The basal expression of the immediate-early gene protein products fos, fos-related antigens (FRA's), jun and krox-24 was examined using immunocytochemical methods in intrastriatal grafts derived from fetal striatal primordia. Whereas very few, if any, normal adult striatal neurons expressed jun, many neurons in the striatal graft expressed jun at high levels. FRA's, but not fos, were also occasionally induced in some grafted striata. krox-24 was expressed in normal adult striatal neurons, and to a lesser extent in transplanted striatal neurons. These results show that neurons of intrastriatal grafts express jun at substantially higher levels than host striatal neurons, and this may be related to the previously reported increased transcription of neuropeptides in striatal grafts, and/or to the possible failure of transplanted neurons to fully establish normal connections with the host tissue.
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http://dx.doi.org/10.1016/0006-8993(91)90785-t | DOI Listing |
Brain Commun
January 2025
Department of Clinical Medicine, Aarhus University Hospital, Aarhus N, 8200 Aarhus, Denmark.
Asymmetric dopaminergic degeneration of the striatum is a characteristic feature of Parkinson's disease, associated with right-left asymmetry in motor function. As such, studying asymmetry provides insights into progressive neurodegeneration between cerebral hemispheres. Given the impact of Lewy pathology on various neurotransmitter systems beyond the dopaminergic, it may be that other neuronal systems in the predominantly affected hemisphere are similarly affected.
View Article and Find Full Text PDFNeuropharmacology
January 2025
Department of Anatomy & Neuroscience, School of Medicine, University College Cork (UCC), Cork, Ireland; APC Microbiome Ireland, UCC, Cork, Ireland. Electronic address:
Degeneration of midbrain nigrostriatal dopaminergic neurons is a pathological hallmark of Parkinson's disease (PD). Peripheral delivery of a compound(s) to arrest or slow this dopaminergic degeneration is a key therapeutic goal. Pan-inhibitors of histone deacetylase (HDAC) enzymes, key epigenetic regulators, have shown therapeutic promise in PD models.
View Article and Find Full Text PDFACS Chem Neurosci
January 2025
College of Pharmacy, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do 28160, Republic of Korea.
The global abuse of stimulant methamphetamine (METH) imposes a significant social burden. Despite this, effective therapeutic interventions for mitigating the harmful effects associated with METH-induced central nervous system (CNS) stimulation remain elusive. (hinoki), containing hinokinin as its active constituent, has been identified to exhibit CNS depressant properties.
View Article and Find Full Text PDFJ Neurosci
January 2025
Laboratory on Neurobiology of Compulsive Behaviors, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, 20892. USA.
Dopamine critically regulates neuronal excitability and promotes synaptic plasticity in the striatum, thereby shaping network connectivity and influencing behavior. These functions establish dopamine as a key neuromodulator, whose release properties have been well-studied in rodents but remain understudied in nonhuman primates. This study aims to close this gap by investigating the properties of dopamine release in macaque striatum and comparing/contrasting them to better-characterized mouse striatum, using ex vivo brain slices from male and female animals.
View Article and Find Full Text PDFNeurosci Res
January 2025
Division of Neuroanatomy, Department of Neuroscience, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, 755-8505, Japan; School of Human Care Studies, Nagoya University of Arts and Sciences, 57 Takenoyama, Iwasaki-cho, Nishin city, Aichi 470-0196, Japan. Electronic address:
Huntingtin-associated protein 1 (HAP1) is an essential constituent of the stigmoid body (STB) and is known as a neuroprotective interactor with causal agents for several neurodegenerative disorders, including huntingtin (HTT) in Huntington's disease. Previous in vitro studies showed that compared to normal HTT, STB/HAP1 exhibited a higher binding affinity for mutant HTT. However, the detailed in vivo relationships of STB/HAP1 with endogenous HTT have not been clarified yet.
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