(lx/-) mice. We conclude that EphB2 forward signaling is required for long-term contextual fear conditioning memory formation. In contrast, EphB2 mediates short-term contextual fear conditioning memory formation in a forward signaling-independent manner. EphA4 mediates long-term contextual fear conditioning memory formation in a kinase-independent manner.