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Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition)

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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: closed (20 January 2026) | Viewed by 17945

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Dr. Manuela Dicarlo

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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; synaptic plasticity; cell biology; irisin; prefrontal cortex; hippocampus; histology; electron microscopy
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Dear Colleagues,

The hippocampus is a fascinating brain region that is primarily devoted to spatial and episodic memory, learning, spatial navigation, and emotional behavior. 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., the 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, e.g., 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

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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

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Published Papers (5 papers)

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Research

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20 pages, 15695 KB

Open AccessArticle

Effects of Pre- and Post-Supplementation of Taurine in the Hippocampus of a Gerbil Model of Transient Global Cerebral Ischemia

by Md Shiblee Sadik Sabuj, Su-Cheol Han, Byung-Yong Park, Hyun-Jin Tae and Sung Min Nam

Int. J. Mol. Sci. 2026, 27(3), 1341; https://doi.org/10.3390/ijms27031341 - 29 Jan 2026

Viewed by 508

Abstract

Taurine is a free amino acid with various effects, such as developing the nervous system, an immune function, an antioxidative effect, enhancing muscle and cardiovascular function, and reducing fatigue. In this study, we investigated the effect of taurine supplementation on ischemic neuronal damage in the hippocampus of gerbils. Taurine (150 mg/kg) was orally administered to gerbils before and after induction of transient ischemia. Histologically, we examined surviving and degenerating neurons by neuronal nuclei immunostaining and fluoro-jade C (FJC) staining. Gliosis was morphologically confirmed by GFAP and Iba1 immunostaining. Compared to the ischemia and pre-treated gerbils, pre- and post-taurine supplementation was neuroprotective by maintaining higher number of mature NeuN-immunoreactive neurons and reducing neuronal death (FJC-stained cells) in the hippocampal CA1 region. Additionally, the ischemia-induced reactive astrocytosis and microgliosis was significantly mitigated by long-term taurine treatment in the gerbil hippocampus. Furthermore, we confirmed that pre- and post-taurine supplementation downregulated ischemia-mediated induction in the MAPK cascade, such as ERK, JNK, and p38, which are involved in oxidative stress, inflammation, apoptosis, and cell differentiation, and this treatment upregulated an ischemia-mediated reduction in antioxidants such as SOD2, GPX4, and anti-apoptotic factor Bcl-2 in the gerbil hippocampus. Pre- and post-taurine supplementation also downregulated again the ischemic injury-mediated activation of transcriptional factor NFkβ, an important gene expression regulator, especially in the inflammatory response, and pro-apoptotic factor Bax in the gerbil hippocampus. Our present results suggest that pre- and post-taurine supplementation has potential in neuroprotection against ischemia-induced neuronal death and glial activation by attenuating oxidative stress and apoptosis. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition))

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17 pages, 9056 KB

Open AccessArticle

Limited Microvascular Remodelling Occurs in the Aged Human Hippocampus in Obstructive Sleep Apnoea

by Cuicui Xu, Jessica E. Owen, Thorarinn Gislason, Bryndis Benediktsdottir, Jiming Ye and Stephen R. Robinson

Int. J. Mol. Sci. 2025, 26(24), 12040; https://doi.org/10.3390/ijms262412040 - 14 Dec 2025

Cited by 1 | Viewed by 559

Abstract

In mice, intermittent hypoxia is associated with an increase in microvessels in the hippocampus, whereas in humans with obstructive sleep apnoea (OSA), microvessels are lost from the heart and retina. The present study investigated microvascular changes in the hippocampus of patients with OSA, and whether patient age or use of continuous positive airway pressure (CPAP) influence microvascularisation. Using autopsy samples from 31 people with confirmed OSA, microvessels were immunolabelled and quantitatively analysed. Compared to the Low OSA group, the High OSA group had larger mean microvessel diameters in the fimbria and CA4, and greater mean microvessel length in the fimbria, which are indicative of microvascular remodelling. An absence of angiogenesis was indicated by similar mean vessel counts in both OSA severity groups. Increased age was associated with microvascular remodelling in the fimbria only. Treatment with CPAP was not associated with changed patterns of microvascularisation. We conclude that: (i) no evidence was found for angiogenesis in the human hippocampus in OSA or ageing; (ii) increased OSA severity is associated with microvascular remodelling in the fimbria and CA4; (iii) microvascular remodelling does not appear to be influenced by CPAP use; (iv) limited adaptability of the microvasculature may underpin the vulnerability of the hippocampus to hypoxic injury, particularly in severe OSA. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition))

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17 pages, 6485 KB

Open AccessArticle

Exogenous Administration of Delta-9-Tetrahydrocannabinol Affects Adult Hippocampal Neurotransmission in Female Wistar Rats

by Ana M. Neves, Sandra Leal, Bruno M. Fonseca and Susana I. Sá

Int. J. Mol. Sci. 2025, 26(13), 6144; https://doi.org/10.3390/ijms26136144 - 26 Jun 2025

Cited by 2 | Viewed by 1576

Abstract

Delta-9-tetrahydrocannabinol (THC) is a psychoactive element of Cannabis sativa and affects the human cannabinoid system through its receptors, CB1R and CB2R. CB1R was found in several brain areas, including the hippocampal formation (HF), and it is responsible for most THC side effects. We investigated THC’s effects in the HF of female Wistar rats to assess changes in its neurotransmission. Female Wister rats (n = 20) were gonadectomized under anesthesia at 8 weeks old. Afterwards, they received estradiol benzoate (EB) and/or THC. Immunohistochemistry was performed to assess the expression of the cholinergic receptor alpha 7 subunit (CHRNA7), the vesicular acetylcholine transporter (VAChT), the vesicular glutamate transporter (VGLUT), the gamma-aminobutyric acid type A receptor (GABRA), the CB1 receptor, and estradiol receptor alpha (EBα). In the HF, the expression of CHRNA7 was increased by EB and by THC in the Oil groups but decreased by THC in the EB groups. The same is true for VGLUT expression in the DG and hilum and for GABRA expression in the hilum. The expression of VAChT and CB1 is reduced by EB, while the concomitant administration of THC increases it. GAD expression is reduced by EB administration in CA1, CA3, and DG. Our results may help with decision-making regarding the prescription of low doses of THC as a therapeutical approach. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition))

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13 pages, 1906 KB

Open AccessArticle

by Ainhoa Alberro, Rocío Del Carmen Bravo-Miana, Saioa GS Iñiguez, Andrea Iribarren-López, Marta Arroyo-Izaga, Ander Matheu, Maider Muñoz-Culla and David Otaegui

Int. J. Mol. Sci. 2024, 25(23), 12872; https://doi.org/10.3390/ijms252312872 - 29 Nov 2024

Cited by 2 | Viewed by 1897

Abstract

Small non-coding RNAs (sncRNAs), particularly microRNAs (miRNAs), play an important role in transcriptome regulation by binding to mRNAs and post-transcriptionally inhibiting protein production. This regulation occurs in both physiological and pathological conditions, where the expression of many miRNAs is altered. Previous reports by our group and others have demonstrated that miRNA expression is also altered during aging. However, most studies have analyzed human peripheral blood samples or brain samples from animal models, leaving a gap in knowledge regarding miRNA expression in the human brain. In this work, we analyzed the expression of sncRNAs from coronal sections of human hippocampal samples, a tissue with a high vulnerability to deleterious conditions such as aging. Samples from young (n = 5, 27–49 years old), old (n = 8, 58–88 years old), and centenarian (n = 3, 97, 99, and 100 years old) individuals were included. Our results reveal that sncRNAs, particularly miRNAs, are differentially expressed (DE) in the human hippocampus with aging. Besides, miRNA-mediated regulatory networks revealed significant interactions with mRNAs deregulated in the same hippocampal samples. Surprisingly, 80% of DE mRNA in the centenarian vs. old comparison are regulated by hsa-miR-192-5p and hsa-miR-3135b. Additionally, validated hsa-miR-6826-5p, hsa-let-7b-3p, hsa-miR-7846, and hsa-miR-451a emerged as promising miRNAs that are deregulated with aging and should be further investigated. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition))

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Review

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21 pages, 2794 KB

Open AccessReview

The BDNF-Interactive Model for Sustainable Hippocampal Neurogenesis in Humans: Synergistic Effects of Environmentally-Mediated Physical Activity, Cognitive Stimulation, and Mindfulness

by Mohamed Hesham Khalil

Int. J. Mol. Sci. 2024, 25(23), 12924; https://doi.org/10.3390/ijms252312924 - 1 Dec 2024

Cited by 25 | Viewed by 12549

Abstract

This paper bridges critical gaps through proposing a novel, environmentally mediated brain-derived neurotrophic factor (BDNF)-interactive model that promises to sustain adult hippocampal neurogenesis in humans. It explains how three environmental enrichment mechanisms (physical activity, cognitive stimulation, and mindfulness) can integratively regulate BDNF and other growth factors and neurotransmitters to support neurogenesis at various stages, and how those mechanisms can be promoted by the physical environment. The approach enables the isolation of specific environmental factors and their molecular effects to promote sustainable BDNF regulation by testing the environment’s ability to increase BDNF immediately or shortly before it is consumed for muscle repair or brain update. This model offers a novel, feasible method to research environment enrichment and neurogenesis dynamics in real-world human contexts at the immediate molecular level, overcoming the confounds of complex environment settings and challenges of long-term exposure and structural plasticity changes. The model promises to advance understanding of environmental influences on the hippocampus to enhance brain health and cognition. This work bridges fundamental gaps in methodology and knowledge to facilitate more research on the enrichment–neuroplasticity interplay for humans without methodological limitations. Full article

(This article belongs to the Special Issue Focus on Hippocampus Biology: From Neurophysiology to Dysfunctions (2nd Edition))

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