Posterior Amygdala Research Articles

The multi-stage plasticity in the aggression circuit underlying the winner effect.

Winning increases the readiness to attack and the probability of winning, a widespread phenomenon known as the "winner effect." Here, we reveal a transition from target-specific to generalized aggression enhancement over 10days of winning in male mice. This behavioral change is supported by three causally linked plasticity events in the ventrolateral part of the ventromedial hypothalamus (VMHvl), a critical node for aggression. Over 10days of winning, VMHvl cells experience monotonic potentiation of long-range excitatory inputs, transient local connectivity strengthening, and a delayed excitability increase. Optogenetically coactivating the posterior amygdala (PA) terminals and VMHvl cells potentiates the PA-VMHvl pathway and triggers the same cascade of plasticity events observed during repeated winning. Optogenetically blocking PA-VMHvl synaptic potentiation eliminates all winning-induced plasticity. These results reveal the complex Hebbian synaptic and excitability plasticity in the aggression circuit during winning, ultimately leading to increased "aggressiveness" in repeated winners.

The multi-stage plasticity in the aggression circuit underlying the winner effect.

Winning increases the readiness to attack and the probability of winning, a widespread phenomenon known as the "winner effect". Here, we reveal a transition from target-specific to generalized aggression enhancement over 10 days of winning in male mice, which is supported by three stages of plasticity in the ventrolateral part of the ventromedial hypothalamus (VMHvl), a critical node for aggression. Over 10-day winning, VMHvl cells experience monotonic potentiation of long-range excitatory inputs, a transient local connectivity strengthening, and a delayed excitability increase. These plasticity events are causally linked. Optogenetically coactivating the posterior amygdala (PA) terminals and VMHvl cells potentiates the PA-VMHvl pathway and triggers the cascade of plasticity events as those during repeated winning. Optogenetically blocking PA-VMHvl synaptic potentiation eliminates all winning-induced plasticity. These results reveal the complex Hebbian synaptic and excitability plasticity in the aggression circuit during winning that ultimately leads to an increase in "aggressiveness" in repeated winners.

Clinical symptoms and neuroanatomical substrates of daytime sleepiness in Parkinson’s disease

Clinical and neuroanatomical correlates of daytime sleepiness in Parkinson’s disease (PD) remain inconsistent in the literature. Two studies were conducted here. The first evaluated the interrelation between non-motor and motor symptoms, using a principal component analysis, associated with daytime sleepiness in PD. The second identified the neuroanatomical substrates associated with daytime sleepiness in PD using magnetic resonance imaging (MRI). In the first study, 77 participants with PD completed an extensive clinical, cognitive testing and a polysomnographic recording. In the second study, 29 PD participants also underwent MRI acquisition of T1-weighted images. Vertex-based cortical and subcortical surface analysis, deformation-based morphometry, and voxel-based morphometry were performed to assess the association between daytime sleepiness severity and structural brain changes in participants. In both studies, the severity of daytime sleepiness and the presence of excessive daytime sleepiness (EDS; total score >10) were measured using the Epworth Sleepiness Scale. We found that individuals with EDS had a higher score on a component including higher dosage of dopamine receptor agonists, motor symptoms severity, shorter sleep latency, and greater sleep efficiency. Moreover, increased daytime sleepiness severity was associated with a larger surface area in the right insula, contracted surfaces in the right putamen and right lateral amygdala, and a larger surface in the right posterior amygdala. Hence, daytime sleepiness in PD was associated with dopaminergic receptor agonists dosage, motor impairment, and objective sleep measures. Moreover, neuroanatomical changes in cortical and subcortical regions related to vigilance, motor, and emotional states were associated with more severe daytime sleepiness.

FRI272 Sex-Specific Role Of ProkR2 Neurons Of The Posterior Amygdala In The Integration Of Odors And Neuroendocrine Responses

Abstract Disclosure: B. Cisneros-Larios: None. C.F. Elias: None. Kallmann Syndrome (KS) is characterized by abnormal development of the reproductive axis and olfactory bulb dysgenesis. Genetic studies have revealed that Kallmann Syndrome is caused by loss-of-function mutations in several genes including the prokineticin receptor 2 (PROKR2) gene. Prokr2 null mice exhibit the same phenotype of KS patients. While the role of PROKR2 during development has been linked with GnRH neuron migration, limited data exists on PROKR2 neurons in adult reproduction. PROKR2 mRNA are highly expressed in reproductive control sites. Furthermore, our lab previously found sexually dimorphic expression of PROKR2 mRNA and Prokr2-Cre GFP+ cells in several reproductive control sites. The posterior amygdala had higher PROKR2 expression in males compared to female mice. More recently, we identified expression of sex steroid receptors in PROKR2 expressing cells of the PA. The amygdala is an important site of socio-sexual inputs and reproductive neuroendocrine responses in rodents and primates, including humans. We hypothesize Prokr2-Cre neurons in the PA have a role in male reproductive function. Using genetic tracing techniques, we mapped PA Prokr2-Cre neuronal projections in male mice and found dense innervation to reproductive control sites such as the medial preoptic area and the ventral premammillary nucleus. We found activation of these neurons, via fos expression, after opposite sex soiled bedding exposure (olfactory cues). Lastly, selective activation, using chemogenetic technology DREADDs, of PA Prokr2-Cre cells in males can induce a rise in circulating luteinizing hormone. These data suggest PA Prokr2-Cre cells have a role in pathways integrating olfactory cues and reproductive endocrine responses (e.g., aggression, mating behavior). We expect our studies will contribute to the understanding of the role of PROKR2 neurons in adult reproduction and reproductive deficits associated with PROKR2 mutations. Presentation: Friday, June 16, 2023

Global dissociation of the posterior amygdala from the rest of the brain during REM sleep

Rapid-eye-movement sleep (REMS) or paradoxical sleep is associated with intense neuronal activity, fluctuations in autonomic control, body paralysis and brain-wide hyperemia. The mechanisms and functions of these energy-demanding patterns remain elusive and a global picture of brain activation during REMS is currently missing. In the present work, we performed functional ultrasound imaging on rats over multiple coronal and sagittal brain sections during hundreds of spontaneous REMS episodes to provide the spatiotemporal dynamics of vascular activity in 259 brain regions spanning more than 2/3 of the total brain volume. We first demonstrate a dissociation between basal/midbrain and cortical structures, the first ones sustaining tonic activation during REMS while the others are activated in phasic bouts. Second, we isolated the vascular compartment in our recordings and identified arteries in the anterior part of the brain as strongly involved in the blood supply during REMS episodes. Finally, we report a peculiar activation pattern in the posterior amygdala, which is strikingly disconnected from the rest of the brain during most REMS episodes. This last finding suggests that the amygdala undergoes specific processing during REMS and may be linked to the regulation of emotions and the creation of dream content during this very state.

Higher Rate of Male Sexual Displays Correlates with Larger Ventral Posterior Amygdala Volume and Neuron Soma Volume in Wild-Caught Common Side-Blotched Lizards, Uta stansburiana

Several areas of the vertebrate brain are involved in facilitating and inhibiting the production of sexual behaviors and displays. In the laboratory, a higher rate of sexual displays is correlated with a larger ventral posterior amygdala (VPA), an area of the brain involved in the expression of sexual display behaviors, as well as larger VPA neuronal somas. However, it remains unclear if individuals in the field reflect similar patterns, as there are likely many more selective pressures in the field that may also modulate the VPA architecture. In this study, we examined variation in VPA volume and neuron soma volume in wild-caught common side-blotched lizards (Uta stansburiana) from two different populations. In a population from Nevada, males experience high predation pressure and have decreased sexual display rates during the breeding season, whereas a population in Oregon has lower levels of predation and higher rates of male sexual displays. We found that wild-caught males from the population with lower display rates also exhibited decreased VPA volume and VPA neuron cell soma volume, which may suggest that decreased display rate, possibly due to increased predation rate, covaries with VPA attributes.

Oxytocin Receptor-Expressing Neurons in the Paraventricular Thalamus Regulate Feeding Motivation through Excitatory Projections to the Nucleus Accumbens Core.

Oxytocin receptors (OTR) have been found in the paraventricular thalamus (PVT) for the regulation of feeding and maternal behaviors. However, the functional projections of OTR-expressing PVT neurons remain largely unknown. Here, we used chemogenetic and optogenetic tools to test the role of OTR-expressing PVT neurons and their projections in the regulation of food intake in both male and female OTR-Cre mice. We found chemogenetic activation of OTR-expressing PVT neurons promoted food seeking under trials with a progressive ratio schedule of reinforcement. Using Feeding Experimentation Devices for real-time meal measurements, we found chemogenetic activation of OTR-expressing PVT neurons increased meal frequency but not cumulative food intake because of a compensatory decrease in meal sizes. In combination with anterograde neural tracing and slice patch-clamp recordings, we found optogenetic stimulation of PVT OTR terminals excited neurons in the posterior basolateral amygdala (pBLA) and nucleus accumbens core (NAcC) as well as local PVT neurons through monosynaptic glutamatergic transmissions. Photostimulation of OTR-expressing PVT-NAcC projections promoted food-seeking, whereas selective activation of PVT-pBLA projections produced little effect on feeding. In contrast to selective activation of OTR terminals, photostimulation of a broader population of glutamatergic PVT terminals exerted direct excitation followed by indirect lateral inhibition on neurons in both NAcC and anterior basolateral amygdala. Together, these results suggest that OTR-expressing PVT neurons are a distinct population of PVT glutamate neurons that regulate feeding motivation through projections to NAcC.SIGNIFICANCE STATEMENT The paraventricular thalamus plays an important role in the regulation of feeding motivation. However, because of the diversity of paraventricular thalamic neurons, the specific neuron types promoting food motivation remain elusive. In this study, we provide evidence that oxytocin receptor-expressing neurons are a specific group of glutamate neurons that primarily project to the nucleus accumbens core and posterior amygdala. We found that activation of these neurons promotes the motivation for food reward and increases meal frequency through projections to the nucleus accumbens core but not the posterior amygdala. As a result, we postulate that oxytocin receptor-expressing neurons in the paraventricular thalamus and their projections to the nucleus accumbens core mainly regulate feeding motivation but not food consumption.

The role of posterior pallial amygdala in mediating motor behaviors in pigeons

The posterior pallial amygdala (PoA) is located on the basolateral caudal telencephalon, including the basal division of PoA (PoAb) and the compact division of PoA (PoAc). PoA plays a vital role in emotion regulation and is considered a part of the amygdala in birds. However, the regulatory functions responsible for motor behaviors and emotions between PoAb and PoAc are poorly understood. Therefore, we studied the structure and function of PoA by tract-tracing methods, constant current electrical stimulation, and different dopamine receptor drug injections in pigeons (Columba livia domestica). PoAb connects reciprocally with two nuclear groups in the cerebrum: 1) a continuum comprising the temporo–parieto–occipitalis, corticoidea dorsolateralis, hippocampus, and parahippocampalis areas and 2) rostral areas of the hemisphere, including the nucleus septalis lateralis and nucleus taeniae amygdalae. Extratelencephalic projections of PoAb terminate in the lateral hypothalamic nucleus and are scattered in many limbic midbrain regions. PoAb and PoAc mainly mediated the turning movement. In the ‘open-field’ test, D1 agonist and D2 antagonist could significantly reduce the latency period for entering into the central area and increase the residence time in the central area, whereas D1 antagonist and D2 agonist had the opposite effect. PoAb and PoAc are important brain areas that mediate turning behavior.

Comparative metabolic profiling of posterior parietal cortex, amygdala, and hippocampus in conditioned fear memory

Fear conditioning and retrieval are suitable models to investigate the biological basis of various mental disorders. Hippocampus and amygdala neurons consolidate conditioned stimulus (CS)-dependent fear memory. Posterior parietal cortex is considered important for the CS-dependent conditioning and retrieval of fear memory. Metabolomic screening among functionally related brain areas provides molecular signatures and biomarkers to improve the treatment of psychopathologies. Herein, we analyzed and compared changes of metabolites in the hippocampus, amygdala, and posterior parietal cortex under the fear retrieval condition. Metabolite profiles of posterior parietal cortex and amygdala were similarly changed after fear memory retrieval. While the retrieval of fear memory perturbed various metabolic pathways, most metabolic pathways that overlapped among the three brain regions had high ranks in the enrichment analysis of posterior parietal cortex. In posterior parietal cortex, the most perturbed pathways were pantothenate and CoA biosynthesis, purine metabolism, glutathione metabolism, and NAD+ dependent signaling. Metabolites of posterior parietal cortex including 4′-phosphopantetheine, xanthine, glutathione, ADP-ribose, ADP-ribose 2′-phosphate, and cyclic ADP-ribose were significantly regulated in these metabolic pathways. These results point to the importance of metabolites of posterior parietal cortex in conditioned fear memory retrieval and may provide potential biomarker candidates for traumatic memory-related mental disorders.

Personality Factors' Impact on the Structural Integrity of Mentalizing Network in Old Age: A Combined PET-MRI Study.

The mentalizing network (MN) treats social interactions based on our understanding of other people's intentions and includes the medial prefrontal cortex (mPFC), temporoparietal junction (TPJ), posterior cingulate cortex (PCC), precuneus (PC), and amygdala. Not all elders are equally affected by the aging-related decrease of mentalizing abilities. Personality has recently emerged as a strong determinant of functional connectivity in MN areas. However, its impact on volumetric changes across the MN in brain aging is still unknown. To address this issue, we explored the determinants of volume decrease in MN components including amyloid burden, personality, and APOE genotyping in a previously established cohort of 130 healthy elders with a mean follow-up of 54 months. Personality was assessed with the Neuroticism Extraversion Openness Personality Inventory-Revised. Regression models corrected for multiple comparisons were used to identify predictors of volume loss including time, age, sex, personality, amyloid load, presence of APOE epsilon 4 allele, and cognitive evolution. In cases with higher Agreeableness scores, there were lower volume losses in PCC, PC, and amygdala bilaterally. This was also the case for the right mPFC in elders displaying lower Agreeableness and Conscientiousness. In multiple regression models, the effect of Agreeableness was still observed in left PC and right amygdala and that of Conscientiousness was still observed in right mPFC volume loss (26.3% of variability, significant age and sex). Several Agreeableness (Modesty) and Conscientiousness (order, dutifulness, achievement striving, and self-discipline) facets were positively related to increased volume loss in cortical components of the MN. In conclusion, these data challenge the beneficial role of higher levels of Agreeableness and Conscientiousness in old age, showing that they are associated with an increased rate of volume loss within the MN.

Posterior amygdala regulates sexual and aggressive behaviors in male mice.

Sexual and aggressive behaviors are fundamental to animals’ survival and reproduction. The medial preoptic nucleus (MPN) and ventrolateral part of ventromedial hypothalamus (VMHvl) are essential regions for male sexual and aggressive behaviors, respectively. While key inhibitory inputs to VMHvl and MPN are identified, the extra-hypothalamic excitatory inputs essential for the social behaviors remain elusive. Here we identify estrogen receptor alpha (Esr1) expressing cells in posterior amygdala (PA) as a main source of excitatory inputs to hypothalamus and key mediators for mating and fighting in male mice. We find two largely distinct PA subpopulations that differ in connectivity, gene expression, in vivo responses and social behavior relevance. MPN projecting PAEsr1+ cells are activated during mating and necessary and sufficient for male sexual behaviors, while VMHvl projecting PAEsr1+ are excited during inter-male aggression and promote attacks. These findings place PA as a key node in both male aggression and reproduction circuits.

VMHvl-Projecting Vglut1+ Neurons in the Posterior Amygdala Gate Territorial Aggression

Despite being innate, displays of aggression are influenced by cortical activities. Here, using Vglut1 as a marker for inputs from cortical structures, we identify a small population of excitatory neurons located in the posterior amygdala (PA) that project to the ventrolateral division of ventromedial nucleus of the hypothalamus (VMHvl), a region that critically regulates territorial aggression. Indeed, activities of PA Vglut1+ (PAVglut1) neurons, as analyzed by post hoc c-Fos expression, differentiate trials in which attacks occur, or not, during resident-intruder assays. More importantly, chemogenetic activation of VMHvl-projecting PAVglut1 neurons robustly promote aggression while inhibition of these neurons reduces attacks. Finally, a connectivity map places VMHvl-projecting PAVglut1 neurons at the interface between emotion regulation and aggression as they receive broad inputs from limbic structures and project collaterally to the VMHvl and other targets. Taken together, these results point to VMHvl-projecting PAVglut1 neurons as a potential site for cortical gating of territorial aggression.

Brain Differences Associated with Self-Injurious Thoughts and Behaviors: A Meta-Analysis of Neuroimaging Studies

This meta-analysis aims to evaluate whether the extant literature justifies any definitive conclusions about whether and how SITBs may be associated with brain differences. A total of 77 papers (N = 4,903) published through January 1, 2019 that compared individuals with and without SITBs were included, resulting in 882 coordinates. A pooled meta-analysis assessing for general risk for SITBs indicated a lack of convergence on structural differences. When all types of control groups were considered, functional differences in the left posterior cingulate cortex (PCC), right amygdala, left hippocampus, and right thalamus were significant using multi-level kernel density analysis (pcorrected < 0.05) but nonsignificant using activation-likelihood estimation. These results suggest that a propensity for internally-oriented, emotional processing coupled with under-active pain processing could potentially underlie SITBs, but additional research is needed to test this possibility. Separate analyses for types of SITBs suggested that the brain differences associated with deliberate self-harm were consistent with the overall findings. Checkered moderator effects were detected. Overall, the meta-analytic evidence was not robust. More studies are needed to reach definitive conclusions about whether SITBs are associated with brain differences.

VMHvl-Projecting&amp;nbsp; &lt;i&gt;Vglut1&lt;/i&gt;+Neurons in the Posterior Amygdala Gate Territorial Aggression

Despite being innate, display of aggression is influenced by cortical activities. Here, using Vglut1 as a marker for inputs from cortical structures, we identified a small population of excitatory neurons located in the posterior amygdala (PA) that projects to the ventrolateral division of ventromedial nucleus of the hypothalamus (VMHvl), a region that critically regulate territorial aggression. Indeed, activities of PA Vglut1+ (PA Vglut1 ) neurons, as analyzed by post-hoc c-Fos expression, unequivocally differentiate trials in which attacks occur or not during resident-intruder assays. More importantly, chemogenetic activation of VMHvl-projecting PA Vglut1 neurons robustly promotes aggression while inhibition of these neurons reduces attacks. Finally, connectivity map places VMHvl-projecting PA Vglut1 neurons at the interface between emotion reactivity and aggression as they receive broad inputs from limbic structures and project collaterally to VMHvl and other targets. Taken together, these results point to VMHvl-projecting PA Vglut1 neurons as a potential site for cortical gating of territorial aggression.

Sex dimorphism in a mediatory role of the posterior midcingulate cortex in the association between anxiety and pain sensitivity.

Behavioral studies found greater pain sensitivity in females that vanishes fully or partially when controlling for the emotional state. Furthermore, pain-related brain activation hints at the role of limbic structures in sex differences in pain processing. We aimed to investigate the role of pain-related limbic structures in mediating the relation between subjects' affective state (i.e., anxiety) and pain. Contact heat-evoked potentials (CHEPs) were recorded in 26 healthy subjects (13 males) simultaneously with innocuous (42°C) baseline and target noxious (52°C) series of stimuli administered to the left non-dominant volar forearm. The N2 and P2 components were analyzed, and their generators' activity was estimated using standardized low-resolution brain electromagnetic tomography. Thereafter, structural equation modeling (SEM) was applied separately for females and males, examining the mediatory role of the CHEPs' limbic structures generators [posterior midcingulate cortex (pMCC), insula, amygdala, and hippocampus] in the anxiety-pain sensitivity association. Females exhibited greater P2 amplitudes that were highly associated with larger pMCC activity (r=0.910, p<0.001). This correlation was also evident in males, though with less strength (r=0.578, p=0.039). Moreover, the P2 amplitudes were associated both in females (r=0.645, p=0.017) and males (r=0.608, p=0.028) with the activity of the amygdala\hippocampus\insula. SEM revealed that the relationship between state anxiety and pain ratings was only in females fully mediated via the effect of the pMCC on the P2 amplitude. These findings suggest that sexual dimorphism in anxiety-related brain activity may explain the differences found in CHEPs and the sex-related association between anxiety and pain.

Activity of muscarinic, galanin and cannabinoid receptors in the prodromal and advanced stages in the triple transgenic mice model of Alzheimer’s disease

Neurochemical alterations in Alzheimer’s disease (AD) include cholinergic neuronal loss in the nucleus basalis of Meynert (nbM) and a decrease in densities of the M2 muscarinic receptor subtype in areas related to learning and memory. Neuromodulators present in the cholinergic pathways, such as neuropeptides and neurolipids, control these cognitive processes and have become targets of research in order to understand and treat the pathophysiological and clinical stages of the disease. This is the case of the endocannabinoid and galaninergic systems, which have been found to be up-regulated in AD, and could therefore have a neuroprotective role. In the present study, the functional coupling of Gi/o protein-coupled receptors to GalR1, and the CB1 receptor subtype for endocannabinoids were analyzed in the 3xTg-AD mice model of AD. In addition, the activity mediated by Gi/o protein-coupled M2/4 muscarinic receptor subtypes was also analyzed in brain areas involved in anxiety and cognition. Thus, male mice were studied at 4 and 15months of age (prodromal and advanced stages, respectively) and compared to age-matched non-transgenic (NTg) mice (adult and old, respectively). In 4-month-old 3xTg-AD mice, the [35S]GTPγS binding stimulated by galanin was significantly increased in the hypothalamus, but a decrease of functional M2/4 receptors was observed in the posterior amygdala. The CB1 cannabinoid receptor activity was up-regulated in the anterior thalamus at that age. In 15-month-old 3xTg-AD mice, muscarinic receptor activity was found to be increased in motor cortex, while CB1 activity was decreased in nbM. No changes were found in GalR1-mediated activity at this age. Our results provide further evidence of the relevance of limbic areas in the prodromal stage of AD, the profile of which is characterized by anxiety. The up-regulation of galaninergic and endocannabinoid systems support the hypothesis of their neuroprotective roles, and these are established prior to the onset of clear clinical cognitive symptoms of the disease.

Radial derivatives of the mouse ventral pallium traced with Dbx1-LacZ reporters

The progeny of Dbx1-expressing progenitors was studied in the developing mouse pallium, using two transgenic mouse lines: (1) Dbx1nlslacZ mice, in which the gene of the β-galactosidase reporter (LacZ) is inserted directly under the control of the Dbx1 promoter, allowing short-term lineage tracing of Dbx1-derived cells; and (2) Dbx1CRE mice crossed with a Cre-dependent reporter strain (ROSA26loxP-stop-loxP-LacZ), in which the Dbx1-derived cells result permanently labeled (Bielle et al., 2005). We thus examined in detail the derivatives of the postulated longitudinal ventral pallium (VPall) sector, which has been defined among other features by its selective ventricular zone expression of Dbx1 (the recent ascription by Puelles, 2014 of the whole olfactory cortex primordium to the VPall was tested). Earlier notions about a gradiental caudorostral reduction of Dbx1 signal were corroborated, so that virtually no signal was found at the olfactory bulb and the anterior olfactory area. The piriform cortex was increasingly labeled caudalwards. The only endopiriform grisea labeled were the ventral endopiriform nucleus and the bed nucleus of the external capsule. Anterior and basolateral parts of the whole pallial amygdala also were densely marked, in contrast to the negative posterior parts of these pallial amygdalar nuclei (leaving apart medial amygdalar parts ascribed to subpallial or extratelencephalic sources of Dbx1-derived GABAergic and non-GABAergic neurons). Alternative tentative interpretations are discussed to explain the partial labeling obtained of both olfactory and amygdaloid structures. This includes the hypothesis of an as yet undefined part of the pallium, potentially responsible for the posterior amygdala, or the hypothesis that the VPall may not be wholly characterized by Dbx1 expression (this gene not being necessary for VPall molecular distinctness and histogenetic potency), which would leave a dorsal Dbx1-negative VPall subdomain of variable size that might contribute partially to olfactory and posterior amygdalar structures.

Connectivity and neurochemistry of the commissura anterior of the pigeon (Columba livia).

The anterior commissure (AC) and the much smaller hippocampal commissure constitute the only interhemispheric pathways at the telencephalic level in birds. Since the degeneration study from Zeier and Karten (1973), no detailed description of the topographic organization of the AC has been performed. This information is not only necessary for a better understanding of interhemispheric transfer in birds, but also for a comparative analysis of the evolution of commissural systems in the vertebrate classes. We therefore examined the fiber connections of the AC by using choleratoxin subunit B (CTB) and biotinylated dextran amine (BDA). Injections into subareas of the arcopallium and posterior amygdala (PoA) demonstrated contralateral projection fields within the anterior arcopallium (AA), intermediate arcopallium (AI), PoA, lateral, caudolateral and central nidopallium, dorsal and ventral mesopallium, and medial striatum (MSt). Interestingly, only arcopallial and amygdaloid projections were reciprocally organized, and all AC projections originated within a rather small area of the arcopallium and the PoA. The commissural neurons were not GABA‐positive, and thus possibly not of an inhibitory nature. In sum, our neuroanatomical study demonstrates that a small group of arcopallial and amygdaloid neurons constitute a wide range of contralateral projections to sensorimotor and limbic structures. Different from mammals, in birds the neurons that project via the AC constitute mostly heterotopically organized and unidirectional connections. In addition, the great majority of pallial areas do not participate by themselves in interhemispheric exchange in birds. Instead, commissural exchange rests on a rather small arcopallial and amygdaloid cluster of neurons. J. Comp. Neurol. 524:343–361, 2016. © 2015 The Authors The Journal of Comparative Neurology Published by Wiley Periodicals, Inc.

Nucleus Accumbens and Posterior Amygdala Mediate Cue-Triggered Alcohol Seeking and Suppress Behavior During the Omission of Alcohol-Predictive Cues.

Neurobiological mechanisms that influence behavior in the presence of alcohol-associated stimuli involve processes that organize behavior during the presence of these cues, and separately, regulation of behavior in their absence. However, little is known about anatomical structures that might mediate this regulation. Here we examined nucleus accumbens shell (AcbSh) as a possible neural substrate mediating behavior modulation triggered by the presence and absence of alcohol-associated environmental cues and contexts. We also examined subregions of basal amygdala nuclei- rostral basolateral (BLA) and basal posterior (BAP)- as they provide a major source of glutamatergic input to the AcbSh. Animals were trained to associate an auditory conditioning stimulus with alcohol in a discriminative context and then subsequently tested for conditioned port-entries across contexts either previously associated or not associated with alcohol. We found that, on test to the alcohol cue alone, AcbSh inactivation prevented conditioned port-entries in contexts that either were associated with alcohol or were novel, while also increasing unconditioned port-entries during the intertrial intervals. When tested to alcohol-reinforced cues, AcbSh inactivation produced more cue-trial omissions and elevated unconditioned port-entries. Interestingly, BLA and BAP inactivation produced dissociable effects. BAP but not BLA increased unconditioned port-entries, while both manipulations prevented conditioned port-entries during the alcohol-cue. We conclude that AcbSh is necessary for modulating control over behavior otherwise guided by the presence of alcohol-predictive environmental stimuli and contexts. Moreover, this role may involve integration of functionally segregated inputs from rostral and posterior portions of basal amygdala nuclei.

Fear across the senses: brain responses to music, vocalizations and facial expressions.

Intrinsic emotional expressions such as those communicated by faces and vocalizations have been shown to engage specific brain regions, such as the amygdala. Although music constitutes another powerful means to express emotions, the neural substrates involved in its processing remain poorly understood. In particular, it is unknown whether brain regions typically associated with processing 'biologically relevant' emotional expressions are also recruited by emotional music. To address this question, we conducted an event-related functional magnetic resonance imaging study in 47 healthy volunteers in which we directly compared responses to basic emotions (fear, sadness and happiness, as well as neutral) expressed through faces, non-linguistic vocalizations and short novel musical excerpts. Our results confirmed the importance of fear in emotional communication, as revealed by significant blood oxygen level-dependent signal increased in a cluster within the posterior amygdala and anterior hippocampus, as well as in the posterior insula across all three domains. Moreover, subject-specific amygdala responses to fearful music and vocalizations were correlated, consistent with the proposal that the brain circuitry involved in the processing of musical emotions might be shared with the one that have evolved for vocalizations. Overall, our results show that processing of fear expressed through music, engages some of the same brain areas known to be crucial for detecting and evaluating threat-related information.