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Perception 2017Olfactory perception and its underlying neural mechanisms are not fixed, but rather vary over time, dependent on various parameters such as state, task, or learning... (Review)
Review
Olfactory perception and its underlying neural mechanisms are not fixed, but rather vary over time, dependent on various parameters such as state, task, or learning experience. In olfaction, one of the primary sensory areas beyond the olfactory bulb is the piriform cortex. Due to an increasing number of functions attributed to the piriform cortex, it has been argued to be an associative cortex rather than a simple primary sensory cortex. In fact, the piriform cortex plays a key role in creating olfactory percepts, helping to form configural odor objects from the molecular features extracted in the nose. Moreover, its dynamic interactions with other olfactory and nonolfactory areas are also critical in shaping the olfactory percept and resulting behavioral responses. In this brief review, we will describe the key role of the piriform cortex in the larger olfactory perceptual network, some of the many actors of this network, and the importance of the dynamic interactions among the piriform-trans-thalamic and limbic pathways.
Topics: Humans; Limbic System; Neural Pathways; Olfactory Pathways; Olfactory Perception; Piriform Cortex; Thalamus
PubMed: 27687814
DOI: 10.1177/0301006616663216 -
Revista Brasileira de Psiquiatria (Sao... Dec 2012Mounting evidence suggests that the limbic system is pathologically involved in cases of psychiatric comorbidities in temporal lobe epilepsy (TLE) patients. Our... (Review)
Review
OBJECTIVE
Mounting evidence suggests that the limbic system is pathologically involved in cases of psychiatric comorbidities in temporal lobe epilepsy (TLE) patients. Our objective was to develop a conceptual framework describing how neuropathological and connectivity changes might contribute to the development of psychosis and to the potential neurobiological mechanisms that cause schizophrenia-like psychosis in TLE patients.
METHODS
In this review, clinical and neuropathological findings, especially brain circuitry of the limbic system, were examined together to enhance our understanding of the association between TLE and psychosis. Finally, the importance of animal models in epilepsy and psychiatric disorders was discussed.
CONCLUSIONS
TLE and psychiatric symptoms coexist more frequently than chance would predict. Damage and deregulation among critical anatomical regions, such as the hippocampus, amygdala, thalamus, and the temporal, frontal and cingulate cortices, might predispose TLE brains to psychosis. Studies of the effects of kindling and injection of neuroactive substances on behavior and electrophysiological patterns may offer a model of how limbic seizures in humans increase the vulnerability of TLE patients to psychiatric symptoms.
Topics: Amygdala; Animals; Comorbidity; Epilepsy, Temporal Lobe; Hippocampus; Humans; Limbic System; Models, Animal; Psychotic Disorders; Risk Factors; Thalamus
PubMed: 23429818
DOI: 10.1016/j.rbp.2012.04.007 -
Psychoneuroendocrinology Jan 2019Trauma alters neuroendocrine responses to stress and increases vulnerability to stress-related disorders. Yet, relationships among trauma, stress-induced neural changes...
Trauma alters neuroendocrine responses to stress and increases vulnerability to stress-related disorders. Yet, relationships among trauma, stress-induced neural changes and hypothalamic-pituitary-adrenal (HPA) axis activity have not been determined. The present study used functional magnetic resonance imaging to investigate the impact of life trauma on basal cortisol levels and neural responses to acute stress in 73 healthy individuals during brief stress and neutral-relaxing imagery using a well-established, individualized imagery method. We hypothesized that trauma experience would have a negative impact on brain function, resulting in altered basal cortisol levels via dysregulated neural control over the HPA axis system. Results showed that higher life trauma exposure was significantly associated with lower basal cortisol levels. Neuroimaging results indicated that both higher life trauma and low morning cortisol levels were associated with increased response to acute stress in limbic-medial temporal lobe (MTL) regions including the amygdala and hippocampus. A mediation analysis showed that increased limbic-MTL response to stress mediated the relationship between life trauma and low cortisol levels. Findings revealed a significant impact of lifetime trauma on neural responses to acute stress and HPA axis activity. Life trauma may sensitize limbic-MTL regions and its related peripheral systems, which could compromise stress regulation and HPA axis function, and increase risk for negative stress-related health outcomes.
Topics: Adrenocorticotropic Hormone; Adult; Adverse Childhood Experiences; Amygdala; Female; Hippocampus; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Hypothalamus; Life Change Events; Limbic System; Magnetic Resonance Imaging; Male; Pituitary-Adrenal System; Stress, Psychological
PubMed: 30172968
DOI: 10.1016/j.psyneuen.2018.08.023 -
Frontiers in Neuroendocrinology Oct 2009Vertebrate animals exhibit a spectacular diversity of social behaviors, yet a variety of basic social behavior processes are essential to all species. These include... (Review)
Review
Vertebrate animals exhibit a spectacular diversity of social behaviors, yet a variety of basic social behavior processes are essential to all species. These include social signaling; discrimination of conspecifics and sexual partners; appetitive and consummatory sexual behaviors; aggression and dominance behaviors; and parental behaviors (the latter with rare exceptions). These behaviors are of fundamental importance and are regulated by an evolutionarily conserved, core social behavior network (SBN) of the limbic forebrain and midbrain. The SBN encodes social information in a highly dynamic, distributed manner, such that behavior is most strongly linked to the pattern of neural activity across the SBN, not the activity of single loci. Thus, shifts in the relative weighting of activity across SBN nodes can conceivably produce almost limitless variation in behavior, including diversity across species (as weighting is modified through evolution), across behavioral contexts (as weights change temporally) and across behavioral phenotypes (as weighting is specified through heritable and developmental processes). Individual neural loci may also express diverse relationships to behavior, depending upon temporal variations in their functional connectivity to other brain regions ("neural context"). We here review the basic properties of the SBN and show how behavioral variation relates to functional connectivity of the network, and discuss ways in which neuroendocrine factors adjust network activity to produce behavioral diversity. In addition to the actions of steroid hormones on SBN state, we examine the temporally plastic and evolutionarily labile properties of the nonapeptides (the vasopressin- and oxytocin-like neuropeptides), and show how variations in nonapeptide signaling within the SBN serve to promote behavioral diversity across social contexts, seasons, phenotypes and species. Although this diversity is daunting in its complexity, the search for common "organizing principles" has become increasingly fruitful. We focus on multiple aspects of behavior, including sexual behavior, aggression and affiliation, and in each of these areas, we show how broadly relevant insights have been obtained through the examination of behavioral diversity in a wide range of vertebrate taxa.
Topics: Aggression; Animals; Behavior, Animal; Limbic System; Nerve Net; Neurons; Neurosecretory Systems; Neurotransmitter Agents; Seasons; Social Behavior; Vertebrates
PubMed: 19520105
DOI: 10.1016/j.yfrne.2009.05.007 -
Brain Structure & Function Sep 2008The neural networks that putatively modulate aspects of normal emotional behavior have been implicated in the pathophysiology of mood disorders by converging evidence... (Review)
Review
The neural networks that putatively modulate aspects of normal emotional behavior have been implicated in the pathophysiology of mood disorders by converging evidence from neuroimaging, neuropathological and lesion analysis studies. These networks involve the medial prefrontal cortex (MPFC) and closely related areas in the medial and caudolateral orbital cortex (medial prefrontal network), amygdala, hippocampus, and ventromedial parts of the basal ganglia, where alterations in grey matter volume and neurophysiological activity are found in cases with recurrent depressive episodes. Such findings hold major implications for models of the neurocircuits that underlie depression. In particular evidence from lesion analysis studies suggests that the MPFC and related limbic and striato-pallido-thalamic structures organize emotional expression. The MPFC is part of a larger "default system" of cortical areas that include the dorsal PFC, mid- and posterior cingulate cortex, anterior temporal cortex, and entorhinal and parahippocampal cortex, which has been implicated in self-referential functions. Dysfunction within and between structures in this circuit may induce disturbances in emotional behavior and other cognitive aspects of depressive syndromes in humans. Further, because the MPFC and related limbic structures provide forebrain modulation over visceral control structures in the hypothalamus and brainstem, their dysfunction can account for the disturbances in autonomic regulation and neuroendocrine responses that are associated with mood disorders. This paper discusses these systems together with the neurochemical systems that impinge on them and form the basis for most pharmacological therapies.
Topics: Animals; Brain; Depression; Emotions; Humans; Limbic System; Mood Disorders; Nerve Net; Prefrontal Cortex
PubMed: 18704495
DOI: 10.1007/s00429-008-0189-x -
Reviews in the Neurosciences 2012The addictive properties of psychostimulants such as cocaine are rooted in their ability to activate the mesocorticolimbic dopamine (DA) system. This system consists... (Review)
Review
The addictive properties of psychostimulants such as cocaine are rooted in their ability to activate the mesocorticolimbic dopamine (DA) system. This system consists primarily of dopaminergic projections arising from the ventral tegmental area (VTA) and projecting to the limbic and cortical brain regions, such as the nucleus accumbens (NAc) and prefrontal cortex (PFC). While the basic anatomy and functional relevance of the mesocorticolimbic DA system is relatively well-established, a key challenge remaining in addiction research is to understand where and how molecular adaptations and corresponding changes in function of this system facilitate a pathological desire to seek and take drugs. Several lines of evidence indicate that inhibitory signaling, particularly signaling mediated by the Gi/o class of heterotrimeric GTP-binding proteins (G proteins), plays a key role in the acute and persistent effects of drugs of abuse. Moreover, recent evidence argues that these signaling pathways are targets of drug-induced adaptations. In this review we discuss inhibitory signaling pathways involving DA and the inhibitory neurotransmitter GABA in two brain regions - the VTA and PFC - that are central to the effects of acute and repeated cocaine exposure and represent sites of adaptations linked to addiction-related behaviors including sensitization, craving, and relapse.
Topics: Adaptation, Physiological; Animals; Cerebral Cortex; Cocaine; Dopamine Uptake Inhibitors; Humans; Limbic System; Neural Inhibition; Neural Pathways; Receptors, G-Protein-Coupled; Signal Transduction
PubMed: 22944653
DOI: 10.1515/revneuro-2012-0045 -
Current Neuropharmacology 2017In 1990, Blum and associates provided the first confirmed genetic link between the DRD2 polymorphisms and alcoholism. This finding was based on an earlier conceptual... (Review)
Review
BACKGROUND
In 1990, Blum and associates provided the first confirmed genetic link between the DRD2 polymorphisms and alcoholism. This finding was based on an earlier conceptual framework, which served as a blueprint for their seminal genetic association discovery they termed "Brain Reward Cascade." These findings were followed by a new way of understanding all addictive behaviors (substance and non-substance) termed "Reward Deficiency Syndrome" (RDS). RDS incorporates a complex multifaceted array of inheritable behaviors that are polygenic.
OBJECTIVE
In this review article, we attempt to clarify these terms and provide a working model to accurately diagnose and treat these unwanted behaviors.
METHOD
We are hereby proposing the development of a translational model we term "Reward Deficiency Solution System™" that incorporates neurogenetic testing and meso-limbic manipulation of a "hypodopaminergic" trait/state, which provides dopamine agonistic therapy (DAT) as well as reduced "dopamine resistance," while embracing "dopamine homeostasis."
RESULT
The result is better recovery and relapse prevention, despite DNA antecedents, which could impact the recovery process and relapse. Understanding the commonality of mental illness will transform erroneous labeling based on symptomatology, into a genetic and anatomical etiology. WC: 184.
Topics: Animals; Behavior, Addictive; Disease Models, Animal; Dopamine; Dopamine Agonists; Genetic Predisposition to Disease; Humans; Limbic System; Reward
PubMed: 27174576
DOI: 10.2174/1570159x13666160512150918 -
Hearing Research Jul 2007A synthesis of cat auditory cortex (AC) organization is presented in which the extrinsic and intrinsic connections interact to derive a unified profile of the auditory... (Review)
Review
A synthesis of cat auditory cortex (AC) organization is presented in which the extrinsic and intrinsic connections interact to derive a unified profile of the auditory stream and use it to direct and modify cortical and subcortical information flow. Thus, the thalamocortical input provides essential sensory information about peripheral stimulus events, which AC redirects locally for feature extraction, and then conveys to parallel auditory, multisensory, premotor, limbic, and cognitive centers for further analysis. The corticofugal output influences areas as remote as the pons and the cochlear nucleus, structures whose effects upon AC are entirely indirect, and it has diverse roles in the transmission of information through the medial geniculate body and inferior colliculus. The distributed AC is thus construed as a functional network in which the auditory percept is assembled for subsequent redistribution in sensory, premotor, and cognitive streams contingent on the derived interpretation of the acoustic events. The confluence of auditory and multisensory streams likely precedes cognitive processing of sound. The distributed AC constitutes the largest and arguably the most complete representation of the auditory world. Many facets of this scheme may apply in rodent and primate AC as well. We propose that the distributed auditory cortex contributes to local processing regimes in regions as disparate as the frontal pole and the cochlear nucleus to construct the acoustic percept.
Topics: Acetylcholine; Animals; Auditory Cortex; Auditory Pathways; Auditory Perception; Cats; Cognition; Limbic System; Neurochemistry; Neuronal Plasticity; Thalamus; gamma-Aminobutyric Acid
PubMed: 17329049
DOI: 10.1016/j.heares.2007.01.017 -
Epilepsia 1999Status epilepticus (SE) is associated with both acute and permanent pathological sequellae. One common long term consequence of SE is the subsequent development of a... (Review)
Review
Status epilepticus (SE) is associated with both acute and permanent pathological sequellae. One common long term consequence of SE is the subsequent development of a chronic epileptic condition, with seizures frequently originating from and involving the limbic system. Following SE, many studies have demonstrated selective loss of neurons within the hilar region of the dentate gyrus, CA1 and CA3 pyramidal neurons. Selective loss of distinct subpopulations of interneurons throughout the hippocampus is also frequently evident, although interneurons as a whole are selectively spared relative to principal cells. Accompanying this loss of neurons are circuit rearrangements, the most widely studied being the sprouting of dentate granule cell (DGC) axons back onto the inner molecular layer of the dentate gyrus, termed mossy fiber sprouting. Less studied are the receptor properties of the surviving neurons within the epileptic hippocampus following SE. DGCs in epileptic animals exhibit marked alterations in the functional and pharmacological properties of gamma-aminobutyric acid (GABA) receptors. DGCs have a significantly elevated density of GABA(A) receptors in chronically epileptic animals. In addition, the pharmacological properties of GABA(A) receptors in post-SE epileptic animals are quite different compared to controls. In particular, GABA(A) receptors in DGCs from epileptic animals show an enhanced sensitivity to blockade by zinc, and a markedly altered sensitivity to modulation by benzodiazepines. These pharmacological differences may be due to a decreased expression of alpha1 subunits of the GABA(A) receptor relative to other alpha subunits in DGCs of post-SE epileptic animals. These GABA(A) receptor alterations precede the onset of spontaneous seizures in post-SE DGCs, and so are temporally positioned to contribute to the process of epileptogenesis in the limbic system. The presence of zinc sensitive GABA receptors combined with the presence of zinc-containing "sprouted" mossy fiber terminals innervating the proximal dendrites of DGCs in the post-SE epileptic hippocampus prompted the development of the hypothesis that repetitive activation of the DG in the epileptic brain could result in the release of zine. This zinc in turn may diffuse to and block "epileptic" zinc-sensitive GABA(A) receptors in DGCs, leading to a catastrophic failure of inhibition and concomitant enhanced seizure propensity in the post-SE epileptic limbic system.
Topics: Animals; Blotting, Southern; Dentate Gyrus; Disease Models, Animal; Gene Expression; Hippocampus; Humans; Ion Channels; Limbic System; Mossy Fibers, Hippocampal; RNA, Messenger; Receptors, GABA-A; Reverse Transcriptase Polymerase Chain Reaction; Status Epilepticus
PubMed: 10421558
DOI: 10.1111/j.1528-1157.1999.tb00875.x -
Neuropsychopharmacology : Official... Jan 2011In this review, we consider affective cognition, responses to emotional stimuli occurring in the context of cognitive evaluation. In particular, we discuss emotion... (Review)
Review
In this review, we consider affective cognition, responses to emotional stimuli occurring in the context of cognitive evaluation. In particular, we discuss emotion categorization, biasing of memory and attention, as well as social/moral emotion. We discuss limited neuropsychological evidence suggesting that affective cognition depends critically on the amygdala, ventromedial frontal cortex, and the connections between them. We then consider neuroimaging studies of affective cognition in healthy volunteers, which have led to the development of more sophisticated neural models of these processes. Disturbances of affective cognition are a core and specific feature of mood disorders, and we discuss the evidence supporting this claim, both from behavioral and neuroimaging perspectives. Serotonin is considered to be a key neurotransmitter involved in depression, and there is a considerable body of research exploring whether serotonin may mediate disturbances of affective cognition. The final section presents an overview of this literature and considers implications for understanding the pathophysiology of mood disorder as well as developing and evaluating new treatment strategies.
Topics: Affect; Animals; Brain; Brain Chemistry; Cognition; Depressive Disorder; Humans; Limbic System; Mood Disorders; Neural Pathways; Prefrontal Cortex; Serotonin
PubMed: 20571485
DOI: 10.1038/npp.2010.77