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Uro-Angiographic Contrast Agents—The Holy Grail
Published in Christoph de Haën, X-Ray Contrast Agent Technology, 2019
In 1952 the zoology student at Uppsala University, Jan-Erik Kihlström, in connection with using solutions of iodopyracet meglumine for the determination of the density of sperm, set out to find the osmolalities of solutions in concentrations up to 80% (w/v) (Kihlström 1952). He realized that the freezing behavior of such solutions did not meet the validity requirements for cryoscopic measurements, a fact since confirmed by others (Børdalen, Wang, and Holtermann 1970). He built and then applied a vapor pressure osmometer. This pioneering effort could have signaled a breakthrough in characterization of contrast media. Unreasonably he analyzed solutions of iodopyracet and meglumine in an ill-defined stoichiometry but clearly very different from the 1:1 stoichiometry of radiological preparations. In defiance of the fact that his results were useless for the concrete case of UMBRADIL™ (iodopyracet meglumine), he was able to publish them in a radiological journal. Such was the radiological culture in the field of osmolality.
Stress-Responsive Neurohormones in Depression and Anxiety
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Ströhle Andreas, Holsboer Florian
Most studies exploring behavioral effects of CRH in animals have used intracerebro-ventricular or site-specific effects of CRH, and all agree that CRH mediates numerous anxiogenic and fear-related aspects of stress. These include the CRH-induced potentiation of acoustic startle, suppression of social interaction, and an increase in stress-induced freezing behavior [8]. This is further supported by transgenic mice overexpressing CRH. These mice have deficits in emotionality and were used as a genetic model of anxiogenic behavior [9]. As shown in Figure 1, most of the signs and symptoms induced by CRH administration correspond to symptoms of today’s diagnostic algorithms for depression and anxiety disorders.
The Impact of Insulin on Brain Serotonergic System: Consequences on Diabetes-Associated Mood Disorders 1
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Hugo Martin, Sebastian Bullich, Bruno P. Guiard, Xavier Fioramonti
Several interconnected biological mechanisms have been suggested to explain the comorbidity diabetes/psychiatric disorders including oxidative stress, inflammation, and insulin resistance. For this chapter, we only address the potential involvement of brain insulin resistance in the development of diabetes-associated mood disorders and the eventuality that the serotonin system is impacted by such pathological conditions. Supporting this hypothesis, a clinical study recently reported that depressive symptoms correlate with insulin resistance (8). Preclinical studies also consolidate this concept, as high-fat diet (HFD)-induced insulin resistance has been repeatedly shown to cause anxiety and depressive-like phenotypes in mice or rats (9–12). For instance, depressive-like symptoms are observed in genetic models of T2D such as in leptin-receptor deficient mice (db/db) or Zucker fa/fa rats (13, 14). These behavioral abnormalities are not limited to T2D, as streptozotocin (STZ) injection-induced T1D in mice also promotes anxiety and depressive-like symptoms (15–17). Conversely, animal studies showed that chronic mild stress, social defeat, or dexamethasone-induced depressive-like symptoms are associated with peripheral insulin resistance (17–19). Nevertheless, in these models, it has never been shown whether metabolic impairments are a cause or a consequence of mood disorders. Of particular note, several preclinical studies have examined the potential therapeutic effects of insulin or antidiabetic drugs in these models of T1D or T2D. They concur to demonstrate their beneficial effects on emotionality in association with enhancement of peripheral insulin signaling and/or anti-inflammatory properties. For example, in a rat model of T2D, chronic intraperitoneal administration of insulin elicits a comparable antidepressant-like response than the selective serotonin reuptake inhibitor (SSRI) sertraline (20). An important question that remains unresolved is whether the impairment of peripheral and/or central insulin signaling contributes to modifying brain circuits involved in depression. The observation that subchronic intraperitoneal insulin treatment reverses freezing behavior without attenuating hyperglycemia in an STZ-T1D mouse model (15), strongly suggests that the stimulation of insulin signaling may promote a therapeutic independently from an improvement of peripheral metabolism. This review summarizes the arguments in favor of the hypothesis that insulin resistance in the brain is key to these deleterious effects of diabetes on behavior.
A novel stress re-stress model: modification of re-stressor cue induces long-lasting post-traumatic stress disorder-like symptoms in rats
Published in International Journal of Neuroscience, 2020
Santosh Kumar Prajapati, Neha Singh, Debapriya Garabadu, Sairam Krishnamurthy
SRS model also has some limitations as there are no measures of fear responses which are considered to be responsible for the development of most of the symptoms. Further, forced-swim paradigm can interfere with the results of the depressive-like behavior as animals are weekly exposed to forced swim test (FST) as a re-stress cue. Furthermore, treatment with paroxetine did not modulate FST-induced decrease in plasma corticosterone (CORT) level, suggesting a lack of predictive validity related to HPA dysfunction [7]. Therefore, it is necessary to develop a suitable model which mimics most of the clinical symptoms of PTSD. Recently, Guo et al. [23] reported that inescapable foot shock (FS) (0.8 mA, 10 sec) develops long-lasting manifestations of anxiety as well as depression-like behavior even after four weeks to the initial exposure in rats [23]. The exposure of FS also induces freezing response which is reliable to measure contextual fear response and intrusive memory [24]. The neuronal mechanism underlying fear conditioning is also involved in the development of intrusive memory [25]. Enhanced freezing behavior is considered as an indicator for formation of intrusive response [26]. Reports suggest that inescapable FS exposure of 0.5 mA for 5 sec exhibit long-lasting cognitive dysfunction [27], and 1 mA for 1 sec pulse per 60 sec affects different brain regions such as locus coeruleus, ventral tegmental area and medial prefrontal cortex and leads to HPA-axis dysfunction [28].
Small damage of brain parenchyma reliably triggers spreading depolarization
Published in Neurological Research, 2020
Lyudmila V. Vinogradova, Maria P. Rysakova, Irina V Pavlova
To investigate behavioral manifestations of injury-induced SD, video-recordings of rat behavior were analyzed. During the first post-injury minute, when SD traveled over the neocortex, the most frequent behavior was grooming that was observed in 50% of cortical SDs. Later, starting from 81 ± 6 s, i.e. when SD left the neocortex and reached deep sites of the temporal lobe, all rats demonstrated repeated brief episodes of freezing behavior (no movements except the respiratory ones). The episodes were initially short-lasting (4–10 s) but became longer with time (20–80 s). The delayed freezing behavior was the most reliable behavioral sign of cortical SD observed during 89% (25/28) of cortical SDs for which the behavior could be identified. During the period from 225 ± 6 s till 268 ± 9 s post-injury, when SD invaded the striatum, rats exhibited turning behavior (Figure 1e). It started with forced head turning and evolved in the whole body circling towards contralateral to SD side (up to six full body circles, Figure 1f). After termination of the SD-related circling, freezing behavior re-appeared and lasted till 313 ± 6 s. If cortical SD did not penetrate the striatum, no turning behavior was observed.
The effect of traumatic-like stress exposure on alterations in the temporal social behavior of a rodent population
Published in Stress, 2020
Mengfei Han, Haoshuang Luo, Yunjing Bai, Shichun Zheng, Fenghua Li, Juan Fu, Shaofei Jiang, Zhengkui Liu, Xigeng Zheng
Behavior indices such as the total freezing time, time spent in the central area, number of rearings and total distance traveled were videotaped and analyzed with Xeye. Specifically, freezing behavior was used to assess the fear response, which was defined as no movements other than those associated with respiration (Fu et al., 2016). Time spent in the central area was used to assess anxiety-like behaviors. In the test, a designated rectangular area (43 × 18 cm) in the center of the open-field chamber was specified as the central area. The number of rearings included both free leaning and non-free leaning to assess exploratory behaviors. Motility was assessed by the total distance that the rats traveled.