Afferent projections to the different medial amygdala subdivisions: a retrograde tracing study in the mouse

Cádiz-Moretti, Bernardita; Otero-García, Marcos; Martínez‐Garciá, Fernando; Lanuza, Enrique

doi:10.1007/s00429-014-0954-y

Cited by 80 publications

(65 citation statements)

References 138 publications

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“…We then quantified c-Fos-ir specifically within MeA tdTomato + (MeA Kiss ) neurons in response to urine exposure and observed raised c-Fos levels in MeA Kiss neurons throughout the MeA, but this was most significant in the MeApd. Our data are supported by anatomical tracing studies that show the AOB provides dense input to all three MeA subdivisions [34], but neurons sensitive to volatile molecules which induce reproductive neuroendocrine effects (oestrous induction, puberty acceleration or delay) terminate principally in the MeApd [35, 36]. Reciprocal connections between MeApd MeA Kiss neurons and the anterior AOB have been identified previously [14], suggesting that these neurons are directly targeted by pheromonal pathways but also may feedback to the AOB.…”

Section: Discussionsupporting

confidence: 81%

Medial Amygdala Kiss1 Neurons Mediate Female Pheromone Stimulation of Luteinizing Hormone in Male Mice

et al. 2018

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Background/Aims: The medial amygdala (MeA) responds to olfactory stimuli and alters reproductive physiology. However, the neuronal circuit that relays signals from the MeA to the reproductive axis remains poorly defined. This study aimed to test whether MeA kisspeptin (MeA^Kiss) neurons in male mice are sensitive to sexually relevant olfactory stimuli and transmit signals to alter reproductive physiology. We also investigated whether MeA^Kiss neurons have the capacity to elaborate glutamate and GABA neurotransmitters and potentially contribute to reproductive axis regulation. Methods: Using female urine as a pheromone stimulus, MeA^Kiss neuronal activity was analysed and serum luteinizing hormone (LH) was measured in male mice. Next, using a chemogenetic approach, MeA^Kiss neurons were bi-directionally modulated to measure the effect on serum LH and evaluate the activation of the preoptic area. Lastly, using in situ hybridization, we identified the proportion of MeA^Kiss neurons that express markers for GABAergic (Vgat) and glutamatergic (Vglut2) neurotransmission. Results: Male mice exposed to female urine showed a two-fold increase in the number of c-Fos-positive MeA^Kiss neurons concomitant with raised LH. Chemogenetic activation of MeA^Kiss neurons significantly increased LH in the absence of urine exposure, whereas inhibition of MeA^Kiss neurons did not alter LH. In situ hybridization revealed that MeA^Kiss neurons are a mixed neuronal population in which 71% express Vgat mRNA, 29% express Vglut2 mRNA, and 6% express both. Conclusions: Our results uncover, for the first time, that MeA^Kiss neurons process sexually relevant olfactory signals to influence reproductive hormone levels in male mice, likely through a complex interplay of neuropeptide and neurotransmitter signalling.

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Section: Discussionsupporting

confidence: 81%

Medial Amygdala Kiss1 Neurons Mediate Female Pheromone Stimulation of Luteinizing Hormone in Male Mice

et al. 2018

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“…One recent study in rats obtained restricted injections in the CxA (Pro-Sistiaga et al, 2007), but reported only the resulting labeling in the olfactory bulbs. In mice, our laboratory has previously reported the projections from the CxA to the ventral striatum, using both anterograde and retrograde tracing (Novejarque et al, 2011), as well as the connections with the vomeronasal amygdala (medial nucleus: Pardo-Bellver et al, 2012; Cadiz-Moretti et al, 2016; and posteromedial cortical nucleus: Gutierrez-Castellanos et al, 2014). It is important to note that most of the previous neuroanatomical works did not differentiate between the Pir and the CxA, and it is necessary to study their descriptions and illustrations to assign the observed labeling in the ventral part of the Pir (at the appropriate rostrocaudal levels) to what we considered now is the CxA according to the ChAT labeling ( Figure 1 ) and the atlas of Paxinos and Franklin (2004).…”

Section: Discussionmentioning

confidence: 99%

Afferent and Efferent Connections of the Cortex-Amygdala Transition Zone in Mice

et al. 2016

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The transitional zone between the ventral part of the piriform cortex and the anterior cortical nucleus of the amygdala, named the cortex-amygdala transition zone (CxA), shows two differential features that allow its identification as a particular structure. First, it receives dense cholinergic and dopaminergic innervations as compared to the adjacent piriform cortex and amygdala, and second, it receives projections from the main and accessory olfactory bulbs. In this work we have studied the pattern of afferent and efferent projections of the CxA, which are mainly unknown, by using the retrograde tracer Fluorogold and the anterograde tracer biotinylated dextranamine. The results show that the CxA receives a relatively restricted set of intratelencephalic connections, originated mainly by the olfactory system and basal forebrain, with minor afferents from the amygdala. The only relevant extratelencephalic afference originates in the ventral tegmental area (VTA). The efferent projections of the CxA reciprocate the inputs from the piriform cortex and olfactory amygdala. In addition, the CxA projects densely to the basolateral amygdaloid nucleus and the olfactory tubercle. The extratelencephalic projections of the CxA are very scarce, and target mainly hypothalamic structures. The pattern of connections of the CxA suggests that it is indeed a transitional area between the piriform cortex and the cortical amygdala. Double labeling with choline acetyltransferase indicates that the afferent projection from the basal forebrain is the origin of its distinctive cholinergic innervation, and double labeling with dopamine transporter shows that the projection from the VTA is the source of dopaminergic innervation. These connectivity and neurochemical features, together with the fact that it receives vomeronasal in addition to olfactory information, suggest that the CxA may be involved in processing olfactory information endowed with relevant biological meaning, such as odors related to reproductive or defensive behaviors.

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“…6C). CNO effects last several hours (Alexander et al, 2009) so administration of CNO 1 h before footshock does not allow discrimination between effects at the stages of acquisition and initial encoding of fear memory or its consolidation over the next few hours. To address this issue, we injected a separate cohort of MeA hM4Di-expressing PTH2R-Cre mice with CNO immediately after footshock (within 3-4 min).…”

Section: Inhibition Of Mea Pth2r Neurons At the Time Of Footshock Enhmentioning

confidence: 99%

Incubation of Fear Is Regulated by TIP39 Peptide Signaling in the Medial Nucleus of the Amygdala

et al. 2015

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Fear-related psychopathologies such as post-traumatic stress disorder are characterized by impaired extinction of fearful memories. Recent behavioral evidence suggests that the neuropeptide tuberoinfundibular peptide of 39 residues (TIP39), via its receptor, the parathyroid hormone 2 receptor (PTH2R), modulates fear memory. Here we examined the anatomical and cellular localization of TIP39 signaling that contributes to the increase in fear memory over time following a traumatic event, called fear memory incubation. Contextual freezing, a behavioral sign of fear memory, was significantly greater in PTH2R knock-out than wild-type male mice 2 and 4 weeks after a 2 s 1.5 mA footshock. PTH2R knock-out mice had significantly reduced c-Fos activation in the medial amygdala (MeA) following both footshock and fear recall, but had normal activation in the hypothalamic paraventricular nucleus and the amygdalar central nucleus compared with wild-type. We therefore investigated the contribution of MeA TIP39 signaling to fear incubation. Similar to the effect of global TIP39 signaling loss, blockade of TIP39 signaling in the MeA by lentivirus-mediated expression of a secreted PTH2R antagonist augmented fear incubation. Ablation of MeA PTH2R-expressing neurons also strengthened the fear incubation effect. Using the designer receptor exclusively activated by designer drug pharmacogenetic approach, transient inhibition of MeA PTH2R-expressing neurons before or immediately after the footshock, but not at the time of fear recall, enhanced fear incubation. Collectively, the findings demonstrate that TIP39 signaling within the MeA at the time of an aversive event regulates the increase over time in fear associated with the event context.

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Afferent projections to the different medial amygdala subdivisions: a retrograde tracing study in the mouse

Cited by 80 publications

References 138 publications

Medial Amygdala <b><i>Kiss1</i></b> Neurons Mediate Female Pheromone Stimulation of Luteinizing Hormone in Male Mice

Medial Amygdala <b><i>Kiss1</i></b> Neurons Mediate Female Pheromone Stimulation of Luteinizing Hormone in Male Mice

Afferent and Efferent Connections of the Cortex-Amygdala Transition Zone in Mice

Incubation of Fear Is Regulated by TIP39 Peptide Signaling in the Medial Nucleus of the Amygdala

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