In the hippocampus, a functional role of dopamine D1 receptors (D1R) in synaptic plasticity and memory processes has been suggested by electrophysiological and pharmacological studies. However, comprehension of their function remains elusive due to the lack of knowledge on the precise localization of D1R expression among the diversity of interneuron populations. Using BAC transgenic mice expressing enhanced green fluorescent protein under the control of D1R promoter, we examined the molecular identity of D1R-containing neurons within the CA1 subfield of the dorsal hippocampus. In agreement with previous findings, our analysis revealed that these neurons are essentially GABAergic interneurons, which express several neurochemical markers, including calcium-binding proteins, neuropeptides, and receptors among others. Finally, by using different tools comprising cell type-specific isolation of mRNAs bound to tagged-ribosomes, we provide solid data indicating that D1R is present in a large proportion of interneurons expressing dopamine D2 receptors. Altogether, our study indicates that D1Rs are expressed by different classes of interneurons in all layers examined and not by pyramidal cells, suggesting that CA1 D1R mostly acts via modulation of GABAergic interneurons.
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http://dx.doi.org/10.1007/s00429-016-1314-x | DOI Listing |
Sci Rep
January 2025
Department of Psychiatry, University of Wisconsin School of Medicine & Public Health, Madison, WI, USA.
Childhood abuse represents one of the most potent risk factors for the development of psychopathology during childhood, accounting for 30-60% of the risk for onset. While previous studies have separately associated reductions in gray matter volume (GMV) with childhood abuse and internalizing psychopathology (IP), it is unclear whether abuse and IP differ in their structural abnormalities, and which GMV features are related to abuse and IP at the individual level. In a pooled multisite, multi-investigator sample, 246 child and adolescent females between the ages of 8-18 were recruited into studies of interpersonal violence (IPV) and/or IP (i.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Laboratory of Exercise Biochemistry and Neuroendocrinology, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan; Division of Sport Neuroscience, Kokoro Division, Advanced Research Initiative for Human High Performance (ARIHHP), Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan. Electronic address:
Exercise benefits the brain, particularly the learning and memory center-the dorsal hippocampus (dHPC)-and holds promise for therapeutic applications addressing age-related cognitive deficits. While moderate-to-vigorous-intensity exercise is commonly recommended for health benefits, our translational research proposes the effectiveness of very-light-intensity exercise in enhancing cognitive functions. However, the intensity-dependent characteristics of HPC activation have yet to be fully delineated; therefore, there is no evidence of whether such easily accessible exercises for people of all ages and most fitness levels can activate HPC neurons.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Iowa, Iowa City, IA, USA.
Background: It is increasingly apparent that tau pathology in Alzheimer's disease (AD) begins in the brainstems of middle-aged patients, decades before the onset of symptoms. Most studies are, however, based on brain-bank cohorts and focus on patients dying of natural causes. The true incidence of tau pathology in the brainstem thus remains unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology & Technology, ACECR, Tehran, NY, Iran (Islamic Republic of).
Background: Alzheimer's disease (AD) is a degenerative condition characterized by a progressive decline in cognitive function, predominantly affecting older individuals. AD is associated with a range of histopathological alterations, including the gradual demise of neuronal cells, the accumulation of amyloid plaques, and the formation of neurofibrillary tangles. Furthermore, research suggests that the brain tissue of AD patients is subject to oxidative stress, which manifests as the oxidation of proteins, lipids, DNA, and the process of glycoxidation, throughout the disease progression.
View Article and Find Full Text PDFCurr Top Behav Neurosci
January 2025
Department of Experimental Psychology, University of Oxford, Oxford, UK.
A decline in hippocampal function has long been associated with the progression of cognitive impairments in patients with Alzheimer's disease (AD). The disruption of hippocampal synaptic plasticity [primarily the reduction of long-term potentiation LTP] by excess production of soluble beta-amyloid (Aβ) has long been accepted as the mechanism by which AD pathology impairs memory, at least during the early stages of AD pathogenesis. However, the premise that hippocampal LTP underpins the formation of associative, long-term memories has been challenged.
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