scholarly journals Cognitive impairments from developmental exposure to serotonergic drugs: citalopram and MDMA

2013 ◽  
Vol 16 (6) ◽  
pp. 1383-1394 ◽  
Author(s):  
Tori L. Schaefer ◽  
Curtis E. Grace ◽  
Amanda A. Braun ◽  
Robyn M. Amos-Kroohs ◽  
Devon L. Graham ◽  
...  
Keyword(s):  
Brain Development ◽  
Cognitive Deficits ◽  
System Development ◽  
Third Trimester ◽  
Learning Deficits ◽  
Developmental Exposure ◽  
Target Field ◽  
Field Organization ◽  
Serotonergic Drugs

Abstract We previously showed that developmental 3,4-methylenedioxymethamphetamine (MDMA) treatment induces long-term spatial and egocentric learning and memory deficits and serotonin (5-HT) reductions. During brain development, 5-HT is a neurotrophic factor influencing neurogenesis, synaptogenesis, migration, and target field organization. MDMA (10 mg/kg × 4/d at 2 h intervals) given on post-natal day (PD) 11–20 in rats (a period of limbic system development that approximates human third trimester brain development) induces 50% reductions in 5-HT during treatment and 20% reductions when assessed as adults. To determine whether the 5-HT reduction is responsible for the cognitive deficits, we used citalopram (Cit) pretreatment to inhibit the effects of MDMA on 5-HT reuptake in a companion study. Cit attenuated MDMA-induced 5-HT reductions by 50% (Schaefer et al., 2012). Here we tested whether Cit (5 or 7.5 mg/kg × 2/d) pretreatment attenuates the cognitive effects of MDMA. Within each litter, different offspring were treated on PD11–20 with saline (Sal) + MDMA, Cit + MDMA, Cit + Sal or Sal + Sal. Neither spatial nor egocentric learning/memory was improved by Cit pretreatment. Unexpectedly, Cit + Sal (at both doses) produced spatial and egocentric learning deficits as severe as those caused by Sal + MDMA. These are the first data showing cognitive deficits resulting from developmental exposure to a selective serotonin reuptake inhibitor. These data indicate the need for further research on the long-term safety of antidepressants during pregnancy.

Word Memory in Non-Psychotic Depression

1980 ◽  
Vol 51 (3) ◽  
pp. 699-705 ◽  
Author(s):  
Henry Davis ◽  
W. R. Unruh
Keyword(s):  
Free Recall ◽  
Cognitive Deficits ◽  
Verbal Learning ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Short Term ◽  
Learning Deficits ◽  
Word Memory ◽  
Learning Tasks

Two diverging explanations can be given for the fact that depressed persons often show deficits on verbal learning tasks: (a) researchers have suggested that memory deficits are the result of interference in the transfer from short- to long-term memory; (b) other researchers have suggested that depressives may not have cognitive deficits but may instead simply show deficits in performance. The present study assessed differences in recognition memory, free recall, organization in multitrial free recall, and final free recall among short-term and long-term non-psychotic depressives ( ns = 15) to determine whether such depressed adults show deficits on verbal learning tasks. No verbal learning deficits were demonstrated for 30 depressives relative to 30 nondepressives. The implications of these findings are discussed in terms of interference and the possibility that poor verbal learning in depression is a problem of performance and not learning.

Long-term learning deficits following developmental exposure to the flame retardant decaBDE

2007 ◽  
Vol 29 (5) ◽  
pp. 590 ◽  
Author(s):  
K.D. Onos ◽  
E.R. Kenny ◽  
D.C. Rice ◽  
V.P. Markowski
Keyword(s):  
Flame Retardant ◽  
Learning Deficits ◽  
Developmental Exposure

Learning Deficits Accompanied by Microglial Proliferation After the Long-Term Post-Injection of Alzheimer’s Disease Brain Extract in Mouse Brains

2021 ◽  
Vol 79 (4) ◽  
pp. 1701-1711
Author(s):  
Tetsuo Hayashi ◽  
Shotaro Shimonaka ◽  
Montasir Elahi ◽  
Shin-Ei Matsumoto ◽  
Koichi Ishiguro ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Brain ◽  
Functional Decline ◽  
Brain Regions ◽  
Insoluble Fraction ◽  
Brain Extract ◽  
Post Injection ◽  
Learning Deficits

Background: Human tauopathy brain injections into the mouse brain induce the development of tau aggregates, which spread to functionally connected brain regions; however, the features of this neurotoxicity remain unclear. One reason may be short observational periods because previous studies mostly used mutated-tau transgenic mice and needed to complete the study before these mice developed neurofibrillary tangles. Objective: To examine whether long-term incubation of Alzheimer’s disease (AD) brain in the mouse brain cause functional decline. Methods: We herein used Tg601 mice, which overexpress wild-type human tau, and non-transgenic littermates (NTg) and injected an insoluble fraction of the AD brain into the unilateral hippocampus. Results: After a long-term (17–19 months) post-injection, mice exhibited learning deficits detected by the Barnes maze test. Aggregated tau pathology in the bilateral hippocampus was more prominent in Tg601 mice than in NTg mice. No significant changes were observed in the number of Neu-N positive cells or astrocytes in the hippocampus, whereas that of Iba-I-positive microglia increased after the AD brain injection. Conclusion: These results potentially implicate tau propagation in functional decline and indicate that long-term changes in non-mutated tau mice may reflect human pathological conditions.

Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice

2016 ◽  
Vol 53 ◽  
pp. 290-300 ◽  
Author(s):  
Yu Hu ◽  
Jinsheng Lai ◽  
Baoquan Wan ◽  
Xingfa Liu ◽  
Yemao Zhang ◽  
...  
Keyword(s):  
Cognitive Deficits ◽  
Tau Hyperphosphorylation

scholarly journals Developmental exposure to silver nanoparticles leads to long term gut dysbiosis and neurobehavioral alterations

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zhen Lyu ◽  
Shreya Ghoshdastidar ◽  
Karamkolly R. Rekha ◽  
Dhananjay Suresh ◽  
Jiude Mao ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Body Fat ◽  
Repetitive Behaviors ◽  
Developmental Exposure ◽  
Male And Female ◽  
Female Mice ◽  
Gut Dysbiosis ◽  
Study Results ◽  
Wide Range

AbstractDue to their antimicrobial properties, silver nanoparticles (AgNPs) are used in a wide range of consumer products that includes topical wound dressings, coatings for biomedical devices, and food-packaging to extend the shelf-life. Despite their beneficial antimicrobial effects, developmental exposure to such AgNPs may lead to gut dysbiosis and long-term health consequences in exposed offspring. AgNPs can cross the placenta and blood–brain-barrier to translocate in the brain of offspring. The underlying hypothesis tested in the current study was that developmental exposure of male and female mice to AgNPs disrupts the microbiome–gut–brain axis. To examine for such effects, C57BL6 female mice were exposed orally to AgNPs at a dose of 3 mg/kg BW or vehicle control 2 weeks prior to breeding and throughout gestation. Male and female offspring were tested in various mazes that measure different behavioral domains, and the gut microbial profiles were surveyed from 30 through 120 days of age. Our study results suggest that developmental exposure results in increased likelihood of engaging in repetitive behaviors and reductions in resident microglial cells. Echo-MRI results indicate increased body fat in offspring exposed to AgNPs exhibit. Coprobacillus spp., Mucispirillum spp., and Bifidobacterium spp. were reduced, while Prevotella spp., Bacillus spp., Planococcaceae, Staphylococcus spp., Enterococcus spp., and Ruminococcus spp. were increased in those developmentally exposed to NPs. These bacterial changes were linked to behavioral and metabolic alterations. In conclusion, developmental exposure of AgNPs results in long term gut dysbiosis, body fat increase and neurobehavioral alterations in offspring.

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

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