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Frontiers in Human Neuroscience 2018The psycho-physiological changes in brain-body interaction observed in most of meditative and relaxing practices rely on voluntary slowing down of breath frequency....
The psycho-physiological changes in brain-body interaction observed in most of meditative and relaxing practices rely on voluntary slowing down of breath frequency. However, the identification of mechanisms linking breath control to its psychophysiological effects is still under debate. This systematic review is aimed at unveiling psychophysiological mechanisms underlying slow breathing techniques (<10 breaths/minute) and their effects on healthy subjects. A systematic search of MEDLINE and SCOPUS databases, using keywords related to both breathing techniques and to their psychophysiological outcomes, focusing on cardio-respiratory and central nervous system, has been conducted. From a pool of 2,461 abstracts only 15 articles met eligibility criteria and were included in the review. The present systematic review follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The main effects of slow breathing techniques cover autonomic and central nervous systems activities as well as the psychological status. Slow breathing techniques promote autonomic changes increasing Heart Rate Variability and Respiratory Sinus Arrhythmia paralleled by Central Nervous System (CNS) activity modifications. EEG studies show an increase in alpha and a decrease in theta power. Anatomically, the only available fMRI study highlights increased activity in cortical (e.g., prefrontal, motor, and parietal cortices) and subcortical (e.g., pons, thalamus, sub-parabrachial nucleus, periaqueductal gray, and hypothalamus) structures. Psychological/behavioral outputs related to the abovementioned changes are increased comfort, relaxation, pleasantness, vigor and alertness, and reduced symptoms of arousal, anxiety, depression, anger, and confusion. Slow breathing techniques act enhancing autonomic, cerebral and psychological flexibility in a scenario of mutual interactions: we found evidence of links between parasympathetic activity (increased HRV and LF power), CNS activities (increased EEG alpha power and decreased EEG theta power) related to emotional control and psychological well-being in healthy subjects. Our hypothesis considers two different mechanisms for explaining psychophysiological changes induced by voluntary control of slow breathing: one is related to a voluntary regulation of internal bodily states (enteroception), the other is associated to the role of mechanoceptors within the nasal vault in translating slow breathing in a modulation of olfactory bulb activity, which in turn tunes the activity of the entire cortical mantle.
PubMed: 30245619
DOI: 10.3389/fnhum.2018.00353 -
Frontiers in Neural Circuits 2022Itch-induced scratching is an evolutionarily conserved behavioral response that protects organisms from potential parasites/irritants in their immediate vicinity. How... (Review)
Review
Itch-induced scratching is an evolutionarily conserved behavioral response that protects organisms from potential parasites/irritants in their immediate vicinity. How the exposure to a pruritogen is translated to the perception of itch and how that perception drives scratching directed towards the site of exposure remains poorly understood. In this review, we focus on the recent findings that shed light on the neural pathways in the brain that underlie itch-induced scratching. We compare the molecularly defined itch pathways with the known pain circuits as they have anatomical and functional overlap. We review the roles played by the neurons in the spinoparabrachial pathway-comprising of the neurons in the spinal cord and the parabrachial nucleus (PBN), which acts as a hub for transmitting itch information across the brain. Lastly, we deliberate on scratching as a behavioral measure of the intensity of itch and its implication in unraveling the underlying supraspinal mechanisms. In summary, we provide a resource on the recent advances and discuss a path forward on our understanding of the neural circuits for itch.
Topics: Humans; Neural Pathways; Neurons; Parabrachial Nucleus; Pruritus; Spinal Cord
PubMed: 35250493
DOI: 10.3389/fncir.2022.805831 -
Nature Communications Dec 2022Feeding behavior is adaptively regulated by external and internal environment, such that feeding is suppressed when animals experience pain, sickness, or fear. While the...
Feeding behavior is adaptively regulated by external and internal environment, such that feeding is suppressed when animals experience pain, sickness, or fear. While the lateral parabrachial nucleus (lPB) plays key roles in nociception and stress, neuronal pathways involved in feeding suppression induced by fear are not fully explored. Here, we investigate the parasubthalamic nucleus (PSTN), located in the lateral hypothalamus and critically involved in feeding behaviors, as a target of lPB projection neurons. Optogenetic activation of lPB-PSTN terminals in male mice promote avoidance behaviors, aversive learning, and suppressed feeding. Inactivation of the PSTN and lPB-PSTN pathway reduces fear-induced feeding suppression. Activation of PSTN neurons expressing pituitary adenylate cyclase-activating polypeptide (PACAP), a neuropeptide enriched in the PSTN, is sufficient for inducing avoidance behaviors and feeding suppression. Blockade of PACAP receptors impaires aversive learning induced by lPB-PSTN photomanipulation. These findings indicate that lPB-PSTN pathway plays a pivotal role in fear-induced feeding suppression.
Topics: Mice; Male; Animals; Parabrachial Nucleus; Fear; Pain; Hypothalamic Area, Lateral; Pituitary Adenylate Cyclase-Activating Polypeptide
PubMed: 36585411
DOI: 10.1038/s41467-022-35634-2 -
Cerebral Cortex (New York, N.Y. : 1991) Jul 2020The parabrachial nucleus (PB) in the upper brain stem tegmentum includes several neuronal subpopulations with a wide variety of connections and functions. A...
The parabrachial nucleus (PB) in the upper brain stem tegmentum includes several neuronal subpopulations with a wide variety of connections and functions. A subpopulation of PB neurons projects axons directly to the cerebral cortex, and limbic areas of the cerebral cortex send a return projection directly to the PB. We used retrograde and Cre-dependent anterograde tracing to identify genetic markers and characterize this PB-cortical interconnectivity in mice. Cortical projections originate from glutamatergic PB neurons that contain Lmx1b (81%), estrogen receptor alpha (26%), and Satb2 (20%), plus mRNA for the neuropeptides cholecystokinin (Cck, 48%) and calcitonin gene-related peptide (Calca, 13%), with minimal contribution from FoxP2+ PB neurons (2%). Axons from the PB produce an extensive terminal field in an unmyelinated region of the insular cortex, extending caudally into the entorhinal cortex, and arcing rostrally through the dorsolateral prefrontal cortex, with a secondary terminal field in the medial prefrontal cortex. In return, layer 5 neurons in the insular cortex and other prefrontal areas, along with a dense cluster of cells dorsal to the claustrum, send a descending projection to subregions of the PB that contain cortically projecting neurons. This information forms the neuroanatomical basis for testing PB-cortical interconnectivity in arousal and interoception.
Topics: Animals; Cerebral Cortex; Female; Male; Mice; Mice, Inbred C57BL; Neural Pathways; Parabrachial Nucleus
PubMed: 32383444
DOI: 10.1093/cercor/bhaa072 -
Nature Neuroscience Mar 2024Fear-related disorders (for example, phobias and anxiety) cause a substantial public health problem. To date, studies of the neural basis of fear have mostly focused on...
Fear-related disorders (for example, phobias and anxiety) cause a substantial public health problem. To date, studies of the neural basis of fear have mostly focused on the amygdala. Here we identify a molecularly defined amygdala-independent tetra-synaptic pathway for olfaction-evoked innate fear and anxiety in male mice. This pathway starts with inputs from the olfactory bulb mitral and tufted cells to pyramidal neurons in the dorsal peduncular cortex that in turn connect to cholecystokinin-expressing (Cck) neurons in the superior part of lateral parabrachial nucleus, which project to tachykinin 1-expressing (Tac1) neurons in the parasubthalamic nucleus. Notably, the identified pathway is specifically involved in odor-driven innate fear. Selective activation of this pathway induces innate fear, while its inhibition suppresses odor-driven innate fear. In addition, the pathway is both necessary and sufficient for stress-induced anxiety-like behaviors. These findings reveal a forebrain-to-hindbrain neural substrate for sensory-triggered fear and anxiety that bypasses the amygdala.
Topics: Mice; Male; Animals; Odorants; Amygdala; Anxiety; Fear; Smell; Olfactory Bulb
PubMed: 38347199
DOI: 10.1038/s41593-023-01562-7 -
Cell Reports Apr 2024Pain that persists beyond the time required for tissue healing and pain that arises in the absence of tissue injury, collectively referred to as nociplastic pain, are...
Pain that persists beyond the time required for tissue healing and pain that arises in the absence of tissue injury, collectively referred to as nociplastic pain, are poorly understood phenomena mediated by plasticity within the central nervous system. The parabrachial nucleus (PBN) is a hub that relays aversive sensory information and appears to play a role in nociplasticity. Here, by preventing PBN Calca neurons from releasing neurotransmitters, we demonstrate that activation of Calca neurons is necessary for the manifestation and maintenance of chronic pain. Additionally, by directly stimulating Calca neurons, we demonstrate that Calca neuron activity is sufficient to drive nociplasticity. Aversive stimuli of multiple sensory modalities, such as exposure to nitroglycerin, cisplatin, or lithium chloride, can drive nociplasticity in a Calca-neuron-dependent manner. Aversive events drive nociplasticity in Calca neurons in the form of increased activity and excitability; however, neuroplasticity also appears to occur in downstream circuitry.
Topics: Animals; Parabrachial Nucleus; Neurons; Mice; Neuronal Plasticity; Male; Mice, Inbred C57BL
PubMed: 38583149
DOI: 10.1016/j.celrep.2024.114057 -
Physiological Reports Jun 2018Fluid satiation, or quenching of thirst, is a critical homeostatic signal to stop drinking; however, its underlying neurocircuitry is not well characterized.... (Review)
Review
Fluid satiation, or quenching of thirst, is a critical homeostatic signal to stop drinking; however, its underlying neurocircuitry is not well characterized. Cutting-edge genetically encoded tools and techniques are now enabling researchers to pinpoint discrete neuronal populations that control fluid satiation, revealing that hindbrain regions, such as the nucleus of the solitary tract, area postrema, and parabrachial nucleus, primarily inhibit fluid intake. By contrast, forebrain regions such as the lamina terminalis, primarily stimulate thirst and fluid intake. One intriguing aspect of fluid satiation is that thirst is quenched tens of minutes before water reaches the circulation, and the amount of water ingested is accurately calibrated to match physiological needs. This suggests that 'preabsorptive' inputs from the oropharyngeal regions, esophagus or upper gastrointestinal tract anticipate the amount of fluid required to restore fluid homeostasis, and provide rapid signals to terminate drinking once this amount has been consumed. It is likely that preabsorptive signals are carried via the vagal nerve to the hindbrain. In this review, we explore our current understanding of the fluid satiation neurocircuitry, its inputs and outputs, and its interconnections within the brain, with a focus on recent studies of the hindbrain, particularly the parabrachial nucleus.
Topics: Brain; Brain Mapping; Drinking; Homeostasis; Humans; Neural Pathways; Prosencephalon; Rhombencephalon; Satiation; Thirst
PubMed: 29932494
DOI: 10.14814/phy2.13744 -
Neuropharmacology Oct 2021Our understanding of the role of the parabrachial nucleus (PBN) has evolved as technology has advanced, in part due to cell-specific studies and complex behavioral... (Review)
Review
Our understanding of the role of the parabrachial nucleus (PBN) has evolved as technology has advanced, in part due to cell-specific studies and complex behavioral assays. This is reflected in the heterogeneous neuronal populations within the PBN to the extended amygdala (EA) circuits which encompass the bed nucleus of the stria terminalis (BNST) and central amygdala (CeA) circuitry, as they differentially modulate aspects of behavior in response to diverse threat-like contexts necessary for survival. Here we review how the PBN→CeA and PBN→BNST pathways differentially modulate fear-like behavior, innate and conditioned, through unique changes in neurotransmission in response to stress-inducing contexts. Furthermore, we hypothesize how in specific instances the PBN→CeA and PBN→BNST circuits are redundant and in part intertwined with their respective reciprocal projections. By deconstructing the interoceptive and exteroceptive components of affect- and stress related behavioral paradigms, evidence suggests that the PBN→CeA circuit modulates innate response to physical stimuli and fear conditioning. Conversely, the PBN→BNST circuit modulates distress-like stress in unpredictable contexts. Thereby, the PBN provides a pathway for alarming interoceptive and exteroceptive stimuli to be processed and relayed to the EA to induce stress-relevant affect. Additionally, we provide a framework for future studies to detail the cell-type specific intricacies of PBN→EA circuits in mediating behavioral responses to threats, and the relevance of the PBN in drug-use as it relates to threat and negative reinforcement. This article is part of the special Issue on 'Neurocircuitry Modulating Drug and Alcohol Abuse'.
Topics: Affect; Amygdala; Animals; Fear; Humans; Parabrachial Nucleus; Septal Nuclei; Stress, Psychological
PubMed: 34461068
DOI: 10.1016/j.neuropharm.2021.108757 -
Neuropeptides Aug 2019Neurotensin (Nts) is a neuropeptide implicated in the regulation of many facets of physiology, including cardiovascular tone, pain processing, ingestive behaviors,...
Neurotensin (Nts) is a neuropeptide implicated in the regulation of many facets of physiology, including cardiovascular tone, pain processing, ingestive behaviors, locomotor drive, sleep, addiction and social behaviors. Yet, there is incomplete understanding about how the various populations of Nts neurons distributed throughout the brain mediate such physiology. This knowledge gap largely stemmed from the inability to simultaneously identify Nts cell bodies and manipulate them . One means of overcoming this obstacle is to study mice crossed onto a Cre-inducible green fluorescent reporter line ( mice), as these mice permit both visualization and modulation of specific populations of Nts neurons (using Cre-inducible viral and genetic tools) to reveal their function. Here we provide a comprehensive characterization of the distribution and relative densities of the Nts-GFP populations observed throughout the male mouse brain, which will pave the way for future work to define their physiologic roles. We also compared the distribution of Nts-GFP neurons with - Hybridization (-ISH) data from the adult mouse brain. By comparing these data sets we can distinguish Nts-GFP populations that may only transiently express Nts during development but not in the mature brain, and hence which populations may not be amenable to Cre-mediated manipulation in adult mice. This atlas of Nts-GFP neurons will facilitate future studies using the line to describe the physiological functions of individual Nts populations and how modulating them may be useful to treat disease.
Topics: Animals; Atlases as Topic; Brain; Male; Mice, Inbred C57BL; Mice, Transgenic; Neurons; Neurotensin
PubMed: 31079844
DOI: 10.1016/j.npep.2019.05.001 -
Neuron Jan 2022Humans and animals alike perform behaviors-like putting on a sweater or building a warm nest-to regulate body temperature. In this issue of Neuron, Jung et al. (2022)...
Humans and animals alike perform behaviors-like putting on a sweater or building a warm nest-to regulate body temperature. In this issue of Neuron, Jung et al. (2022) reveal a parabrachial nucleus-to-lateral hypothalamus circuit that regulates thermoregulatory behavior, a circuit distinct from that which governs motivated feeding behavior.
Topics: Animals; Body Temperature Regulation; Feeding Behavior; Hunger; Hypothalamic Area, Lateral; Neurons
PubMed: 35051361
DOI: 10.1016/j.neuron.2021.12.030