Hemoglobin autofluorescence as potential long‐term glycemic marker in the rat animal model

2021 ◽  
Author(s):  
Han‐Wen Guo ◽  
Te‐Yu Tseng ◽  
Chih‐Ju Lin ◽  
Chen‐Yuan Dong
Keyword(s):  
Animal Model ◽  
Rat Animal Model

scholarly journals Disruption of the astrocyte–neuron interaction is responsible for the impairments in learning and memory in 5XFAD mice: an Alzheimer’s disease animal model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Moonseok Choi ◽  
Sang-Min Lee ◽  
Dongsoo Kim ◽  
Heh-In Im ◽  
Hye-Sun Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Stat3 Phosphorylation ◽  
Neuron Interactions ◽  
5Xfad Mice

AbstractThe morphological dynamics of astrocytes are altered in the hippocampus during memory induction. Astrocyte–neuron interactions on synapses are called tripartite synapses. These control the synaptic function in the central nervous system. Astrocytes are activated in a reactive state by STAT3 phosphorylation in 5XFAD mice, an Alzheimer’s disease (AD) animal model. However, changes in astrocyte–neuron interactions in reactive or resting-state astrocytes during memory induction remain to be defined. Here, we investigated the time-dependent changes in astrocyte morphology and the number of astrocyte–neuron interactions in the hippocampus over the course of long-term memory formation in 5XFAD mice. Hippocampal-dependent long-term memory was induced using a contextual fear conditioning test in 5XFAD mice. The number of astrocytic processes increased in both wild-type and 5XFAD mice during memory formation. To assess astrocyte–neuron interactions in the hippocampal dentate gyrus, we counted the colocalization of glial fibrillary acidic protein and postsynaptic density protein 95 via immunofluorescence. Both groups revealed an increase in astrocyte–neuron interactions after memory induction. At 24 h after memory formation, the number of tripartite synapses returned to baseline levels in both groups. However, the total number of astrocyte–neuron interactions was significantly decreased in 5XFAD mice. Administration of Stattic, a STAT3 phosphorylation inhibitor, rescued the number of astrocyte–neuron interactions in 5XFAD mice. In conclusion, we suggest that a decreased number of astrocyte–neuron interactions may underlie memory impairment in the early stages of AD.

A dual approach to self-stimulation and locomotor trace affected by chronic methamphetamine treatment for an animal model of schizophrenia

1993 ◽  
Vol 71 (5-6) ◽  
pp. 321-325 ◽  
Author(s):  
Morikuni Takigawa ◽  
Hiroshi Maeda ◽  
Kenichi Ueyama ◽  
Hidefumi Tominaga ◽  
Kei Matsumoto
Keyword(s):  
Animal Model ◽  
Negative Symptoms ◽  
Disease Model ◽  
Stereotyped Behavior ◽  
Dependent Manner ◽  
Dual Approach ◽  
Reverse Tolerance ◽  
Self Stimulation ◽  
Dose Dependent

The effect of long-term methamphetamine (MAP) treatment on intracranial self-stimulation of the lateral hypotholamus and locomotor traces was assessed. An attempt was made to provide a useful animal model for understanding anhedonia, stereotypy, and reoccurrence of liability, which are analogous to symptoms of schizophrenia. The frequency of intracranial self-stimulation (ICSS) as used as a measure of the animals' "hedonic–anhedonic" state. Following long-term MAP treatment (3 mg/kg), rats gradually showed stereotyped behavior, and became inactive and unresponsive to ICSS. These behavioral changes and decreased ICSS lasted several weeks after cessation of chronic MAP treatment and seemed to suggest post-MAP chronic psychosis and (or) anhedonia, two of the negative symptoms of schizophrenia. The traces of rat behavior affected by chronic MAP treatment were classified into three types, peripheral, mixed, and fixed, occurring in a dose-dependent manner. Reverse tolerance, similar to the reoccurrence of schizophrenic symptoms, was observed as a fixed stereotypy associated with loss of ICSS. These abnormal phenomena were suppressed by pretreatment with haloperidol. In the present study, the combination of ICSS and locomotor trace affected by chronic MAP treatment was proposed as an animal model of schizophrenia and as a useful technique for gauging the effect of neuroleptics.Key words: self-stimulation, anhedonia, stereotypy, reverse tolerance, animal disease model, schizophrenia, methamphetamine.

Laser thresholds in pulp exposure: a rat animal model

1995 ◽  
Author(s):  
Joel M. White ◽  
Harold E. Goodis ◽  
Joel J. Kudler
Keyword(s):  
Animal Model ◽  
Pulp Exposure ◽  
Rat Animal Model

scholarly journals Application of a collagen scaffold saturated with platelet-rich plasma in prevention of bisphosphonate-related osteonecrosis of the jaw in the rat animal model

Heliyon ◽  
2021 ◽  
Vol 7 (5) ◽  
pp. e06930
Author(s):  
Farnoosh Razmara ◽  
Mohammad Bayat ◽  
Sadegh Shirian ◽  
Ghazal Shabankare ◽  
Abdolreza Mohamadnia ◽  
...  
Keyword(s):  
Animal Model ◽  
Platelet Rich Plasma ◽  
Collagen Scaffold ◽  
Osteonecrosis Of The Jaw ◽  
Rat Animal Model

CNS Stimulant Controversies

1989 ◽  
Vol 23 (4) ◽  
pp. 497-502 ◽  
Author(s):  
Florence Levy
Keyword(s):  
Central Nervous System ◽  
Animal Model ◽  
Nervous System ◽  
High Dose ◽  
Ethical Considerations ◽  
Hyperactivity Disorder ◽  
Central Nervous System Stimulant ◽  
Stimulant Medications ◽  
Cns Stimulant

Controversies in the use of central nervous system stimulant medications in children with attention deficit hyperactivity disorder are discussed. Diagnostic issues, age of optimal use, side effects, effects on learning and ethical considerations are current issues. An animal model for the effects of chronic long-term high dose regimes is proposed.

scholarly journals Successful Amelioration of Mitochondrial Optic Neuropathy Using the Yeast NDI1 Gene in a Rat Animal Model

PLoS ONE ◽  
2010 ◽  
Vol 5 (7) ◽  
pp. e11472 ◽  
Author(s):  
Mathieu Marella ◽  
Byoung Boo Seo ◽  
Biju B. Thomas ◽  
Akemi Matsuno-Yagi ◽  
Takao Yagi
Keyword(s):  
Animal Model ◽  
Optic Neuropathy ◽  
Rat Animal Model ◽  
Mitochondrial Optic Neuropathy

scholarly journals The Developmental Role of Serotonin: A Comparison of Short- and Long-term Blockade of the Serotonin Transporter on Behavioural Outcomes in Adulthood

2021 ◽  
Author(s):  
◽  
Amy O'Connell
Keyword(s):  
Animal Model ◽  
Serotonin Transporter ◽  
Anxiety And Depression ◽  
Depression And Anxiety ◽  
Critical Periods ◽  
Significant Group ◽  
Fluoxetine Treatment ◽  
Short And Long Term

<p>Serotonin is an important neurotransmitter that regulates a range of processes within the brain and is implicated in several psychiatric disorders. In addition, serotonin acts as a developmental signal during critical periods of prenatal development, influencing processes such as neuronal proliferation, migration, and synaptogenesis (Gaspar et al., 2003). The serotonin transporter (5- HTT) plays a key role in regulating extracellular serotonin levels and is the main target of selective-serotonin reuptake inhibitors (SSRIs), a class of drugs that have anti-anxiety and anti- depressive activity. SSRIs cause an acute increase in extracellular serotonin and are commonly prescribed as a treatment for depression and anxiety during pregnancy (Tran & Robb, 2015). Given that these drugs alter serotonin transmission and can pass to the developing fetus via the placenta, it is vital that the outcomes of prenatal SSRI exposure are investigated. In humans, a genetic variant of the gene that codes for the 5-HTT (SLC6A4) has been linked to increased risk for developing depression and anxiety (Caspi et al., 2003). The functional consequences of this genetic polymorphism are life-long alterations in 5-HTT activity, resulting in increased extracellular levels of serotonin (Nakamura et al., 2000). Given prenatal SSRI exposure results in a time-locked blockade of 5-HTT during critical periods of development, it follows that alterations in serotonin during development might similarly result in enhanced risk for depression and anxiety later in life. Outcomes in children prenatally exposed to SSRIs are difficult to study due to confounds of pre- existing maternal depression. Therefore, the current thesis presents two experiments that aimed to further investigate the role of altered extracellular serotonin levels during development in an animal model. Experiment one aimed to develop a method of voluntary oral administration of the SSRI fluoxetine to pregnant rat dams. This method was then applied in experiment two to create a time-locked blockade of 5-HTT during critical periods of development in an animal model of life-long 5-HTT blockade. The aim of experiment two was to directly assess the contribution of short- and long-term 5-HTT blockade on anxiety and depression phenotypes in adult male offspring. In addition, maternal behaviour was assessed to determine whether fluoxetine treatment had an influence on mother-pup interactions that could confound results. To test for anxiety and depression phenotypes, the novel affective disorder test (ADT) was used to assess anxiety behaviour and the deficits in anticipatory pleasure indicative of anhedonia. In the current study, fluoxetine treatment did not have an effect on litter outcomes or mother-pup interactions. Crucially, no significant group differences were found indicating that neither short- nor long- term blockade of 5-HTT resulted in increased anxiety- or depressive-like behaviours in the current experiment. However, limitations with methodological design limit the translatability of these results to the broader literature, and validation of the ADT is required before these results can be generalised beyond this thesis.</p>

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