Haloperidol induces Fos and related molecules (Fos-related antigens, FRAs) in adult striatal neurons. We tested whether a similar induction of Fos and FRAs by haloperidol injection would occur in fetal striatal neurons transplanted into adult quinolinic acid-lesioned striatum. We found that Fos and FRAs were induced in striatal neurons after haloperidol. This induction had a time course in transplanted neurons that was identical to the time course of induction in normal adult striatum. Furthermore, the relative numbers of Fos- and FRA-immunopositive neurons induced by haloperidol were identical for both transplanted and normal striatal neurons. These results provide the first demonstration that neurons in intrastriatal grafts derived from fetal striatal primordia have similar intracellular biochemical characteristics to normal adult striatal neurons.
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http://dx.doi.org/10.1016/0006-8993(90)91300-6 | 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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