Galanin inhibits the release of several neurotransmitters and produces performance deficits in a variety of spatial and aversive learning and memory tasks. The experiments in this study investigated the role galanin has in emotional learning and memory using a standard delay cued and contextual fear conditioning task. Rats were administered galanin into the lateral ventricles before training, and scored for freezing behavior in the same context and in a novel context with and without an auditory cue (CS) that had been paired previously with an aversive stimulus (US). Galanin-overexpressing transgenic mice were tested in an identical behavioral protocol. The galanin-administered rats and the transgenic mice were not significantly different from their respective controls on this task. A more challenging trace cued and contextual fear conditioning procedure was administered to separate groups of galanin-treated rats and galanin-overexpressing transgenic mice. Subjects were trained with the same CS and US, however, a 2.5-sec delay was inserted between CS offset and US onset. Following the trace conditioning, rats administered galanin and mice overexpressing galanin both exhibited significantly less freezing to the CS in the novel context as compared with their control groups. These results indicate that the observed disruption of cued fear conditioning was specific to the more difficult trace conditioning task. These findings are the first demonstration that galanin impairs performance on an emotional memory task and support the hypothesis that galanin-induced deficits are specific to more difficult cognitive tasks.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC182584PMC
http://dx.doi.org/10.1101/m.49502DOI Listing

Publication Analysis

Top Keywords

fear conditioning
16
transgenic mice
16
galanin-overexpressing transgenic
12
trace cued
8
cued fear
8
galanin-treated rats
8
rats galanin-overexpressing
8
learning memory
8
cued contextual
8
contextual fear
8

Similar Publications

Rationale: Clinical literature indicates there may be a therapeutic use of cannabidiol (CBD) for stress-related disorders. Preclinical literature remains conflicted regarding the underlying neurobehavioral mechanisms, reporting mixed effects of CBD (increased, decreased, or no effect) on anxiety- and fear-related behaviors. Preclinical data demonstrated that CBD modulates hypothalamus-pituitary-adrenal (HPA) axis gene expression; it is unknown whether CBD changes HPA axis responsivity and how this relates to altered behavior.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

Background: The prevalence of sepsis and delirium in the elderly is a risk factor for subsequent diagnosis of Alzheimer's disease and related dementias (ADRD). Post-sepsis impairments include changes in memory, attention, emotional function, and neuromuscular strength. Studies have shown a link between the prolonged activation of microglia after infection.

View Article and Find Full Text PDF

Background: We previously identified the novel mechanism of pathological tau transfer via extracellular vesicles (EVs) in Alzheimer's disease (AD). Targeting EV secretion to mitigate tau transfer is therefore a promising therapeutic approach for AD. P2X purinoreceptor 7 (P2RX7), an ATP-gated cationic channel, regulates microvesicle shedding or secretion of multivesicular body-derived exosomes.

View Article and Find Full Text PDF

Background: A drug cocktail targeting different processes of aging was tested in an aging mouse model of Alzheimer's disease (AD) neuropathologic change as an intervention to improve behaviors corresponding to cognitive dysfunction in AD.

Method: A cocktail of acarbose/rapamycin/phenylbutyrate or a control treatment was administered (medicated vs. non-medicated chow) chronically to 22 months-old mice that received viral vector injections to induce amyloid and tau pathology in the hippocampus at 24 months of age.

View Article and Find Full Text PDF

Background: Neurodegenerative disorders such as Alzheimer's Disease (AD) are increasingly associated with irregular lipid accumulation. Dysfunction in the catabolism of sphingolipids leads to many neurodegenerative disorders but has only recently garnered interest in AD. Excess ceramide deposition has been observed in Aβ-plaques, plasma, and cerebrospinal fluid in AD patients and AD mouse models.

View Article and Find Full Text PDF

Want 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!