Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 6103

Share This Special Issue

Special Issue Editor

Dr. Manuela Dicarlo

E-Mail Website
Guest Editor

Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), University of Bari Aldo Moro, Piazza Giulio Cesare 11, 70124 Bari, Italy
Interests: neurodegenerative diseases; Alzheimer’s disease; depression; anxiety; memory; learning; ageing; neuroinflammation; neurotrophic factors; sinaptic plasticity; cell biology; irisin; prefrontal cortex; hippocampus; histology; electron microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The hippocampus is a fascinating brain region that is majorly devoted to spatial and episodic memory, learning, spatial navigation, and emotional behaviour. Electrophysiological, biochemical, and molecular techniques have evidenced that these hippocampus-dependent functions are guaranteed by the complex and plastic neural circuits that connect the main hippocampal regions (i.e., Cornu ammonis and dentate gyrus) with their surrounding cerebral areas, and the adult neurogenesis in the dentate gyrus. However, hippocampal networks exhibit pronounced vulnerability to deleterious conditions such as ischemia, chronic stress, neuroinflammation, aging, etc., which may damage the hippocampal cytoarchitecture and lead to various neurological and psychiatric disorders.

Therefore, this Special Issue of the International Journal of Molecular Sciences aims to advance investigations into the hippocampus and warmly encourages the submission of original research articles and exhaustive reviews that examine the physiopathology of the hippocampus from a molecular and cellular perspective.

Dr. Manuela Dicarlo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

hippocampus
dentate gyrus
cornu ammonis (CA)
spatial memory
episodic memory
learning
spatial navigation
synaptic plasticity
neuroplasticity
neurogenesis
ischemia
neuroinflammation
chronic stress
aging
neurodegenerative diseases
Alzheimer’s disease
epilepsy
depression
anxiety

Published Papers (5 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

16 pages, 16571 KiB

Open AccessArticle

Complex Hippocampal Response to Thermal Skin Injury and Protocols with Hyperbaric Oxygen Therapy and Filipendula ulmaria Extract in Rats

by Bojana Krstic, Dragica Selakovic, Nemanja Jovicic, Milos Krstic, Jelena S. Katanic Stankovic, Sara Rosic, Dragan Milovanovic and Gvozden Rosic

Int. J. Mol. Sci. 2024, 25(5), 3033; https://doi.org/10.3390/ijms25053033 - 06 Mar 2024

Viewed by 534

Abstract

The aim of this study was to evaluate the alterations of the hippocampal function that may be related to anxiogenic response to thermal skin injury, including the morpho-functional alterations, and the effects of hyperbaric oxygen (HBO) and Filipendula ulmaria (FU) extract in the treatment of anxiety-like behavior that coincides with thermal skin injury. A rat thermal skin injury experimental model was performed on 2-month-old male Wistar albino rats. The evaluated therapeutic protocols included HBO and/or antioxidant supplementation. HBO was applied for 7 days in the hyperbaric chamber (100% O₂, 2.5 ATA, 60 min). Oral administration of FU extract (final concentration of 100 mg/kg b.w.) to achieve antioxidant supplementation was also applied for 7 days. Anxiety level was estimated in the open field and elevated plus-maze test, which was followed by anesthesia, sacrifice, and collection of hippocampal tissue samples. HBO treatment and FU supplementation significantly abolished anxiogenic response to thermal skin injury. This beneficial effect was accompanied by the reduction in hippocampal pro-inflammatory and pro-apoptotic indicators, and enhanced BDNF and GABA-ARα2S gene expression, previously observed in untreated burns. The hippocampal relative gene expression of melatonin receptors and NPY positively responded to the applied protocols, in the same manner as µ and δ opioid receptors, while the opposite response was observed for κ receptors. The results of this study provide some confirmations that adjuvant strategies, such as HBO and antioxidant supplementation, may be simultaneously applied in the treatment of the anxiety-like behavior that coincides with thermal skin injury. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions)

► Show Figures

Figure 1

16 pages, 4629 KiB

Open AccessArticle

Increased Dentate Gyrus Excitability in the Intrahippocampal Kainic Acid Mouse Model for Temporal Lobe Epilepsy

by Marijke Vergaelen, Simona Manzella, Kristl Vonck, Erine Craey, Jeroen Spanoghe, Mathieu Sprengers, Evelien Carrette, Wytse Jan Wadman, Jean Delbeke, Paul Boon, Lars Emil Larsen and Robrecht Raedt

Int. J. Mol. Sci. 2024, 25(1), 660; https://doi.org/10.3390/ijms25010660 - 04 Jan 2024

Cited by 1 | Viewed by 1131

Abstract

The intrahippocampal kainic acid (IHKA) mouse model is an extensively used in vivo model to investigate the pathophysiology of mesial temporal lobe epilepsy (mTLE) and to develop novel therapies for drug-resistant epilepsy. It is characterized by profound hippocampal sclerosis and spontaneously occurring seizures with a major role for the injected damaged hippocampus, but little is known about the excitability of specific subregions. The purpose of this study was to electrophysiologically characterize the excitability of hippocampal subregions in the chronic phase of the induced epilepsy in the IHKA mouse model. We recorded field postsynaptic potentials (fPSPs) after electrical stimulation in the CA1 region and in the dentate gyrus (DG) of hippocampal slices of IHKA and healthy mice using a multielectrode array (MEA). In the DG, a significantly steeper fPSP slope was found, reflecting higher synaptic strength. Population spikes were more prevalent with a larger spatial distribution in the IHKA group, reflecting a higher degree of granule cell output. Only minor differences were found in the CA1 region. These results point to increased neuronal excitability in the DG but not in the CA1 region of the hippocampus of IHKA mice. This method, in which the excitability of hippocampal slices from IHKA mice is investigated using a MEA, can now be further explored as a potential new model to screen for new interventions that can restore DG function and potentially lead to novel therapies for mTLE. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions)

► Show Figures

Figure 1

11 pages, 2868 KiB

Open AccessArticle

The Effects of Stress on Hippocampal Neurogenesis and Behavior in the Absence of Lipocalin-2

by Ana Catarina Ferreira and Fernanda Marques

Int. J. Mol. Sci. 2023, 24(21), 15537; https://doi.org/10.3390/ijms242115537 - 24 Oct 2023

Viewed by 953

Abstract

Lipocalin-2 (LCN2) is an acute phase protein able to bind iron when complexed with bacterial siderophores. The recent identification of a mammalian siderophore also suggested a physiological role for LCN2 in the regulation of iron levels and redox state. In the central nervous system, the deletion of LCN2 induces deficits in neural stem cells proliferation and commitment, with an impact on the hippocampal-dependent contextual fear discriminative task. Additionally, stress is a well-known regulator of cell genesis and is known to decrease adult hippocampal cell proliferation and neurogenesis. Although voluntary running, another well-known regulator of neurogenesis, is sufficient to rescue the defective hippocampal neurogenesis and behavior in LCN2-null mice by promoting stem cells’ cell cycle progression and maturation, the relevance of LCN2-regulated hippocampal neurogenesis in response to stress has never been explored. Here, we show a lack of response by LCN2-null mice to the effects of chronic stress exposure at the cellular and behavioral levels. Together, these findings implicate LCN2 as a relevant mediator of neuronal plasticity and brain function in the adult mammalian brain. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions)

► Show Figures

Figure 1

20 pages, 2545 KiB

Open AccessArticle

Dorsal–Ventral Gradient of Activin Regulates Strength of GABAergic Inhibition along Longitudinal Axis of Mouse Hippocampus in an Activity-Dependent Fashion

by Maria Jesus Valero-Aracama, Fang Zheng and Christian Alzheimer

Int. J. Mol. Sci. 2023, 24(17), 13145; https://doi.org/10.3390/ijms241713145 - 24 Aug 2023

Cited by 2 | Viewed by 658

Abstract

The functional and neurophysiological distinction between the dorsal and ventral hippocampus affects also GABAergic inhibition. In line with this notion, ventral CA1 pyramidal cells displayed a more dynamic and effective response to inhibitory input compared to their dorsal counterparts. We posit that this difference is effected by the dorsal–ventral gradient of activin A, a member of the transforming growth factor-β family, which is increasingly recognized for its modulatory role in brain regions involved in cognitive functions and affective behavior. Lending credence to this hypothesis, we found that in slices from transgenic mice expressing a dominant-negative mutant of activin receptor IB (dnActRIB), inhibitory transmission was enhanced only in CA1 neurons of the dorsal hippocampus, where the basal activin A level is much higher than in the ventral hippocampus. We next asked how a rise in endogenous activin A would affect GABAergic inhibition along the longitudinal axis of the hippocampus. We performed ex vivo recordings in wild-type and dnActRIB mice after overnight exposure to an enriched environment (EE), which engenders a robust increase in activin A levels in both dorsal and ventral hippocampi. Compared to control mice from standard cages, the behaviorally induced surge in activin A produced a decline in ventral inhibition, an effect that was absent in slices from dnActRIB mice. Underscoring the essential role of activin in the EE-associated modulation of ventral inhibition, this effect was mimicked by acute application of recombinant activin A in control slices. In summary, both genetic and behavioral manipulations of activin receptor signaling affected the dorsal–ventral difference in synaptic inhibition, suggesting that activin A regulates the strength of GABAergic inhibition in a region-specific fashion. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions)

► Show Figures

Figure 1

Review

Jump to: Research

24 pages, 1052 KiB

Open AccessReview

Glucose Transport and Utilization in the Hippocampus: From Neurophysiology to Diabetes-Related Development of Dementia

by Caio Yogi Yonamine, Maria Luiza Estimo Michalani, Rafael Junges Moreira and Ubiratan Fabres Machado

Int. J. Mol. Sci. 2023, 24(22), 16480; https://doi.org/10.3390/ijms242216480 - 18 Nov 2023

Cited by 1 | Viewed by 1689

Abstract

The association of diabetes with cognitive dysfunction has at least 60 years of history, which started with the observation that children with type 1 diabetes mellitus (T1D), who had recurrent episodes of hypoglycemia and consequently low glucose supply to the brain, showed a deficit of cognitive capacity. Later, the growing incidence of type 2 diabetes mellitus (T2D) and dementia in aged populations revealed their high association, in which a reduced neuronal glucose supply has also been considered as a key mechanism, despite hyperglycemia. Here, we discuss the role of glucose in neuronal functioning/preservation, and how peripheral blood glucose accesses the neuronal intracellular compartment, including the exquisite glucose flux across the blood–brain barrier (BBB) and the complex network of glucose transporters, in dementia-related areas such as the hippocampus. In addition, insulin resistance-induced abnormalities in the hippocampus of obese/T2D patients, such as inflammatory stress, oxidative stress, and mitochondrial stress, increased generation of advanced glycated end products and BBB dysfunction, as well as their association with dementia/Alzheimer’s disease, are addressed. Finally, we discuss how these abnormalities are accompained by the reduction in the expression and translocation of the high capacity insulin-sensitive glucose transporter GLUT4 in hippocampal neurons, which leads to neurocytoglycopenia and eventually to cognitive dysfunction. This knowledge should further encourage investigations into the beneficial effects of promising therapeutic approaches which could improve central insulin sensitivity and GLUT4 expression, to fight diabetes-related cognitive dysfunctions. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions)

► Show Figures

Journal Menu

Journal Browser

Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (5 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI