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Neuropeptides in Brain Health and Disease: From Molecular Mechanisms to Therapeutic Potential

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: 20 May 2026 | Viewed by 549

Special Issue Editor

Dr. Alessandro Castorina

E-Mail Website
Guest Editor
School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia
Interests: nervous system diseases; neuropharmacology; anatomy; biomolecular; musculoskeletal disorders; neuropathic pain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuropeptides play key roles in neural development, synaptic transmission, neuroimmune interactions, and the regulation of inflammation, myelination, and regeneration. Understanding their signaling pathways and receptor dynamics at the molecular level is crucial to uncovering their impact on brain function and dysfunction. This Special Issue will encompass topics that explore the molecular functions and mechanisms of neuropeptides in the central nervous system (CNS), both under physiological and pathological conditions.

We welcome original research articles, reviews, systematic reviews, and meta-analyses that address neuropeptide-related mechanisms in healthy states as well as in neurodegenerative diseases, demyelinating disorders, neuropsychiatric conditions, or brain injury. Special emphasis will be placed on studies investigating intracellular signalling, gene and protein expression changes, receptor-ligand interactions, and cross-talk between neurons and glial cells.

Submissions highlighting translational aspects, such as neuropeptides as biomarkers or therapeutic targets, are encouraged, provided the work is supported by clear molecular or mechanistic data. Clinical studies and surveys without molecular analysis do not meet the journal’s scope.

This Special Issue aims to foster a deeper understanding of neuropeptide biology and promote research that bridges basic molecular insights with therapeutic development for CNS disorders.

Dr. Alessandro Castorina
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 250 words) can be sent to the Editorial Office for assessment.

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

  • neuropeptides
  • brain function
  • neuroinflammation
  • regeneration
  • neurodegeneration
  • biomarkers
  • therapy
  • CNS
  • brain disorders
  • demyelination

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Published Papers (1 paper)

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Research

18 pages, 3432 KB  
Article
Kölliker–Fuse/Parabrachial Complex PACAP—Glutamate Pathway to the Extended Amygdala Couples Rapid Autonomic and Delayed Endocrine Responses to Acute Hypotension
by Vito S. Hernández, Pedro Segura-Chama and Limei Zhang
Int. J. Mol. Sci. 2025, 26(23), 11405; https://doi.org/10.3390/ijms262311405 - 25 Nov 2025
Viewed by 317
Abstract
The calyx of Held is a giant axo-somatic synapse classically confined to the auditory brainstem. We recently identified morphologically similar calyx-like terminals in the extended amygdala (EA) that arise from the ventrolateral parabrachial complex and co-express PACAP, CGRP, VAChT, VGluT1, and VGluT2, targeting [...] Read more.
The calyx of Held is a giant axo-somatic synapse classically confined to the auditory brainstem. We recently identified morphologically similar calyx-like terminals in the extended amygdala (EA) that arise from the ventrolateral parabrachial complex and co-express PACAP, CGRP, VAChT, VGluT1, and VGluT2, targeting PKCδ+/GluD1+ EA neurons. Here, we asked whether this parabrachial–EA pathway participates in compensation during acute hypotension. In rats given hydralazine (10 mg/kg, i.p.), we quantified Fos protein during an early phase (60 min) and a late phase (120 min). Early after hypotension, Fos surged in a discrete subpopulation of the parabrachial Kölliker–Fuse (KF) region and in the EA, whereas magnocellular neurons of the supraoptic and paraventricular nuclei (SON/PVN) remained largely silent. By 120 min, magnocellular SON/PVN neurons were robustly Fos-positive. Confocal immunohistochemistry showed that most Fos+ PKCδ+/GluD1+ EA neurons were encircled by PACAP+ perisomatic terminals (80.8%), of which the majority co-expressed VGluT1 (88.1%). RNAscope in situ hybridization further identified a selective KF population co-expressing Adcyap1 (PACAP) and Slc17a7 (VGluT1) that became fos-positive during the early phase. Together, these data suggest that a KF PACAP+/VGluT1+ projection forms calyceal terminals around PKCδ+/GluD1+ EA neurons, providing a high-fidelity route for rapid autonomic rebound to falling blood pressure, while slower endocrine support is subsequently recruited via neurohormone-magnocellular activation. This work links multimodal parabrachial output to temporally layered autonomic–neuroendocrine control. Full article
(This article belongs to the Special Issue Neuropeptides in Brain Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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