We examined if axon terminals of dopaminergic neurons might make synapses upon neurokinin-1 receptor (NK1R)-expressing intrinsic neurons in the rat striatum. In a double-immunocytochemical ultrastructural study, dopaminergic terminals were labeled by the immunoperoxidase method for tyrosine hydroxylase (TH), while NK1R-immunoreactivity (-IR) was revealed by the immunogold-silver labeling method. Some TH-immunoreactive (-ir) axon terminals formed synapses of the symmetric or intermediate type on NK1R-ir neuronal profiles; usually on dendritic profiles and rarely on somatic profiles. It was further confirmed by means of triple-immunofluorescence histochemistry that NK1R-ir neurons in close association with TH-ir axon terminals showed nitric oxide synthase (NOS)- or vesicular acetylcholine transporter-IR. Since NK1R-expressing striatal neurons are segregated into cholinergic and somatostatin/NOS-containing intrinsic neurons (Brain Res. 631 (1993) 297; Neurosci. Lett. 310 (2001) 109), the present results indicate that dopaminergic neurons make synapses upon these intrinsic neurons in the striatum.
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http://dx.doi.org/10.1016/s0304-3940(02)00138-6 | DOI Listing |
Neurobiol Dis
January 2025
Division of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. Electronic address:
The consequences of non-pathogenic huntingtin (HTT) reduction in the mature brain are of substantial importance as clinical trials for numerous HTT-lowering therapies are underway; many of which are non-selective in that they reduce both mutant and wild type protein variants. In this study, we injected CaMKII-promoted AAV-Cre directly into the hippocampus of adult HTT floxed mice to explore the role of wild-type huntingtin (wtHTT) in adult hippocampal pyramidal neurons and the broader implications of its loss. Our findings reveal that wtHTT depletion results in profound macroscopic morphological abnormalities in hippocampal structure, accompanied by significant reactive gliosis.
View Article and Find Full Text PDFJ Neurochem
January 2025
Centre for Discovery Brain Sciences, Hugh Robson Building, George Square, University of Edinburgh, Edinburgh, Scotland, UK.
Synaptic vesicle protein 2A (SV2A) is an abundant synaptic vesicle cargo with an as yet unconfirmed role in presynaptic function. It is also heavily implicated in epilepsy, firstly being the target of the leading anti-seizure medication levetiracetam and secondly with loss of function mutations culminating in human disease. A range of potential presynaptic functions have been proposed for SV2A; however its interaction with the calcium sensor for synchronous neurotransmitter release, synaptotagmin-1 (Syt1), has received particular attention over the past decade.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Hale Building for Transformative Medicine, Room 10006, 60 Fenwood Road, Boston, MA, 02115, USA.
α-Synuclein (αS) is a 140 amino-acid neuronal protein highly enriched in presynaptic nerve terminals. Its progressive accumulation in Lewy bodies and neurites is the hallmark of Parkinson's disease (PD). A growing number of studies highlights a critical interplay between lipid metabolism and αS biology.
View Article and Find Full Text PDFFront Neural Circuits
January 2025
Department of Neurobiology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
A strong repetitive stimulus can occasionally enhance axonal excitability, leading to the generation of afterdischarge. This afterdischarge outlasts the stimulus period and originates either from the physiological spike initiation site, typically the axon initial segment, or from ectopic sites for spike generation. One of the possible mechanisms underlying the stimulus-induced ectopic afterdischarge is the local depolarization due to accumulated potassium ions surrounding the axonal membranes of the distal portion.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Compelling evidence has demonstrated that rehabilitation through physical exercise, a non-invasive and non-surgical intervention, enhances muscle reinnervation and motor recovery after peripheral nerve injury (PNI) by increasing muscle-derived brain-derived neurotrophic factor (BDNF) expression and triggering TrkB-dependent axonal plasticity. Adenosine has been widely acknowledged to trigger TrkB via A2A receptor (A2AR). Since motor nerve terminals co-express TrkBs and A2ARs and depolarizing conditions increase muscle release of BDNF and adenosine, we examined whether A2ARs activation could recapitulate the functional recovery benefits of intermittent exercise after a nerve crush.
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