scholarly journals Dorsal hippocampus contributes to model-based planning

2016 ◽  
Author(s):  
Kevin J. Miller ◽  
Matthew M. Botvinick ◽  
Carlos D. Brody

AbstractPlanning can be defined as a process of action selection that leverages an internal model of the environment. Such models provide information about the likely outcomes that will follow each selected action, and their use is a key function underlying complex adaptive behavior. However, the neural mechanisms supporting this ability remain poorly understood. In the present work, we adapt for rodents recent advances from work on human planning, presenting for the first time a task for animals which produces many trials of planned behavior per session, allowing the experimental toolkit available for use in trial-by-trial tasks for rodents to be applied to the study of planning. We take advantage of one part of this toolkit to address a perennially controversial issue in planning research: the role of the dorsal hippocampus. Although prospective representations in the hippocampus have been proposed to support model-based planning, intact planning in hippocampally damaged animals has been observed in a number of assays. Combining formal algorithmic behavioral analysis with muscimol inactivation, we provide the first causal evidence directly linking dorsal hippocampus with planning behavior. The results reported, and the methods introduced, open the door to new and more detailed investigations of the neural mechanisms of planning, in the hippocampus and throughout the brain.

2020 ◽  
Author(s):  
Kevin Miller ◽  
Sarah Jo Venditto

Decisions in the natural world are rarely made in isolation. Each action that an organism selects will affect the future situations in which it finds itself, and those situations will in turn affect the future actions that are available. Achieving real-world goals often requires successfully navigating a sequence of many actions. An efficient and flexible way to achieve such goals is to construct an internal model of the environment, and use it to plan behavior multiple steps into the future. This process is known as multi-step planning, and its neural mechanisms are only beginning to be understood. Here, we review recent advances in our understanding of these mechanisms, many of which take advantage of multi-step decision tasks for humans and animals.


2021 ◽  
Vol 11 ◽  
Author(s):  
Saboor Ahmad ◽  
Shahmshad Ahmed Khan ◽  
Khalid Ali Khan ◽  
Jianke Li

Hypopharyngeal glands (HGs) are the most important organ of hymenopterans which play critical roles for the insect physiology. In honey bees, HGs are paired structures located bilaterally in the head, in front of the brain between compound eyes. Each gland is composed of thousands of secretory units connecting to secretory duct in worker bees. To better understand the recent progress made in understanding the structure and function of these glands, we here review the ontogeny of HGs, and the factors affecting the morphology, physiology, and molecular basis of the functionality of the glands. We also review the morphogenesis of HGs in the pupal and adult stages, and the secretory role of the glands across the ages for the first time. Furthermore, recent transcriptome, proteome, and phosphoproteome analyses have elucidated the potential mechanisms driving the HGs development and functionality. This adds a comprehensive novel knowledge of the development and physiology of HGs in honey bees over time, which may be helpful for future research investigations.


2009 ◽  
Vol 296 (1) ◽  
pp. R51-R56 ◽  
Author(s):  
Lori Asarian

To investigate the role of serotonin 2C receptors (2CR), which are expressed only in the central nervous system, in the satiating actions of the gut peptides CCK and glucagon-like peptide 1 (GLP-1), we examined 1) the effect of null mutations of serotonin 2CR (2CR KO) on the eating-inhibitory potencies of dark-onset intraperitoneal injections of 0.9, 1.7, or 3.5 nmol/kg (1, 2, or 4 μg/kg) CCK and 100, 200, and 400 nmol/kg (33, 66, or 132 μg/kg) GLP-1, and 2) the effects of intraperitoneal injections of 1.7 nmol//kg CCK and 100 nmol/kg GLP-1 on neuronal activation in the brain, as measured by c-Fos expression. All CCK and GLP-1 doses decreased 30-min food intake in wild-type (WT) mice, but none of them did in 2CR KO mice. CCK increased the number of cells expressing c-Fos in the nucleus tractus solitarii (NTS) of WT, but not 2CR KO mice. CCK induced similar degrees of c-Fos expression in the paraventricular (PVN) and arcuate (Arc) nuclei of the hypothalamus of both genotypes. GLP-1, on the other hand, increased c-Fos expression similarly in the NTS of both genotypes and increased c-Fos expression more in the PVN and Arc of 2CR KO mice, but not WT mice. These results indicate that serotonin signaling via serotonin 2CR is necessary for the full satiating effects of CCK and GLP-1. In addition, they suggest that the satiating effects of the two peptides are mediated by different neural mechanisms.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Marta Vicente-Rodríguez ◽  
Rosalía Fernández-Calle ◽  
Esther Gramage ◽  
Carmen Pérez-García ◽  
María P. Ramos ◽  
...  

Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine. To test this hypothesis, we studied astrogliosis and microglial response induced by amphetamine (10 mg/kg i.p. four times, every 2 h) in different brain areas of MK−/− mice and wild type (WT) mice. We found that amphetamine-induced microgliosis and astrocytosis are enhanced in the striatum of MK−/− mice in a region-specific manner. Surprisingly, LPS-induced astrogliosis in the striatum was blocked in MK−/− mice. Since striatal neuroinflammation induced by amphetamine-type stimulants correlates with the cognitive deficits induced by these drugs, we also tested the long-term effects of periadolescent amphetamine treatment (3 mg/kg i.p. daily for 10 days) in a memory task in MK−/− and WT mice. Significant deficits in the Y-maze test were only observed in amphetamine-pretreated MK−/− mice. The data demonstrate for the first time that MK is a novel modulator of neuroinflammation depending on the inflammatory stimulus and the brain area considered. The data indicate that MK limits amphetamine-induced striatal neuroinflammation. In addition, our data demonstrate that periadolescent amphetamine treatment in mice results in transient disruption of learning and memory processes in absence of endogenous MK.


2021 ◽  
Author(s):  
Amy Cheung ◽  
Aya Matsui ◽  
Manabu Abe ◽  
Kenji Sakimura ◽  
Toshikuni Sasaoka ◽  
...  

Extensive serotonin (5-HT) innervation throughout the brain corroborates 5-HT’s modulatory role in numerous cognitive activities. Volume transmission is the major mode for 5-HT transmission but mechanisms underlying 5-HT signaling are still largely unknown. Abnormal brain 5-HT levels and function have been implicated in autism spectrum disorder (ASD). Neurexin (Nrxn) genes encode presynaptic cell adhesion molecules important for the regulation of synaptic neurotransmitter release, notably glutamatergic and GABAergic transmission. Mutations in Nrxn genes are associated with neurodevelopmental disorders including ASD. However, the role of Nrxn genes in the 5-HT system is poorly understood. Here, we generated a mouse model with all three Nrxn genes disrupted specifically in 5-HT neurons to study how Nrxns affect 5-HT transmission. Loss of Nrxns in 5-HT neurons impaired 5-HT release in the dorsal raphe nucleus and dorsal hippocampus and decreased serotonin transporter distribution in specific brain areas. Furthermore, 5-HT neuron-specific Nrxn knockout reduced sociability and increased depressive-like behavior. Our results highlight functional roles for Nrxns in 5-HT neurotransmission and the execution of complex behaviors.


2021 ◽  
Vol 48 (2) ◽  
Author(s):  
Videsha Bansal ◽  
◽  
Indranath Chatterjee ◽  

Schizophrenia is a psychological disorder, way tougher to diagnose than other psychological disorders, as it shares similar symptoms with psychosis. As we know, schizophrenia occurs due to chemical imbalance in the brain; identifying the role of neurotransmitters in schizophrenia poses a vital area to study. Neurotransmitters being the sole carrier of different brain activities, researchers have already initiated studies to investigate their role and effect in disorder. Firstly, this paper performs a critical review of the literature that dealt with different neurotransmitters in schizophrenia. Secondly, we identify the most important neurotransmitters and broadly elaborate on their functional roles and effects on the disorder. Finally, we have successfully identified various gaps and unexplored research questions to investigate these neurochemicals' role. Studies show that neurotransmitters like dopamine, glutamate, GABA, serotonin, and oxytocin are majorly responsible for schizophrenia, among which dopamine contributes the most. To the best of our knowledge, this paper encapsulates all the neurotransmitters, enzymes, and chemicals for the first time and explores their related literature. This study also identifies the most responsible chemicals involved in schizophrenia and unfolds the research community's unsolved problem.


2020 ◽  
Author(s):  
Ilaria Zuliani ◽  
Chiara Lanzillotta ◽  
Antonella Tramutola ◽  
Antonio Francioso ◽  
Sara Pagnotta ◽  
...  

AbstractProtein O-GlcNAcylation is a nutrient-related post-translational modification that, since its discovery some 30 years ago, has been associated with the development of neurodegenerative diseases. As reported in Alzheimer’s disease (AD), flaws in the cerebral glucose uptake translate into reduced hexosamine biosynthetic pathway flux and subsequently lead to aberrant protein O-GlcNAcylation. Notably, the reduction of O-GlcNAcylated proteins involves also tau and APP, thus promoting their aberrant phosphorylation in AD brain and the onset of AD pathological markers. Down syndrome (DS) individuals are characterized by the early development of AD by the age of 60 and, although the two conditions present the same pathological hallmarks and share the alteration of many molecular mechanisms driving brain degeneration, no evidence has been sought on the implication of O-GlcNAcylation in DS pathology. Our study aimed to unravel for the first time the role of protein O-GlcNacylation in DS brain alterations positing the attention of potential trisomy-related mechanisms triggering the aberrant regulation of OGT/OGA cycle. We demonstrate the disruption of O-GlcNAcylation homeostasis, as an effect of altered OGT and OGA regulatory mechanism, and confirm the relevance of O-GlcNAcylation in the appearance of AD hallmarks in the brain of a murine model of DS. Furthermore, we provide evidence for the neuroprotective effects of brain-targeted OGA inhibition. Indeed, the rescue of OGA activity was able to restore protein O-GlcNAcylation, and reduce AD-related hallmarks and decreased protein nitration, possibly as effect of induced autophagy.


1942 ◽  
Vol 88 (371) ◽  
pp. 275-281 ◽  
Author(s):  
E. L. Hutton

I have been fortunate in having the opportunity of studying several of the 15 patients treated by prefrontal leucotomy in connection with the Burden Neurological Institute. I do not propose to discuss the clinical results; it is much too early as yet for any authoritative opinion to be given, and a brief review of the literature and of the early results of the first 8 cases in this series was recently published in the Lancet. It may be mentioned, however, that the results are such as to justify the cautious adoption of this operation for therapeutic purposes. Although obviously any procedure of this kind is only justifiable on therapeutic grounds, its value for psychological medicine is far more than the mere addition of another effective therapeutic method, since for the first time in history an opportunity has been presented for the study of changes in personality produced by a relatively standardized local lesion of the brain, enabling us to investigate as never before the role of the frontal lobe in normal and abnormal mental states. This investigation involves the study and correlation of both neurological and psychological data, and encounters all the difficulties inherent in such correlation.I am only too well aware of the extremely hypothetical nature of much that follows, and of the crying need for experimental evidence to confirm or refute the view here propounded, but I believe that our knowledge of mental disorders would be immeasurably advanced could we but discover the rationale underlying our present empirical methods of therapy.


2018 ◽  
Vol 29 (10) ◽  
pp. 4154-4168 ◽  
Author(s):  
Lisa Marieke Kluen ◽  
Lisa Catherine Dandolo ◽  
Gerhard Jocham ◽  
Lars Schwabe

Abstract Updating established memories in light of new information is fundamental for memory to guide future behavior. However, little is known about the brain mechanisms by which existing memories can be updated. Here, we combined functional magnetic resonance imaging and multivariate representational similarity analysis to elucidate the neural mechanisms underlying the updating of consolidated memories. To this end, participants first learned face–city name pairs. Twenty-four hours later, while lying in the MRI scanner, participants were required to update some of these associations, but not others, and to encode entirely new pairs. Updating success was tested again 24 h later. Our results showed increased activity of the dorsolateral prefrontal cortex (dlPFC) specifically during the updating of existing associations that was significantly stronger than when simple retrieval or new encoding was required. The updating-related activity of the dlPFC and its functional connectivity with the hippocampus were directly linked to updating success. Furthermore, neural similarity for updated items was markedly higher in the dlPFC and this increase in dlPFC neural similarity distinguished individuals with high updating performance from those with low updating performance. Together, these findings suggest a key role of the dlPFC, presumably in interaction with the hippocampus, in the updating of established memories.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Benjamin Wingfield ◽  
Coral Lapsley ◽  
Andrew McDowell ◽  
Georgios Miliotis ◽  
Margaret McLafferty ◽  
...  

AbstractA growing body of evidence supports an important role for alterations in the brain-gut-microbiome axis in the aetiology of depression and other psychiatric disorders. The potential role of the oral microbiome in mental health has received little attention, even though it is one of the most diverse microbiomes in the body and oral dysbiosis has been linked to systemic diseases with an underlying inflammatory aetiology. This study examines the structure and composition of the salivary microbiome for the first time in young adults who met the DSM-IV criteria for depression (n = 40) and matched controls (n = 43) using 16S rRNA gene-based next generation sequencing. Subtle but significant differences in alpha and beta diversity of the salivary microbiome were observed, with clear separation of depressed and healthy control cohorts into distinct clusters. A total of 21 bacterial taxa were found to be differentially abundant in the depressed cohort, including increased Neisseria spp. and Prevotella nigrescens, while 19 taxa had a decreased abundance. In this preliminary study we have shown that the composition of the oral microbiome is associated with depression in young adults. Further studies are now warranted, particuarly investigations into whether such shifts play any role in the underling aetiology of depression.


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