This study shows that ongoing electrical stimulation of the dopaminergic ventral midbrain can modify neuronal activity in the auditory cortex of awake primates for several seconds. This was reflected in a decrease of the spontaneous firing and in a bidirectional modification of the power of auditory evoked potentials. We consider that both effects are due to an increase in the dopamine tone in auditory cortex induced by the electrical stimulation. Thus, the dopaminergic ventral midbrain may contribute to the tonic activity in auditory cortex that has been proposed to be involved in associating events of auditory tasks (Brosch et al. Hear Res 271:66-73, 2011) and may modulate the signal-to-noise ratio of the responses to auditory stimuli.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s00429-014-0950-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Inter- and intra-hemispheric lateralization alterations in auditory verbal hallucinations of Schizophrenia: insights from resting-state functional connectivity.
Eur Arch Psychiatry Clin Neurosci
January 2025
Department of Psychiatry, National Clinical Research Center for Mental Disorders, and National Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha, 310016, Hunan, China.
Auditory verbal hallucinations (AVHs) in schizophrenia are hypothesized to involve alterations in hemispheric lateralization, but the specific neural mechanisms remain unclear. This study investigated functional intra- and inter-hemispheric connectivity to identify lateralization patterns unique to AVHs. Resting-state fMRI data were collected from 60 schizophrenia patients with persistent AVHs (p-AVH group), 39 patients without AVHs (n-AVH group), and 59 healthy controls (HC group).
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Miami, Miami, FL, USA.
Background: Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Johns Hopkins University, Baltimore, MD, USA.
Background: Alzheimer's disease is a progressive form of dementia where cognitive capacities deteriorate due to neurodegeneration. Interestingly, Alzheimer's patients exhibit cognitive fluctuations during all stages of the disease. Though it is thought that contextual factors are critical for unlocking these hidden memories, understanding the neural basis of cognitive fluctuations has been hampered due to the lack of behavioral approaches to dissociate memories from contextual-performance.
View Article and Find Full Text PDFClinical Manifestations.
Alzheimers Dement
December 2024
Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Background: Prior longitudinal studies among older adults have documented associations between hearing loss and changes in brain morphology. Whether interventions involving hearing aids can reduce age-related atrophy is unknown. A substudy within the Aging and Cognitive Health Evaluation in Elders (ACHIEVE, Clinicaltrials.
View Article and Find Full Text PDFHyperactive delta isoform of PI3Kinase enables long distance regeneration of adult rat corticospinal tract.
Mol Ther
January 2025
Institute of Experimental Medicine CAS, Department of Neuroregeneration, Videnska 1083, 142 20, Prague, Czech Republic. Electronic address:
Neurons in the central nervous system (CNS) lose regenerative potential with maturity, leading to minimal corticospinal tract (CST) axon regrowth after spinal cord injury (SCI). In young rodents, knockdown of PTEN, which antagonises PI3K signalling by hydrolysing PIP3, promotes axon regeneration following SCI. However, this effect diminishes in adults, potentially due to lower PI3K activation leading to reduced PIP3.
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!