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Journal articles on the topic 'Limbic circuit'

Author: Grafiati

Published: 2 November 2024

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1

Mehlman, Max L., Shawn S. Winter, Stephane Valerio, and Jeffrey S. Taube. "Functional and anatomical relationships between the medial precentral cortex, dorsal striatum, and head direction cell circuitry. I. Recording studies." Journal of Neurophysiology 121, no. 2 (February 1, 2019): 350–70. http://dx.doi.org/10.1152/jn.00143.2018.

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Head direction (HD) cells fire as a function of the animal’s directional heading and provide the animal with a sense of direction. In rodents, these neurons are located primarily within the limbic system, but small populations of HD cells are found in two extralimbic areas: the medial precentral cortex (PrCM) and dorsal striatum (DS). HD cell activity in these structures could be driven by output from the limbic HD circuit or generated intrinsically. We examined these possibilities by recording the activity of PrCM and DS neurons in control rats and in rats with anterodorsal thalamic nucleus (ADN) lesions, a manipulation that disrupts the limbic HD signal. HD cells in the PrCM and DS of control animals displayed characteristics similar to those of limbic HD cells, and these extralimbic HD signals were eliminated in animals with complete ADN lesions, suggesting that the PrCM and DS HD signals are conveyed from the limbic HD circuit. Angular head velocity cells recorded in the PrCM and DS were unaffected by ADN lesions. Next, we determined if the PrCM and DS convey necessary self-motion signals to the limbic HD circuit. Limbic HD cell activity recorded in the ADN remained intact following combined lesions of the PrCM and DS. Collectively, these experiments reveal a unidirectional functional relationship between the limbic HD circuit and the PrCM and DS; the limbic system generates the HD signal and transmits it to the PrCM and DS, but these extralimbic areas do not provide critical input or feedback to limbic HD cells. NEW & NOTEWORTHY Head direction (HD) cells have been extensively studied within the limbic system. The lesion and recording experiments reported here examined two relatively understudied populations of HD cells located outside of the canonical limbic HD circuit in the medial precentral cortex and dorsal striatum. We found that HD cell activity in these two extralimbic areas is driven by output from the limbic HD circuit, revealing that HD cell circuitry functionally extends beyond the limbic system.

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2

Joel, Daphna. "The limbic basal-ganglia-thalamocortical circuit and goal-directed behavior." Behavioral and Brain Sciences 22, no. 3 (June 1999): 525–26. http://dx.doi.org/10.1017/s0140525x99292047.

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Depue & Collins's model of incentive-motivational modulation of goal-directed behavior subserved by a medial orbital prefrontal cortical (MOC) network is appealing, but it leaves several questions unanswered: How are the stimuli that elicit an incentive motivational state selected? How does the incentive motivational state created by the MOC network modulate behavior? What is the function of the dopaminergic input to the striatum? This commentary suggests possible answers, based on the open-interconnected model of basal-ganglia-thalamocortical circuits, in which the limbic circuit selects goals and, via its connections with the motor and the associative circuits, directs behavior according to those goals, elaborating on the role of dopamine.

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Kaushal, Parth Sarthi, Brijesh Saran, Abhay Bazaz, and Harshit Tiwari. "A brief review of limbic system anatomy, function, and its clinical implication." Santosh University Journal of Health Sciences 10, no. 1 (January 2024): 26–32. http://dx.doi.org/10.4103/sujhs.sujhs_19_24.

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ABSTRACT Introduction: The limbic system, also known as the paleomammalian cortex, is a complex network of brain regions that plays a crucial role in our behavior, memory, and emotional experiences. Objective: This review aims to explore the structure, role, and clinical implications of the limbic system. It also seeks to understand how the concept of the limbic system has evolved over time, from Broca’s large limbic lobe to MacLean’s triune brain theory. Methods: The study involves an in-depth exploration of the limbic system’s constituent parts, including the limbic cortex, hippocampal formation, amygdala, septal area, and hypothalamus. It also examines the Papez and Yakovlev circuits, which are vital for emotion control. Result: The limbic system is involved in various processes, including long-term memory, spatial memory, autonomic function regulation, and the regulation of emotional reactions and behaviors. It is also essential for smell, hunger, sleep, dreams, and memory consolidation. The limbic system plays a significant role in several diseases, including epilepsy, limbic encephalitis, dementia, affective disorders, schizophrenia, KluverBucy syndrome, autism, attention deficit/hyperactivity disorder, Korsakoff’s psychosis, and anxiety disorders. Conclusion: Understanding the functional neuroanatomy of the limbic system is crucial for comprehending human behavior and its anomalies. This review updates the original Papez circuit and emphasizes the role of the limbic system in behavior and neuropsychiatric disorders. It provides valuable insights into a range of neuropsychiatric disorders.

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Mehlman, Max L., Shawn S. Winter, and Jeffrey S. Taube. "Functional and anatomical relationships between the medial precentral cortex, dorsal striatum, and head direction cell circuitry. II. Neuroanatomical studies." Journal of Neurophysiology 121, no. 2 (February 1, 2019): 371–95. http://dx.doi.org/10.1152/jn.00144.2018.

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An animal’s directional heading within its environment is encoded by the activity of head direction (HD) cells. In rodents, these neurons are found primarily within the limbic system in the interconnected structures that form the limbic HD circuit. In our accompanying report in this issue, we describe two HD cell populations located outside of this circuit in the medial precentral cortex (PrCM) and dorsal striatum (DS). These extralimbic areas receive their HD signals from the limbic system but do not provide critical input or feedback to limbic HD cells (Mehlman ML, Winter SS, Valerio S, Taube JS. J Neurophysiol 121: 350–370, 2019.). In this report, we complement our previous lesion and recording experiments with a series of neuroanatomical tracing studies in rats designed to examine patterns of connectivity between the PrCM, DS, limbic HD circuit, and related spatial processing circuitry. Retrograde tracing revealed that the DS receives direct input from numerous structures known to contain HD cells and/or other spatially tuned cell types. Importantly, these projections preferentially target and converge within the most medial portion of the DS, the same area in which we previously recorded HD cells. The PrCM receives direct input from a subset of these spatial processing structures. Anterograde tracing identified indirect pathways that could permit the PrCM and DS to convey self-motion information to the limbic HD circuit. These tracing studies reveal the anatomical basis for the functional relationships observed in our lesion and recording experiments. Collectively, these findings expand our understanding of how spatial processing circuitry functionally and anatomically extends beyond the limbic system into the PrCM and DS. NEW & NOTEWORTHY Head direction (HD) cells are located primarily within the limbic system, but small populations of extralimbic HD cells are found in the medial precentral cortex (PrCM) and dorsal striatum (DS). The neuroanatomical tracing experiments reported here explored the pathways capable of transmitting the HD signal to these extralimbic areas. We found that projections arising from numerous spatial processing structures converge within portions of the PrCM and DS that contain HD cells.

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5

Frenois, F. "A Specific Limbic Circuit Underlies Opiate Withdrawal Memories." Journal of Neuroscience 25, no. 6 (February 9, 2005): 1366–74. http://dx.doi.org/10.1523/jneurosci.3090-04.2005.

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6

Kalin, Ned H. "Prefrontal Cortical and Limbic Circuit Alterations in Psychopathology." American Journal of Psychiatry 176, no. 12 (December 1, 2019): 971–73. http://dx.doi.org/10.1176/appi.ajp.2019.19101036.

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7

Gabriel, Michael, and David M. Smith. "What does the limbic memory circuit actually do?" Behavioral and Brain Sciences 22, no. 3 (June 1999): 451. http://dx.doi.org/10.1017/s0140525x99282039.

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We applaud Aggleton & Brown's affirmation of limbic diencephalic-hippocampal interaction as a key memory substrate. However, we do not agree with a thesis of diencephalic-hippocampal strict dedication to episodic memory. Instead, this circuitry supports the production of context-specific patterns of activation that subserve retrieval for a broad class of memory phenomena, including goal-directed instrumental behavior of animals and episodic memory of humans.

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Pleil, K. E., J. F. DiBerto, A. M. Kendra, A. Shirke, S. Chien, and T. L. Kash. "A thalamo-limbic neuropeptide circuit driving binge drinking behavior." Alcohol 60 (May 2017): 223. http://dx.doi.org/10.1016/j.alcohol.2017.02.269.

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9

Panzer, Annie, and Margaretha Viljoen. "The mother as hidden regulator." Suid-Afrikaanse Tydskrif vir Natuurwetenskap en Tegnologie 22, no. 4 (September 26, 2003): 103–5. http://dx.doi.org/10.4102/satnt.v22i4.218.

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A human baby is born with a decidedly immature brain, and is absolutely dependent on an intense relationship with its mother (or primary caregiver) for brain maturation. In the short term, maternal regulation contributes to a more joyful baby, while in the long term it leads to the internalisation and development of self-regulatory capabilities. The ability to regulate one’s own emotional states is based on the development of right orbitofrontal dominance of dual limbic circuits, i.e. the excitatory sympathetic ventral tegmental circuit, and the inhibitory parasympathetic lateral tegmental circuit. Thus the child will be able to calm down after nigh overwhelming emotions by activating the parasympathetic system, but also to bounce back after setbacks by activating the sympathetic system. The mother influences the parcellation of the two limbic systems and thus the permanent excitation-inhibition autonomic balance of its prefrontal regulatory system. Repeated unregulated emotional states in the practicing period from 12-18 months pave the way for various psychological and psychiatric disorders in adulthood. It is worrisome that many children pass through this critical time in nursery schools, where a shortage of adult staff may lead to the scenario where a child’s emotions are repeatedly not modulated, with dire consequences for the internalisation of its future self-regulating capabilities.

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Keser, Zafer, Arash Kamali, Kyan Younes, Paul E. Schulz, Flavia M. Nelson, and Khader M. Hasan. "Yakovlev's Basolateral Limbic Circuit in Multiple Sclerosis Related Cognitive Impairment." Journal of Neuroimaging 28, no. 6 (June 12, 2018): 596–600. http://dx.doi.org/10.1111/jon.12531.

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11

Brody, Arthur L., Michael W. Barsom, Robert G. Bota, and Sanjaya Saxena. "Prefrontal-subcortical and limbic circuit mediation of major depressive disorder." Seminars in Clinical Neuropsychiatry 6, no. 2 (April 2001): 102–12. http://dx.doi.org/10.1053/scnp.2001.21837.

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12

Nanda, Saheba, Krishna Priya, Tasmia Khan, Puja Patel, Heela Azizi, Deepa Nuthalapati, Christen Paul, et al. "Combined Parietal-Insular-Striatal Cortex Stroke with New-Onset Hallucinations: Supporting the Salience Network Model of Schizophrenia." Psychiatry Journal 2020 (January 24, 2020): 1–6. http://dx.doi.org/10.1155/2020/4262050.

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Brain imaging studies have identified multiple neuronal networks and circuits in the brain with altered functioning in patients with schizophrenia. These include the hippocampo-cerebello-cortical circuit, the prefrontal-thalamic-cerebellar circuit, functional integration in the bilateral caudate nucleus, and the salience network consisting of the insular cortex, parietal anterior cingulate cortex, and striatum, as well as limbic structures. Attributing psychotic symptoms to any of these networks in schizophrenia is confounded by the disruption of these networks in schizophrenic patients. Such attribution can be done with isolated dysfunction in any of these networks with concurrent psychotic symptoms. We present the case of a patient who presents with new-onset hallucinations and a stroke in brain regions similar to the salience network (insular cortex, parietal cortex, and striatum). The implication of these findings in isolating psychotic symptoms of the salience network is discussed.

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Smith, David M., Yan Yu Yang, Dev Laxman Subramanian, Adam M. P. Miller, David A. Bulkin, and L. Matthew Law. "The limbic memory circuit and the neural basis of contextual memory." Neurobiology of Learning and Memory 187 (January 2022): 107557. http://dx.doi.org/10.1016/j.nlm.2021.107557.

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Porter, W. A., J. C. Marsh, A. Herskovic, B. T. Gielda, J. Smart, and J. V. Turian. "Why Do Intracranial Metastases Spare the Limbic Circuit? A Volumetric Analysis." International Journal of Radiation Oncology*Biology*Physics 75, no. 3 (November 2009): S243. http://dx.doi.org/10.1016/j.ijrobp.2009.07.560.

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15

Levine, Olivia, Mary Jane Skelly, John Millerx, Jean Rivera, Pasha Ghazal, Jeffrey DiBerto, Thomas L. Kash, and Kristen Pleil. "Sex-Dependent Plasticity in a Thalamo-Limbic Circuit for Binge Drinking." Alcohol 109 (June 2023): 85. http://dx.doi.org/10.1016/j.alcohol.2023.03.077.

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Vega-Zelaya, Lorena, and Jesús Pastor. "The Network Systems Underlying Emotions: The Rational Foundation of Deep Brain Stimulation Psychosurgery." Brain Sciences 13, no. 6 (June 12, 2023): 943. http://dx.doi.org/10.3390/brainsci13060943.

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Science and philosophy have tried to understand the origin of emotions for centuries. However, only in the last 150 years have we started to try to understand them in a neuroscientific scope. Emotions include physiological changes involving different systems, such as the endocrine or the musculoskeletal, but they also cause a conscious experience of those changes that are embedded in memory. In addition to the cortico-striato-thalamo-cortical circuit, which is the most important of the basal ganglia, the limbic system and prefrontal circuit are primarily involved in the process of emotion perceptions, thoughts, and memories. The purpose of this review is to describe the anatomy and physiology of the different brain structures involved in circuits that underlie emotions and behaviour, underlying the symptoms of certain psychiatric pathologies. These circuits are targeted during deep brain stimulation (DBS) and knowledge of them is mandatory to understand the clinical-physiological implications for the treatment. We summarize the main outcomes of DBS treatment in several psychiatric illness such as obsessive compulsive disorder, refractory depression, erethism and other conditions, aiming to understand the rationale for selecting these neural systems as targets for DBS.

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Volkow, Nora D., Gene-Jack Wang, Joanna S. Fowler, and Frank Telang. "Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1507 (July 24, 2008): 3191–200. http://dx.doi.org/10.1098/rstb.2008.0107.

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Drugs and food exert their reinforcing effects in part by increasing dopamine (DA) in limbic regions, which has generated interest in understanding how drug abuse/addiction relates to obesity. Here, we integrate findings from positron emission tomography imaging studies on DA's role in drug abuse/addiction and in obesity and propose a common model for these two conditions. Both in abuse/addiction and in obesity, there is an enhanced value of one type of reinforcer (drugs and food, respectively) at the expense of other reinforcers, which is a consequence of conditioned learning and resetting of reward thresholds secondary to repeated stimulation by drugs (abuse/addiction) and by large quantities of palatable food (obesity) in vulnerable individuals (i.e. genetic factors). In this model, during exposure to the reinforcer or to conditioned cues, the expected reward (processed by memory circuits) overactivates the reward and motivation circuits while inhibiting the cognitive control circuit, resulting in an inability to inhibit the drive to consume the drug or food despite attempts to do so. These neuronal circuits, which are modulated by DA, interact with one another so that disruption in one circuit can be buffered by another, which highlights the need of multiprong approaches in the treatment of addiction and obesity.

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Lenge, Matteo, Carla Marini, Edoardo Canale, Antonio Napolitano, Salvatore De Masi, Marina Trivisano, Davide Mei, et al. "Quantitative MRI-Based Analysis Identifies Developmental Limbic Abnormalities in PCDH19 Encephalopathy." Cerebral Cortex 30, no. 11 (June 25, 2020): 6039–50. http://dx.doi.org/10.1093/cercor/bhaa177.

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Abstract Protocadherin-19 (PCDH19) is a calcium dependent cell-adhesion molecule involved in neuronal circuit formation with prevalent expression in the limbic structures. PCDH19-gene mutations cause a developmental encephalopathy with prominent infantile onset focal seizures, variably associated with intellectual disability and autistic features. Diagnostic neuroimaging is usually unrevealing. We used quantitative MRI to investigate the cortex and white matter in a group of 20 PCDH19-mutated patients. By a statistical comparison between quantitative features in PCDH19 brains and in a group of age and sex matched controls, we found that patients exhibited bilateral reductions of local gyrification index (lGI) in limbic cortical areas, including the parahippocampal and entorhinal cortex and the fusiform and lingual gyri, and altered diffusivity features in the underlying white matter. In patients with an earlier onset of seizures, worse psychiatric manifestations and cognitive impairment, reductions of lGI and diffusivity abnormalities in the limbic areas were more pronounced. Developmental abnormalities involving the limbic structures likely represent a measurable anatomic counterpart of the reduced contribution of the PCDH19 protein to local cortical folding and white matter organization and are functionally reflected in the phenotypic features involving cognitive and communicative skills as well as local epileptogenesis.

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Fridgeirsson, Egill Axfjord, Martijn Figee, Judy Luigjes, Pepijn van den Munckhof, P. Richard Schuurman, Guido van Wingen, and Damiaan Denys. "Deep brain stimulation modulates directional limbic connectivity in obsessive-compulsive disorder." Brain 143, no. 5 (April 30, 2020): 1603–12. http://dx.doi.org/10.1093/brain/awaa100.

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Abstract Deep brain stimulation is effective for patients with treatment-refractory obsessive-compulsive disorder. Deep brain stimulation of the ventral anterior limb of the internal capsule rapidly improves mood and anxiety with optimal stimulation parameters. To understand these rapid effects, we studied functional interactions within the affective amygdala circuit. We compared resting state functional MRI data during chronic stimulation versus 1 week of stimulation discontinuation in patients, and obtained two resting state scans from matched healthy volunteers to account for test-retest effects. Imaging data were analysed using functional connectivity analysis and dynamic causal modelling. Improvement in mood and anxiety following deep brain stimulation was associated with reduced amygdala-insula functional connectivity. Directional connectivity analysis revealed that deep brain stimulation increased the impact of the ventromedial prefrontal cortex on the amygdala, and decreased the impact of the amygdala on the insula. These results highlight the importance of the amygdala circuit in the pathophysiology of obsessive-compulsive disorder, and suggest a neural systems model through which negative mood and anxiety are modulated by stimulation of the ventral anterior limb of the internal capsule for obsessive-compulsive disorder and possibly other psychiatric disorders.

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Zhang, X., S. Wang, and Q. Gong. "Gray Matter Deficits of Cortical-striatal-limbic Circuit in Social Anxiety Disorder." European Psychiatry 65, S1 (June 2022): S399—S400. http://dx.doi.org/10.1192/j.eurpsy.2022.1012.

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Introduction The extant findings have been of great heterogeneity due to partial volume effects in the investigation of cortical gray matter volume (GMV), high comorbidity with other psychiatric disorders, and concomitant therapy in the neuroimaging studies of social anxiety disorder (SAD). Objectives To identity gray matter deficits in cortical and subcortical structures in non-comorbid never-treated patients, so as to explore the “pure” SAD-specific pathophysiology and neurobiology. Methods Thirty-two non-comorbid free-of-treatment patients with SAD and 32 demography-matched healthy controls were recruited to undergo high-resolution 3.0-Tesla T1-weighted MRI. Cortical thickness (CT) and subcortical GMV were estimated using FreeSurfer; then the whole-brain vertex-wise analysis was performed to compare group differences in CT. Besides, differences in subcortical GMV of priori selected regions-of-interest: amygdala, hippocampus, putamen, and pallidum were compared by an analysis of covariance with age, gender, and total subcortical GMV as covariates. Results The SAD patients demonstrated significantly decreased CT near-symmetrically in the bilateral prefrontal cortex (Monte Carlo simulations of P < 0.05). Besides, smaller GMV in the left hippocampus and pallidum were also observed in the SAD cohort (two-sample t-test of P < 0.05). Conclusions For the first time, the current study investigated the structural alterations of CT and subcortical GMV in non-comorbid never-treated patients with SAD. Our findings provide preliminary evidences that structural deficits in cortical-striatal-limbic circuit may contribute to the psychopathological basis of SAD, and offer more detailed structural substrates for the involvement of such aberrant circuit in the imbalance between defective bottom-up response and top-down control to external stimuli in SAD. Disclosure No significant relationships.

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21

Micevych, Paul E., Clair B. Eckersell, Nicholas Brecha, and Krista L. Holland. "Estrogen Modulation of Opioid and Cholecystokinin Systems in the Limbic-Hypothalamic Circuit." Brain Research Bulletin 44, no. 4 (January 1997): 335–43. http://dx.doi.org/10.1016/s0361-9230(97)00212-8.

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22

Nazem-Zadeh, Mohammad-Reza, Christopher H. Chapman, Theodore L. Lawrence, Christina I. Tsien, and Yue Cao. "Radiation therapy effects on white matter fiber tracts of the limbic circuit." Medical Physics 39, no. 9 (August 24, 2012): 5603–13. http://dx.doi.org/10.1118/1.4745560.

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23

Wang, Zan, Zhengsheng Zhang, Chunming Xie, Hao Shu, Duan Liu, and Zhijun Zhang. "Identification of the Neural Circuit Underlying Episodic Memory Deficit in Amnestic Mild Cognitive Impairment via Machine Learning on Gray Matter Volume." Journal of Alzheimer's Disease 84, no. 3 (November 23, 2021): 959–64. http://dx.doi.org/10.3233/jad-210579.

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Based on whole-brain gray matter volume (GMV), we used relevance vector regression to predict the Rey’s Auditory Verbal Learning Test Delayed Recall (AVLT-DR) scores of individual amnestic mild cognitive impairment (aMCI) patient. The whole-brain GMV pattern could significantly predict the AVLT-DR scores (r = 0.54, p < 0.001). The most important GMV features mainly involved default-mode (e.g., posterior cingulate gyrus, angular gyrus, and middle temporal gyrus) and limbic systems (e.g., hippocampus and parahippocampal gyrus). Therefore, our results provide evidence supporting the idea that the episodic memory deficit in aMCI patients is associated with disruption of the default-mode and limbic systems.

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Trouillet, Anne-Charlotte, Matthieu Keller, Jan Weiss, Trese Leinders-Zufall, Lutz Birnbaumer, Frank Zufall, and Pablo Chamero. "Central role of G protein Gαi2 and Gαi2+ vomeronasal neurons in balancing territorial and infant-directed aggression of male mice." Proceedings of the National Academy of Sciences 116, no. 11 (February 25, 2019): 5135–43. http://dx.doi.org/10.1073/pnas.1821492116.

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Aggression is controlled by the olfactory system in many animal species. In male mice, territorial and infant-directed aggression are tightly regulated by the vomeronasal organ (VNO), but how diverse subsets of sensory neurons convey pheromonal information to limbic centers is not yet known. Here, we employ genetic strategies to show that mouse vomeronasal sensory neurons expressing the G protein subunit Gαi2 regulate male–male and infant-directed aggression through distinct circuit mechanisms. Conditional ablation of Gαi2 enhances male–male aggression and increases neural activity in the medial amygdala (MeA), bed nucleus of the stria terminalis, and lateral septum. By contrast, conditional Gαi2 ablation causes reduced infant-directed aggression and decreased activity in MeA neurons during male–infant interactions. Strikingly, these mice also display enhanced parental behavior and elevated neural activity in the medial preoptic area, whereas sexual behavior remains normal. These results identify Gαi2 as the primary G protein α-subunit mediating the detection of volatile chemosignals in the apical layer of the VNO, and they show that Gαi2+ VSNs and the brain circuits activated by these neurons play a central role in orchestrating and balancing territorial and infant-directed aggression of male mice through bidirectional activation and inhibition of different targets in the limbic system.

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Kubota, Yasuo, and Michael Gabriel. "Studies of the limbic comparator: Limbic circuit training-induced unit activity and avoidance behavior in rabbits with anterior dorsal thalamic lesions." Behavioral Neuroscience 109, no. 2 (1995): 258–77. http://dx.doi.org/10.1037/0735-7044.109.2.258.

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Takeda, T., T. Uchihara, T. Chikugo, T. Hiraga, M. Kitaguchi, and H. Kojima. "Preferential involvement of the basolateral limbic circuit in an amyotrophic lateral sclerosis patient." European Journal of Neurology 14, no. 12 (November 15, 2007): e5-e6. http://dx.doi.org/10.1111/j.1468-1331.2007.01967.x.

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Zhukareva, V., and P. Levitt. "The limbic system-associated membrane protein (LAMP) selectively mediates interactions with specific central neuron populations." Development 121, no. 4 (April 1, 1995): 1161–72. http://dx.doi.org/10.1242/dev.121.4.1161.

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The limbic system-associated membrane protein (LAMP) is a 64–68 × 10(3) M(r) glycoprotein that is expressed by subsets of neurons that are functionally interconnected. LAMP exhibits characteristics that are indicative of a developmentally significant protein, such as an early and restricted pattern of expression and the ability to mediate specific fiber-target interactions. A potential, selective adhesive mechanism by which LAMP may regulate the formation of specific circuits is investigated in the present experiments. LAMP is readily released from intact membranes by phosphatidyl inositol-specific phospholipase C. Purified, native LAMP, isolated by PI-PLC digestion and immunoaffinity chromatography, is capable of mediating fluorescent Covasphere aggregation via homophilic binding. To test the ability of LAMP to selectively facilitate substrate adhesion and growth of neurons from LAMP-positive, in contrast to LAMP-negative regions of the developing brain, purified LAMP was dotted onto nitrocellulose-coated dishes and test cells plated. Limbic neurons from perirhinal cortex bind specifically to substrate-bound LAMP within 4 hours, forming small cell aggregates with short neuritic processes that continue to grow through a 48 hour period of monitoring. Preincubation of cells with anti-LAMP has a modest effect on cell binding but significantly reduces initiation of process growth. Non-limbic neurons from somatosensory cortex and olfactory bulb fail to bind or extend processes on the LAMP substrate to any significant extent. All cell populations bind equally well and form neurites on poly-D-lysine and laminin. The present results provide direct evidence that LAMP can specifically facilitate interactions with select neurons in the CNS during development. The data support the concept that patterned expression of unique cell adhesion molecules in functionally related regions of the mammalian brain can regulate circuit formation.

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Kornilov, Maksim V., and Ilya V. Sysoev. "Mathematical Model of a Main Rhythm in Limbic Seizures." Mathematics 11, no. 5 (March 3, 2023): 1233. http://dx.doi.org/10.3390/math11051233.

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While synchronization in the brain neural networks has been studied, the emergency of the main oscillation frequency and its evolution at different normal and pathological states remains poorly investigated. We propose a new concept of the formation of a main frequency in limbic epilepsy. The idea is that the main frequency is not a result of the activity of a single cell, but is formed due to collective dynamics in a ring of model neurons connected with delay. The individual cells are in an excitable mode providing no self-oscillations without coupling. We considered the ring of a different number of Hodgkin–Huxley neurons connected with synapses with time delay. We have shown that the proposed circuit can generate oscillatory activity with frequencies close to those experimentally observed. The frequency can be varied by changing the number of model neurons, time delay in synapses and coupling strength. The linear dependence of the oscillation period on both coupling delay and the number of neurons in the ring was hypothesized and checked by means of fitting the values obtained from the numerical experiments to the empirical formula for a constant value of coupling coefficient.

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Commons, Kathryn G., K. Ryan Connolley, and Rita J. Valentino. "A Neurochemically Distinct Dorsal Raphe-Limbic Circuit with a Potential Role in Affective Disorders." Neuropsychopharmacology 28, no. 2 (August 9, 2002): 206–15. http://dx.doi.org/10.1038/sj.npp.1300045.

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Duong-Tran, Duy, Ralph Kaufmann, Jiong Chen, Xuan Wang, Sumita Garai, Frederick H. Xu, Jingxuan Bao, et al. "Homological Landscape of Human Brain Functional Sub-Circuits." Mathematics 12, no. 3 (January 31, 2024): 455. http://dx.doi.org/10.3390/math12030455.

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Human whole-brain functional connectivity networks have been shown to exhibit both local/quasilocal (e.g., a set of functional sub-circuits induced by node or edge attributes) and non-local (e.g., higher-order functional coordination patterns) properties. Nonetheless, the non-local properties of topological strata induced by local/quasilocal functional sub-circuits have yet to be addressed. To that end, we proposed a homological formalism that enables the quantification of higher-order characteristics of human brain functional sub-circuits. Our results indicate that each homological order uniquely unravels diverse, complementary properties of human brain functional sub-circuits. Noticeably, the H1 homological distance between rest and motor task was observed at both the whole-brain and sub-circuit consolidated levels, which suggested the self-similarity property of human brain functional connectivity unraveled by a homological kernel. Furthermore, at the whole-brain level, the rest–task differentiation was found to be most prominent between rest and different tasks at different homological orders: (i) Emotion task (H0), (ii) Motor task (H1), and (iii) Working memory task (H2). At the functional sub-circuit level, the rest–task functional dichotomy of the default mode network is found to be mostly prominent at the first and second homological scaffolds. Also at such scale, we found that the limbic network plays a significant role in homological reconfiguration across both the task and subject domains, which paves the way for subsequent investigations on the complex neuro-physiological role of such network. From a wider perspective, our formalism can be applied, beyond brain connectomics, to study the non-localized coordination patterns of localized structures stretching across complex network fibers.

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Fox, Andrew S., Jonathan A. Oler, Alexander J. Shackman, Steven E. Shelton, Muthuswamy Raveendran, D. Reese McKay, Alexander K. Converse, et al. "Intergenerational neural mediators of early-life anxious temperament." Proceedings of the National Academy of Sciences 112, no. 29 (July 6, 2015): 9118–22. http://dx.doi.org/10.1073/pnas.1508593112.

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Understanding the heritability of neural systems linked to psychopathology is not sufficient to implicate them as intergenerational neural mediators. By closely examining how individual differences in neural phenotypes and psychopathology cosegregate as they fall through the family tree, we can identify the brain systems that underlie the parent-to-child transmission of psychopathology. Although research has identified genes and neural circuits that contribute to the risk of developing anxiety and depression, the specific neural systems that mediate the inborn risk for these debilitating disorders remain unknown. In a sample of 592 young rhesus monkeys that are part of an extended multigenerational pedigree, we demonstrate that metabolism within a tripartite prefrontal-limbic-midbrain circuit mediates some of the inborn risk for developing anxiety and depression. Importantly, although brain volume is highly heritable early in life, it is brain metabolism—not brain structure—that is the critical intermediary between genetics and the childhood risk to develop stress-related psychopathology.

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Yang, Jun, Lena Palaniyappan, Chang Xi, Yixin Cheng, Zebin Fan, Chujun Chen, Manqi Zhang, et al. "Aberrant integrity of the cortico-limbic-striatal circuit in major depressive disorder with suicidal ideation." Journal of Psychiatric Research 148 (April 2022): 277–85. http://dx.doi.org/10.1016/j.jpsychires.2022.02.003.

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Tan, Rachel H., Stephanie Wong, Jillian J. Kril, Olivier Piguet, Michael Hornberger, John R. Hodges, and Glenda M. Halliday. "Beyond the temporal pole: limbic memory circuit in the semantic variant of primary progressive aphasia." Brain 137, no. 7 (May 19, 2014): 2065–76. http://dx.doi.org/10.1093/brain/awu118.

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Cha, J., D. DeDora, S. Nedic, J. Ide, T. Greenberg, G. Hajcak, and L. R. Mujica-Parodi. "Clinically Anxious Individuals Show Disrupted Feedback between Inferior Frontal Gyrus and Prefrontal-Limbic Control Circuit." Journal of Neuroscience 36, no. 17 (April 27, 2016): 4708–18. http://dx.doi.org/10.1523/jneurosci.1092-15.2016.

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35

Micevych, Paul, and Catherine Ulibarri. "Development of the Limbic-Hypothalamic Cholecystokinin Circuit: A Model of Sexual Differentiation. pp. 11–22." Developmental Neuroscience 14, no. 1 (1992): 11–22. http://dx.doi.org/10.1159/000111643.

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Micevych, Paul, and Catherine Ulibarri. "Development of the Limbic-Hypothalamic Cholecystokinin Circuit: A Model of Sexual Differentiation pp. 23–34." Developmental Neuroscience 14, no. 1 (1992): 23–34. http://dx.doi.org/10.1159/000111644.

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37

Smith, K. S., and K. C. Berridge. "Opioid Limbic Circuit for Reward: Interaction between Hedonic Hotspots of Nucleus Accumbens and Ventral Pallidum." Journal of Neuroscience 27, no. 7 (February 14, 2007): 1594–605. http://dx.doi.org/10.1523/jneurosci.4205-06.2007.

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Ferrer, J. M. R., M. Cobo, and F. Mora. "The basolateral limbic circuit and self-stimulation of the medial prefrontal cortex in the rat." Physiology & Behavior 40, no. 3 (January 1987): 291–95. http://dx.doi.org/10.1016/0031-9384(87)90049-7.

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39

Lei, Xiaoxia, Juanjuan Ren, Xinyue Teng, Chaoyue Guo, Zenan Wu, Lingfang Yu, Xiaochang Chen, et al. "Characterizing Unipolar and Bipolar Depression by Alterations in Inflammatory Mediators and the Prefrontal-Limbic Structural Network." Depression and Anxiety 2023 (May 24, 2023): 1–11. http://dx.doi.org/10.1155/2023/5522658.

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Objective. The prefrontal-limbic system is closely associated with emotion processing in both unipolar depression (UD) and bipolar depression (BD). Evidence for this link is derived mostly from task-fMRI studies, with limited support from structural findings. Therefore, this study explores the differences in the emotional circuit in these two disorders on a structural, large-scale network basis, coupled with the highly noted inflammatory and growth factors. Methods. In this study, 31 BD patients, 37 UD patients, and 61 age-, sex-, and education-matched healthy controls (HCs) underwent diffusion-weighted imaging (DWI) scanning and serum cytokine sampling. The study compared cytokine levels and prefrontal-limbic network alterations among the three groups and explored potential biological and neurobiological markers to distinguish the two disorders using graph theory, network-based statistics (NBS), and logistic regression. Results. Compared to BD patients, UD patients showed greater s-100β protein levels, higher efficiency of the right amygdala, and significantly elevated prefrontal-cingulate-amygdala subnetwork intensity. Importantly, the altered prefrontal-cingulate-amygdala subnetwork, nodal efficiency of the right amygdala, IL-8, IL-17, and s-100β levels were risk factors for the diagnosis of UD, whereas anxiety symptoms tended to closely correlate with BD. Moreover, binary logistic regression manifested these factors achieved an area under the curve (AUC) of the receiver operating characteristics (ROC) of 0.949, with 0.875 sensitivity and 0.938 specificity in UD vs. BD classification. Conclusions. These findings narrow the gap in the structural network of emotional circuits in bipolar and unipolar depression, pointing to distinct emotion-processing mechanisms in both disorders.

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Rajasekaran, Karthik, Jaideep Kapur, and Edward H. Bertram. "Alterations in GABAA Receptor Mediated Inhibition in Adjacent Dorsal Midline Thalamic Nuclei in a Rat Model of Chronic Limbic Epilepsy." Journal of Neurophysiology 98, no. 5 (November 2007): 2501–8. http://dx.doi.org/10.1152/jn.00139.2007.

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There is evidence that the dorsal midline thalamus is involved in the seizures of limbic epilepsy. However, little is known about the inhibitory synaptic function in this region. In the present study, inhibitory postsynaptic currents (IPSCs) mediated by GABAA receptors were recorded from the mediodorsal (MD) and paraventricular (PV) nuclei from control and epileptic animals. In the MD, the spontaneous (s)IPSCs for epileptic animals had a lower frequency, prolonged rise time, prolonged decay, but unaltered net charge transfer compared with controls. The miniature (m)IPSC parameters were unaltered in the epileptic animals. In contrast, in the PV, both sIPSCs and mIPSCs in the epileptic animals were more frequent with larger amplitudes and there was an increase in the net charge transfer compared with controls. The rise times of the sIPSCs of the PV neurons were significantly prolonged, whereas the weighted decay time of the mIPSC was significantly shortened in epileptic animals. These findings suggest that the changes associated with inhibitory synaptic transmission in limbic epilepsy are not uniform across regions in the thalamus that are part of the seizure circuit.

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Kassel, Michelle T., Julia A. Rao, Sara J. Walker, Emily M. Briceño, Laura B. Gabriel, Anne L. Weldon, Erich T. Avery, et al. "Decreased Fronto-Limbic Activation and Disrupted Semantic-Cued List Learning in Major Depressive Disorder." Journal of the International Neuropsychological Society 22, no. 4 (February 2, 2016): 412–25. http://dx.doi.org/10.1017/s1355617716000023.

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AbstractObjectives: Individuals with major depressive disorder (MDD) demonstrate poorer learning and memory skills relative to never-depressed comparisons (NDC). Previous studies report decreased volume and disrupted function of frontal lobes and hippocampi in MDD during memory challenge. However, it has been difficult to dissociate contributions of short-term memory and executive functioning to memory difficulties from those that might be attributable to long-term memory deficits. Methods: Adult males (MDD, n=19; NDC, n=22) and females (MDD, n=23; NDC, n=19) performed the Semantic List Learning Task (SLLT) during functional magnetic resonance imaging. The SLLT Encoding condition consists of 15 lists, each containing 14 words. After each list, a Distractor condition occurs, followed by cued Silent Rehearsal instructions. Post-scan recall and recognition were collected. Groups were compared using block (Encoding-Silent Rehearsal) and event-related (Words Recalled) models. Results: MDD displayed lower recall relative to NDC. NDC displayed greater activation in several temporal, frontal, and parietal regions, for both Encoding-Silent Rehearsal and the Words Recalled analyses. Groups also differed in activation patterns in regions of the Papez circuit in planned analyses. The majority of activation differences were not related to performance, presence of medications, presence of comorbid anxiety disorder, or decreased gray matter volume in MDD. Conclusions: Adults with MDD exhibit memory difficulties during a task designed to reduce the contribution of individual variability from short-term memory and executive functioning processes, parallel with decreased activation in memory and executive functioning circuits. Ecologically valid long-term memory tasks are imperative for uncovering neural correlates of memory performance deficits in adults with MDD. (JINS, 2016, 22, 412–425)

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van Zessen, R., G. van der Plasse, and R. A. H. Adan. "Contribution of the mesolimbic dopamine system in mediating the effects of leptin and ghrelin on feeding." Proceedings of the Nutrition Society 71, no. 4 (July 17, 2012): 435–45. http://dx.doi.org/10.1017/s0029665112000614.

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Feeding behaviour is crucial for the survival of an organism and is regulated by different brain circuits. Among these circuits the mesolimbic dopamine (DA) system is implicated in the anticipation and motivation for food rewards. This system consists of the dopaminergic neurons in the ventral tegmental area (VTA), and their projections to different cortico-limbic structures such as the nucleus accumbens and medial prefrontal cortex. While the importance of this system in motivational drive for different rewards, including drugs of abuse, has been clearly established, its role in energy balance remains largely unexplored. Evidence suggests that peripheral hormones such as leptin and ghrelin are involved in the anticipation and motivation for food and this might be partially mediated through their effects on the VTA. Yet, it remains to be determined whether these effects are direct effects of ghrelin and leptin onto VTA DA neurons, and to what extent indirect effects through other brain areas contribute. Elucidation of the role of leptin and ghrelin signalling on VTA DA neurons in relation to disruptions of energy balance might provide important insights into the role of this neural circuit in obesity and anorexia nervosa.

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Kishi, Masahiko, Ryuji Sakakibara, Takeshi Ogata, and Emina Ogawa. "Transient phonemic paraphasia by bilateral hippocampus lesion in a case of limbic encephalitis." Neurology International 2, no. 1 (March 29, 2010): 8. http://dx.doi.org/10.4081/ni.2010.e8.

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Although the hippocampus has not typically been identified as part of the language and aphasia circuit, recent evidence suggests that the hippocampus is closely related to naming, word priming, and anomic aphasia. A 59-year old woman with limbic encephalitis of possible autoimmune etiology, after recovery of consciousness, presented with severe memory impairment in both anterograde and retrograde modalities, episodes of fear, hallucination and convulsion, and transient fluent, phonemic paraphasia, together with small sharp waves diffusely by EEG. Brain MRI revealed bilateral symmetric, discrete lesions in the body to the infundibulum of the hippocampus. The transient phonemic paraphasia noted in our patient may have been a result of primary damage in the hippocampus and its fiber connection to the Wernicke’s area or secondary partial status epilepticus that might have originated in the hippocampus.

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Markowitsch, Hans J. "Gestalt view of the limbic system and the Papez circuit – another approach to unity and diversity of brain structures and functions." Behavioral and Brain Sciences 22, no. 3 (June 1999): 459–60. http://dx.doi.org/10.1017/s0140525x99362038.

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The idea of distinct brain systems for the processing of episodic and other forms of memory is welcome. The two brain systems actually proposed however, appear to be stripped of further existing connections and could be integrated with one another. If integrating them, it seems more logical to propose one enlarged system of limbic structures whose individual components make partly different contributions to the forms of memory under discussion.

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Myers, Brent, Eduardo Carvalho-Netto, Dayna Wick-Carlson, Christine Wu, Sam Naser, Matia B. Solomon, Yvonne M. Ulrich-Lai, and James P. Herman. "GABAergic Signaling within a Limbic-Hypothalamic Circuit Integrates Social and Anxiety-Like Behavior with Stress Reactivity." Neuropsychopharmacology 41, no. 6 (October 7, 2015): 1530–39. http://dx.doi.org/10.1038/npp.2015.311.

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Shah, Abhidha, Sukhdeep Singh Jhawar, and Atul Goel. "Analysis of the anatomy of the Papez circuit and adjoining limbic system by fiber dissection techniques." Journal of Clinical Neuroscience 19, no. 2 (February 2012): 289–98. http://dx.doi.org/10.1016/j.jocn.2011.04.039.

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Marsh, James C., Arnold M. Herskovic, Benjamin T. Gielda, Frank F. Hughes, Thomas Hoeppner, Julius Turian, and Ross A. Abrams. "Intracranial Metastatic Disease Spares the Limbic Circuit: A Review of 697 Metastatic Lesions in 107 Patients." International Journal of Radiation Oncology*Biology*Physics 76, no. 2 (February 2010): 504–12. http://dx.doi.org/10.1016/j.ijrobp.2009.02.038.

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48

McDaid, John, Martin P. Graham, and T. Celeste Napier. "Methamphetamine-Induced Sensitization Differentially Alters pCREB and ΔFosB throughout the Limbic Circuit of the Mammalian Brain." Molecular Pharmacology 70, no. 6 (September 1, 2006): 2064–74. http://dx.doi.org/10.1124/mol.106.023051.

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49

Huang, Min-Han, Sheng-Yu Fan, and I.-Mei Lin. "EEG coherences of the fronto-limbic circuit between patients with major depressive disorder and healthy controls." Journal of Affective Disorders 331 (June 2023): 112–20. http://dx.doi.org/10.1016/j.jad.2023.03.055.

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50

McIntosh, A. R., and F. Gonzalez-Lima. "Network interactions among limbic cortices, basal forebrain, and cerebellum differentiate a tone conditioned as a Pavlovian excitor or inhibitor: fluorodeoxyglucose mapping and covariance structural modeling." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1717–33. http://dx.doi.org/10.1152/jn.1994.72.4.1717.

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1. The objective was to examine how opposite learned behavioral responses to the same physical tone were differentiated by the pattern of interactions between extraauditory neural regions. This was pursued using a new approach combining behavior, neuroimaging, and network analysis to integrate information about differences in regional activity with differences in the covariance relationships between brain areas. 2. A tone was used as either a Pavlovian conditioned excitor or inhibitor. Rats were conditioned with reinforced trials of a conditioned excitor (A+) intermixed with nonreinforced trials of a tone-light compound (AX-). The tone was the excitor (A+) for the tone-excitor group and was the inhibitor (X-) for the tone-inhibitor group. After conditioning, all rats were injected with [14C(U)]2-fluoro-2-deoxyglucose (FDG) and presented with the same tone. 3. FDG autoradiography was used to measure regional activity and to generate interregional correlations of activity resulting from the presentation of the tone. A stepwise discriminant analysis was used to select brain regions that differentiated the excitor from the inhibitor effects. 4. Network analysis consisted of constructing an anatomic model of the brain regions, selected by the discriminant analysis, linking the regions with their known anatomical connections. Then, functional models for the tone-excitor and -inhibitor groups were constructed using structural equation modeling. Correlations of activity between regions were decomposed to calculate numerical weights, or path coefficients, for each anatomic path. These path coefficients were used to compare the interactions for the tone-excitor and -inhibitor models. 5. Regional differences in FDG uptake were found in the sulcal frontal cortex (SFC), lateral septum (LS), medial septum/diagonal band (MS/DB), retrosplenial cortex (RS), and dentate-interpositus nuclei of the cerebellum (DEN). Discriminant analysis selected three other regions that significantly discriminated the tone-excitor and -inhibitor groups: perirhinal cortex (PRh), nucleus accumbens (ACB), and the anteroventral nucleus of the thalamus (AVN). 6. Structural equation modeling identified two functional circuits that differentiated the groups. One involved the basal forebrain regions (LS, MS/DB, ACB) and the other limbic thalamocortical structures (SFC, RS, PRh, AVN). Differences in the interactions within these circuits were mainly in sign of the covariance relationships between regions, from positive for the tone-excitor model to negative path coefficients for the tone-inhibitor model. The path coefficient between the basal forebrain circuit and the limbic thalamocortical circuit showed the largest magnitude difference. This quantitative difference was mediated by a path from the MS/DB to PRh.(ABSTRACT TRUNCATED AT 400 WORDS)

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