A major question in neuroscience is to understand how the brain processes social information. A predominant source of information necessary for social recognition is encoded by olfactory and pheromonal signals. The detection of these signals by neuronal populations in the nose and the formation of a memory based on the recognition of these signals play a key role in many social behaviors ranging from feeding, aggression and fear, to reproductive physiology. But, what are the mechanisms by which olfactory stimuli generate their effects on emotion and behavior? Advances in uncovering the molecular mechanism leading to the detection of socially relevant cues by the olfactory system, their influence on innate behavior and reproduction, and the dissection of neural circuits underlying chemosensory induced modulation of social behaviors have set the stage to begin to explore this question. New clues regarding the general structural and functional organization of the mammalian olfactory system have been revealed using multidisciplinary approaches in which investigations at the genetic and molecular level have been combined with cellular and systems level analyses. We now know that the mammalian olfactory system is composed of a number of subsystems, which make distinct neural connections to regions in the olfactory bulb. They can be distinguished by the receptors they express and the signaling mechanisms they employ to detect and transduce chemosensory stimuli. Interrupting the information flow at the primary transduction pathway of odor detection will give rise to various behavioral deficits. Recently, we have used gene targeting to examine the role of the sodium channel Nav1.7 and the G protein Gαo in mouse olfactory function. Both tissue-specific gene deletions cause severe disruptions in olfactory sensing. In the absence of Nav1.7, olfactory neurons are still electrically active and generate odor-evoked action potentials but fail to initiate synaptic signaling causing a total inability to sense odors. More partial deficits, but not less dramatic, are induced in a mouse line carrying the tissue-specific disruption of the Gαo gene. This G protein is essential for the signal transduction in a subpopulation of vomeronasal sensory neurons (VSNs), leading to alterations in membrane potential and calcium entry in these neurons. The cellular Gαo phenotypes are accompanied by striking alterations in aggressive behavior indicating that Gαo is a critical requirement for the neural coding of chemosensory cues that promote aggressive interactions in both male and female mice. The disruptions in sensory detection may help us to decipher the effect of particular chemosensory cues on modulating social behaviors and neural circuits underlying olfactory processing in the brain. As expected by the existence of the different olfactory subsystems, olfactory sensory signals follow distinct neural pathways in the brain. Whereas some signals are relayed through the primary olfactory cortex to higher cortical areas, other signals are transmitted via the amygdala to the hypothalamus and related regions. Currently, new genetic models are being developed with which neural circuits in the brain can be unequivocally identified and targeted. Socially important chemosensory cues have been shown to converge onto a small subset of neurons that produce gonadotropin-releasing hormone (GnRH). We therefore started to investigate the properties of the downstream target cells expressing the GnRH receptor (GnRHR) to ultimately help us in investigating neural circuits involved in olfactory-encoded behaviors.