Women and men can differ in their propensity to take risks and develop impulse control and addiction disorders. Sexual dimorphisms in behavioral control by the mesolimbic dopaminergic reward system may underlie these phenomena, given its sensitivity to gonadal hormones. However, this is hard to test experimentally using humans. Using the rat gambling task (rGT), we investigated what impact acute inhibition of accumbal dopamine had on decision-making and impulsivity in animals of both sexes. We expressed an inhibitory designer receptor exclusively activated by designer drugs (hM4D[Gi]) in the accumbal dopaminergic efferents of female and male transgenic (Tg) rats, engineered to selectively express cre recombinase in neurons synthesizing tyrosine hydroxylase. We then trained the rats to perform the rGT and assessed the effect of an acute clozapine-n-oxide (0-3 mg/kg) challenge. Chemogenetic inhibition of dopaminergic projections to the accumbens did not affect choice in females, perhaps due to low levels of risky choice in Tg+ animals at baseline, but induced a switch from risky to optimal decision-making in males performing the cued rGT. This manipulation also decreased motor impulsivity but only in females. These data support the hypothesis that cue-driven risky choice is mediated, at least in males, by activity of accumbal dopaminergic neurons. However, motor impulsivity is more sensitive to inhibition of accumbal dopamine neurons in female rats. These data may help explain differences in the manifestation of addictions across gender and reinforce the importance of examining both sexes when seeking to attribute control of behavior to specific monoaminergic pathways. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1037/bne0000372 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Adolescent cerebellar nuclei manipulation alters reversal learning and perineuronal net intensity independently in male and female mice.
J Neurosci
January 2025
Arizona State University, Department of Psychology, Tempe, AZ, 85287 USA.
The cerebellum, identified to be active during cognitive and social behavior, has multisynaptic connections through the cerebellar nuclei (CN) and thalamus to cortical regions, yet formation and modulation of these pathways are not fully understood. Perineuronal nets (PNNs) respond to changes in local cellular activity and emerge during development. PNNs are implicated in learning and neurodevelopmental disorders, but their role in the CN during development is unknown.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Linkoping University, Linkoping, Sweden.
Background: Excessive dietary fat is not only a risk factor for metabolic disorders but also for premature cognitive decline and Alzheimer's disease. Recent findings from our study revealed that even a few days of a high-fat diet (HFD) are sufficient to disrupt hippocampal bioenergetics, activate microglia, and induce cognitive decline in mice. We hypothesize that microglia, rather than merely responding to diet-induced damage, play a critical role in disrupting synaptic homeostasis.
View Article and Find Full Text PDFVTA projections to M1 are essential for reorganization of layer 2-3 network dynamics underlying motor learning.
Nat Commun
January 2025
Department of Neuroscience, Technion Medical School, Bat-Galim, Haifa, Israel.
Article Synopsis
- The primary motor cortex (M1) is essential for learning motor skills, and dopaminergic signaling from the ventral-tegmental area (VTA) plays a significant role in this process.
- Using techniques like calcium imaging and chemogenetic inhibition, researchers found that learning a dexterity task leads to a reorganization of M1 layer 2-3, changing how neurons connect and communicate while maintaining overall activity levels.
- Blocking VTA signals during learning halted these neural changes, highlighting the importance of dopaminergic input in developing outcome signaling and refined connectivity in M1, which is crucial for acquiring new motor skills.
A molecularly distinct cell type in the midbrain regulates intermale aggression behaviors in mice.
Theranostics
January 2025
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
: The periaqueductal gray (PAG) is a central hub for the regulation of aggression, whereas the circuitry and molecular mechanisms underlying this regulation remain uncharacterized. In this study, we investigate the role of a distinct cell type, -expressing (Tac2) neurons, located in the dorsomedial PAG (dmPAG) and their modulation of aggressive behavior in mice. : We combined activity mapping, Ca recording, chemogenetic and pharmacological manipulation, and a viral-based translating ribosome affinity purification (TRAP) profiling using a mouse resident-intruder model.
View Article and Find Full Text PDFCoherent Changes in Neural Motor Network Activity during Levodopa-Induced Dyskinesia in a Rat Model of Parkinson's Disease.
J Integr Neurosci
December 2024
Federal State Budgetary Educational Institution, Institute of Theoretical and Experimental Biophysics, 142290 Pushchino, Russia.
Background: Long-term use of levodopa, a metabolic precursor of dopamine (DA) for alleviation of motor symptoms in Parkinson's disease (PD), can cause a serious side effect known as levodopa-induced dyskinesia (LID). With the development of LID, high-frequency gamma oscillations (~100 Hz) are registered in the motor cortex (MCx) in patients with PD and rats with experimental PD. Studying alterations in the activity within major components of motor networks during transition from levodopa-off state to dyskinesia can provide useful information about their contribution to the development of abnormal gamma oscillations and LID.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!