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The firing rate of the mitral/tufted cells in the olfactory bulb is known to undergo significant trial-to-trial variability and is affected by anesthesia. Here we ask whether odorant-elicited changes in firing rate depend on the rate before application of the stimulus in the awake and anesthetized mouse. We find that prestimulus firing rate varies widely on a trial-to-trial basis and that the stimulus-induced change in firing rate decreases with increasing prestimulus firing rate. Interestingly, this prestimulus firing rate dependence was different when the behavioral task did not involve detecting the valence of the stimulus. Finally, when the animal was learning to associate the odor with reward, the prestimulus firing rate was smaller for false alarms compared with correct rejections, suggesting that intrinsic activity reflects the anticipatory status of the animal. Thus, in this sensory modality, changes in behavioral status alter the intrinsic prestimulus activity, leading to a change in the responsiveness of the second-order neurons. We speculate that this trial-to-trial variability in odorant responses reflects sampling of the massive parallel input by subsets of mitral cells. [ABSTRACT FROM AUTHOR]

Studies in different sensory systems indicate that short spike patterns within a spike train that carry items of sensory information can be extracted from the overall train by using field potential oscillations as a reference (Kayser et al., 2012; Panzeri et al., 2014). Here we test the hypothesis that the local field potential (LFP) provides the temporal reference frame needed to differentiate between odors regardless of associated outcome. Experiments were performed in the olfactory system of the mouse (Mus musculus) where the mitral/tufted (M/T) cell spike rate develops differential responses to rewarded and unrewarded odors as the animal learns to associate one of the odors with a reward in a go-no go behavioral task. We found that coherence of spiking in M/T cells with the Y LFP (65 to 95 Hz) differentiates between odors regardless of the associated behavioral outcome of odor presentation. [ABSTRACT FROM AUTHOR]

Sensory neuron input to the olfactory bulb (OB) was activated precisely for different durations with blue light in mice expressing channelrhodopsin-2 in olfactory sensory neurons. Behaviorally the mice discriminated differences of 10 ms in duration of direct glomer-ular activation. In addition, a subset of mitral/tufted cells in the OB of awake mice responded tonically therefore conveying information on stimulus duration. Our study provides evidence that duration of the input to glomeruli not synchronized to sniffing is detected. This potent cue may be used to obtain information on puffs in odor plumes. [ABSTRACT FROM AUTHOR]

Growing evidence suggests that the main olfactory epithelium contains a subset of olfactory sensory neurons (OSNs) responding to pheromones. One candidate subpopulation expresses the calcium activated cation channel TRPM5 (transient receptor potential channel M5). Using GFP driven by the TRPM5 promoter in mice, we show that this subpopulation responds to putative pheromones, urine, and major histocompatibility complex peptides, but not to regular odors or a pheromone detected by other species. In addition, this subpopulation of TRPM5-GFP+ OSNs uses novel transduction. In regular OSNs, odorants elicit activation of the cyclic nucleotide-gated (CNG) channel, leading to Ca2+ gating of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2+-activated Cl- ANO2 (anoctamin 2) channel is not expressed, and pheromones elicit activation of the CNG channel leading to Ca2+ gating of TRPM5. In conclusion, we show that OSNs expressing TRPM5 respond to pheromones, but not to regular odors through the opening of CNG channels leading to Ca2+ gating of TRPM5. [ABSTRACT FROM AUTHOR]

It is believed that odor transduction in the mammalian main olfactory system only involves the cAMP-signaling pathway. Here, we report on odor responsiveness in mice with a disrupted cyclic nucleotide-gated (CNG) channel subunit A2. Several odorants, including putative pheromones, can be detected and discriminated by these mice behaviorally. These odors elicit responses in the olfactory epithelium, main olfactory bulb, and olfactory (piriform) cortex of CNGA2 knock-out mice. In addition, responses to odors detected by CNGA2 knock-out mice are relatively insensitive to inhibitors of the cAMP pathway. These results provide strong evidence that cAMP-independent pathways in the main olfactory system of mammals participate in detecting a subset of odors. [ABSTRACT FROM AUTHOR]

Learning and memory requires coordinated activity between different regions of the brain. Here we studied the interaction between infralimbic medial prefrontal cortex (mPFC) and hippocampal dorsal CA1 during associative odorant discrimination learning in the mouse. We found that as the animal learns to discriminate odorants in a go-no go task, the coupling of high frequency neural oscillations to the phase of theta oscillations (theta-referenced phase-amplitude coupling or tPAC) changes in a manner that results in divergence between rewarded and unrewarded odorant-elicited changes in the theta-phase referenced power (tPRP) for beta and gamma oscillations. In addition, in the proficient animal there was a decrease in the coordinated oscillatory activity between CA1 and mPFC in the presence of the unrewarded odorant. Furthermore, the changes in tPAC resulted in a marked increase in the accuracy for decoding contextual odorant identity from tPRP when the animal became proficient. Finally, we studied the role of Ca 2+ /calmodulin-dependent protein kinase II α (CaMKIIα), a protein involved in learning and memory, in oscillatory neural processing in this task. We find that the accuracy for decoding the contextual odorant identity from tPRP decreases in CaMKIIα knockout mice and that this accuracy correlates with behavioral performance. These results implicate a role for tPAC and CaMKIIα in olfactory go-no go associative learning in the hippocampal-prefrontal circuit. Significance statement Coupling of neural oscillations within and between hippocampal CA1 and medial prefrontal cortex (mPFC) is involved in spatial learning and memory, but the role of oscillation coupling for other learning tasks is not well understood. Here we performed local field potential recording in CA1 and mPFC in mice learning to differentiate rewarded from unrewarded odorants in an associative learning task. We find that odorant-elicited changes in the power of bursts of gamma oscillations at distinct phases of theta oscillations become divergent as the animal becomes proficient allowing decoding of contextual odorant identity. Finally, we find that the accuracy to decode contextual odorant identity decreases in mice deficient for the expression of Ca 2+ /calmodulin-dependent protein kinase II α, a protein involved in synaptic plasticity., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2022 Ramirez-Gordillo et al.)

Fragile X syndrome (FXS) is a neurodevelopmental disorder (NDD) characterized by intellectual disability, autism spectrum disorders (ASDs), and anxiety disorders. The disruption in the function of the FMR1 gene results in a range of alterations in cellular and synaptic function. Previous studies have identified dynamic alterations in inhibitory neurotransmission in early postnatal development in the amygdala of the mouse model of FXS. However, little is known about how these changes alter microcircuit development and plasticity in the lateral amygdala (LA). Using whole-cell patch clamp electrophysiology, we demonstrate that principal neurons (PNs) in the LA exhibit hyperexcitability with a concomitant increase in the synaptic strength of excitatory synapses in the BLA. Further, reduced feed-forward inhibition appears to enhance synaptic plasticity in the FXS amygdala. These results demonstrate that plasticity is enhanced in the amygdala of the juvenile Fmr1 knock-out (KO) mouse and that E/I imbalance may underpin anxiety disorders commonly seen in FXS and ASDs., (Copyright © 2021 Svalina et al.)

Studies in different sensory systems indicate that short spike patterns within a spike train that carry items of sensory information can be extracted from the overall train by using field potential oscillations as a reference (Kayser et al., 2012; Panzeri et al., 2014). Here we test the hypothesis that the local field potential (LFP) provides the temporal reference frame needed to differentiate between odors regardless of associated outcome. Experiments were performed in the olfactory system of the mouse (Mus musculus) where the mitral/tufted (M/T) cell spike rate develops differential responses to rewarded and unrewarded odors as the animal learns to associate one of the odors with a reward in a go-no go behavioral task. We found that coherence of spiking in M/T cells with the ϒ LFP (65 to 95 Hz) differentiates between odors regardless of the associated behavioral outcome of odor presentation., (Copyright © 2015 the authors 0270-6474/15/355808-15$15.00/0.)

Sensory neuron input to the olfactory bulb (OB) was activated precisely for different durations with blue light in mice expressing channelrhodopsin-2 in olfactory sensory neurons. Behaviorally the mice discriminated differences of 10 ms in duration of direct glomerular activation. In addition, a subset of mitral/tufted cells in the OB of awake mice responded tonically therefore conveying information on stimulus duration. Our study provides evidence that duration of the input to glomeruli not synchronized to sniffing is detected. This potent cue may be used to obtain information on puffs in odor plumes., (Copyright © 2014 the authors 0270-6474/14/3416058-07$15.00/0.)

Growing evidence suggests that the main olfactory epithelium contains a subset of olfactory sensory neurons (OSNs) responding to pheromones. One candidate subpopulation expresses the calcium activated cation channel TRPM5 (transient receptor potential channel M5). Using GFP driven by the TRPM5 promoter in mice, we show that this subpopulation responds to putative pheromones, urine, and major histocompatibility complex peptides, but not to regular odors or a pheromone detected by other species. In addition, this subpopulation of TRPM5-GFP+ OSNs uses novel transduction. In regular OSNs, odorants elicit activation of the cyclic nucleotide-gated (CNG) channel, leading to Ca2+ gating of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2+ -activated Cl- ANO2 (anoctamin 2) channel is not expressed, and pheromones elicit activation of the CNG channel leading to Ca2+ gating of TRPM5. In conclusion, we show that OSNs expressing TRPM5 respond to pheromones, but not to regular odors through the opening of CNG channels leading to Ca2+ gating of TRPM5.

It is believed that odor transduction in the mammalian main olfactory system only involves the cAMP-signaling pathway. Here, we report on odor responsiveness in mice with a disrupted cyclic nucleotide-gated (CNG) channel subunit A2. Several odorants, including putative pheromones, can be detected and discriminated by these mice behaviorally. These odors elicit responses in the olfactory epithelium, main olfactory bulb, and olfactory (piriform) cortex of CNGA2 knock-out mice. In addition, responses to odors detected by CNGA2 knock-out mice are relatively insensitive to inhibitors of the cAMP pathway. These results provide strong evidence that cAMP-independent pathways in the main olfactory system of mammals participate in detecting a subset of odors.