Journal articles on the topic 'Histamine, brain, memory, feeding behavior'
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Morimoto, T. "Brain histamine and feeding behavior." Behavioural Brain Research 124, no. 2 (October 15, 2001): 145–50. http://dx.doi.org/10.1016/s0166-4328(01)00225-x.
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Haas, Helmut L., Olga A. Sergeeva, and Oliver Selbach. "Histamine in the Nervous System." Physiological Reviews 88, no. 3 (July 2008): 1183–241. http://dx.doi.org/10.1152/physrev.00043.2007.
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Histamine is a transmitter in the nervous system and a signaling molecule in the gut, the skin, and the immune system. Histaminergic neurons in mammalian brain are located exclusively in the tuberomamillary nucleus of the posterior hypothalamus and send their axons all over the central nervous system. Active solely during waking, they maintain wakefulness and attention. Three of the four known histamine receptors and binding to glutamate NMDA receptors serve multiple functions in the brain, particularly control of excitability and plasticity. H1 and H2 receptor-mediated actions are mostly excitatory; H3 receptors act as inhibitory auto- and heteroreceptors. Mutual interactions with other transmitter systems form a network that links basic homeostatic and higher brain functions, including sleep-wake regulation, circadian and feeding rhythms, immunity, learning, and memory in health and disease.
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Köhler, Cristiano André, Weber Cláudio da Silva, Fernando Benetti, and Juliana Sartori Bonini. "Histaminergic Mechanisms for Modulation of Memory Systems." Neural Plasticity 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/328602.
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Encoding for several memory types requires neural changes and the activity of distinct regions across the brain. These areas receive broad projections originating in nuclei located in the brainstem which are capable of modulating the activity of a particular area. The histaminergic system is one of the major modulatory systems, and it regulates basic homeostatic and higher functions including arousal, circadian, and feeding rhythms, and cognition. There is now evidence that histamine can modulate learning in different types of behavioral tasks, but the exact course of modulation and its mechanisms are controversial. In the present paper we review the involvement of the histaminergic system and the effects histaminergic receptor agonists/antagonists have on the performance of tasks associated with the main memory types as well as evidence provided by studies with knockout models. Thus, we aim to summarize the possible effects histamine has on modulation of circuits involved in memory formation.
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Fukagawa, Koji, Hiroshi Etou, Kazuma Fujimoto, Kazuo Kurata, Kenji Terada, Yasufumi Okabe, and Toshiie Sakata. "Feeding behavior in response to histamine H1-receptor antagonist in the rat brain." Japanese Journal of Pharmacology 40 (1986): 175. http://dx.doi.org/10.1016/s0021-5198(19)59272-1.
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Gotoh, Koro, Takayuki Masaki, Seiichi Chiba, Hisae Ando, Kansuke Fujiwara, Takanobu Shimasaki, Kimihiko Mitsutomi, et al. "Brain-derived neurotrophic factor, corticotropin-releasing factor, and hypothalamic neuronal histamine interact to regulate feeding behavior." Journal of Neurochemistry 125, no. 4 (March 19, 2013): 588–98. http://dx.doi.org/10.1111/jnc.12213.
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Fülöp, András K., Anna Földes, Edit Buzás, Krisztina Hegyi, Ildikó H. Miklós, László Romics, Monika Kleiber, András Nagy, András Falus, and Krisztina J. Kovács. "Hyperleptinemia, Visceral Adiposity, and Decreased Glucose Tolerance in Mice with a Targeted Disruption of the Histidine Decarboxylase Gene." Endocrinology 144, no. 10 (October 1, 2003): 4306–14. http://dx.doi.org/10.1210/en.2003-0222.
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Histamine has been referred to as an anorexic factor that decreases appetite and fat accumulation and affects feeding behavior. Tuberomammillary histaminergic neurons have been implicated in central mediation of peripheral metabolic signals such as leptin, and centrally released histamine inhibits ob gene expression. Here we have characterized the metabolic phenotype of mice that completely lack the ability to produce histamine because of targeted disruption of the key enzyme in histamine biosynthesis (histidine decarboxylase, HDC). Histochemical analyses confirmed the lack of HDC mRNA, histamine immunoreactivity, and histaminergic innervation throughout the brain of gene knockout mouse. Aged histamine-deficient (HDC−/−) mice are characterized by visceral adiposity, increased amount of brown adipose tissue, impaired glucose tolerance, hyperinsulinemia, and hyperleptinemia. Histamine-deficient animals are not hyperphagic but gain more weight and are calorically more efficient than wild-type controls. These metabolic changes presumably are due to the impaired regulatory loop between leptin and hypothalamic histamine that results in orexigenic dominance through decreased energy expenditure, attenuated ability to induce uncoupling protein-1 mRNA in the brown adipose tissue and defect in mobilizing energy stores. Our results further support the role of histamine in regulation of energy homeostasis.
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Schmidt, Stefan, Miriam Richter, Dirk Montag, Tina Sartorius, Verena Gawlik, Anita M. Hennige, Stephan Scherneck, et al. "Neuronal functions, feeding behavior, and energy balance in Slc2a3+/− mice." American Journal of Physiology-Endocrinology and Metabolism 295, no. 5 (November 2008): E1084—E1094. http://dx.doi.org/10.1152/ajpendo.90491.2008.
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Homozygous deletion of the gene of the neuronal glucose transporter GLUT3 ( Slc2a3) in mice results in embryonic lethality, whereas heterozygotes ( Slc2a3+/−) are viable. Here, we describe the characterization of heterozygous mice with regard to neuronal function, glucose homeostasis, and, since GLUT3 might be a component of the neuronal glucose-sensing mechanism, food intake and energy balance. Levels of GLUT3 mRNA and protein in brain were reduced by 50% in Slc2a3+/− mice. Electrographic features examined by electroencephalographic recordings give evidence for slightly but significantly enhanced cerebrocortical activity in Slc2a3+/− mice. In addition, Slc2a3+/− mice were slightly more sensitive to an acoustic startle stimulus (elevated startle amplitude and reduced prepulse inhibition). However, systemic behavioral testing revealed no other functional abnormalities, e.g., in coordination, reflexes, motor abilities, anxiety, learning, and memory. Furthermore, no differences in body weight, blood glucose, and insulin levels were detected between wild-type and Slc2a3+/− littermates. Food intake as monitored randomly or after intracerebroventricular administration of 2-deoxyglucose or d-glucose, or food choice for carbohydrates/fat was not affected in Slc2a3+/− mice. Taken together, our data indicate that, in contrast to Slc2a1, a single allele of Slc2a3 is sufficient for maintenance of neuronal energy supply, motor abilities, learning and memory, and feeding behavior.
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Zhang, Ting, Min Jung Kim, Min Ju Kim, Xuangao Wu, Hye Jeong Yang, Heng Yuan, Shaokai Huang, Sun Myung Yoon, Keun-Nam Kim, and Sunmin Park. "Long-Term Effect of Porcine Brain Enzyme Hydrolysate Intake on Scopolamine-Induced Memory Impairment in Rats." International Journal of Molecular Sciences 23, no. 6 (March 20, 2022): 3361. http://dx.doi.org/10.3390/ijms23063361.
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No study has revealed the effect of porcine brain enzyme hydrolysate (PBEH) on memory impairment. We aimed to examine the hypothesis that PBEH intake modulates memory deficits and cognitive behavior in scopolamine (SC)-induced amnesia rats, and its mechanism, including gut microbiota changes, was determined. Sprague–Dawley male rats had intraperitoneal injections of SC (2 mg/kg body weight/day) at 30 min after daily feeding of casein (MD-control), PBEH (7 mg total nitrogen/mL) at 0.053 mL (Low-PBEH), 0.159 mL (Medium-PBEH), 0.478 mL (High-PBEH), or 10 mg donepezil (Positive-control) per kilogram body weight per day through a feeding needle for six weeks. The Normal-control rats had casein feeding without SC injection. PBEH dose-dependently protected against memory deficits determined by passive avoidance test, Y-maze, water-maze, and novel object recognition test in SC-induced rats compared to the MD-control. The High-PBEH group had a similar memory function to the Positive-control group. Systemic insulin resistance determined by HOMA-IR was lower in the PBEH groups than in the Normal-control but not the Positive-control. In parallel with systemic insulin resistance, decreased cholesterol and increased glycogen contents in the hippocampus in the Medium-PBEH and High-PBEH represented reduced brain insulin resistance. PBEH intake prevented the increment of serum TNF-α and IL-1β concentrations in the SC-injected rats. Hippocampal lipid peroxide and TNF-α contents and mRNA TNF-α and IL-1β expression were dose-dependently reduced in PBEH and Positive-control. PBEH decreased the hippocampal acetylcholinesterase activity compared to the MD-control, but not as much as the Positive-control. PBEH intake increased the α-diversity of the gut microbiota compared to the MD-control, and the gut microbiota community was separated from MD-control. In metagenome function analysis, PBEH increased the energy metabolism-related pathways of the gut microbiota, including citric acid cycle, oxidative phosphorylation, glycolysis, and amino acid metabolism, which were lower in the MD-control than the Normal-control. In conclusion, alleviated memory deficit by PBEH was associated potentially with not only reducing acetylcholinesterase activity but also improving brain insulin resistance and neuroinflammation potentially through modulating gut microbiota. PBEH intake (1.5–4.5 mL of 7 mg total nitrogen/mL for human equivalent) can be a potential therapeutic agent for improving memory impairment.
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MONGE-SANCHEZ, Diana, Marcelıno MONTİEL-HERRERA, Denısse GARCİA VİLLA, Guillermo LOPEZ, J. Abraham DOMÍNGUEZ-AVİLA, and Gustavo GONZÁLEZ-AGUİLAR. "Fasting alters p75NTR and AgRP mRNA expression in rat olfactory bulb and hippocampus." Journal of Cellular Neuroscience and Oxidative Stress 14, no. 2 (January 31, 2023): 1074–84. http://dx.doi.org/10.37212/jcnos.1168800.
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Classic non-homeostatic structures involved in food intake regulation are reciprocally influenced by metabolic signals. Orexigenic peptides expressed in the olfactory bulb (OB) and hippocampus (HP) modulate olfactory processing and memory, respectively. Hypothalamic circuits also modulate feeding behavior by activating and releasing Agouti-related peptide (AgRP) in response to orexigenic signals. An adequate response to fasting requires the expression of p75 neurotrophin receptor (p75NTR) in AgRP neurons. The present study aimed to determine whether there is a role for p75NTR and AgRP in the OB and HP on the feeding behavior of fasted rats. A group of fasted rats (FG) was confronted with a decision-making paradigm in a T-maze containing a standard chow pellet (CP), and the same pellet coated with a phenolic-rich avocado paste extract (AVO) on either end; their OB and HP were then analyzed with histological and molecular tools. FG rats had briefer feeding latencies, as compared to control rats fed ad libitum (median latencies: 55.4 vs 191.7 min, p = 0.032). They also had reduced cell counts in both brain structures, as compared to satiated rats. AgRP mRNA was not expressed in the HP of either group, however, it was found in the OB. p75NTR mRNA was expressed in both brain structures of FG rats. These results suggest that contrasting metabolic states (fasted or satiated) motivate different feeding responses, which are influenced by p75NTR and AgRP mRNA expression in non-homeostatic food intake brain structures.
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Nässel, Dick R. "Leucokinin and Associated Neuropeptides Regulate Multiple Aspects of Physiology and Behavior in Drosophila." International Journal of Molecular Sciences 22, no. 4 (February 16, 2021): 1940. http://dx.doi.org/10.3390/ijms22041940.
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Leucokinins (LKs) constitute a family of neuropeptides identified in numerous insects and many other invertebrates. LKs act on G-protein-coupled receptors that display only distant relations to other known receptors. In adult Drosophila, 26 neurons/neurosecretory cells of three main types express LK. The four brain interneurons are of two types, and these are implicated in several important functions in the fly’s behavior and physiology, including feeding, sleep–metabolism interactions, state-dependent memory formation, as well as modulation of gustatory sensitivity and nociception. The 22 neurosecretory cells (abdominal LK neurons, ABLKs) of the abdominal neuromeres co-express LK and a diuretic hormone (DH44), and together, these regulate water and ion homeostasis and associated stress as well as food intake. In Drosophila larvae, LK neurons modulate locomotion, escape responses and aspects of ecdysis behavior. A set of lateral neurosecretory cells, ALKs (anterior LK neurons), in the brain express LK in larvae, but inconsistently so in adults. These ALKs co-express three other neuropeptides and regulate water and ion homeostasis, feeding, and drinking, but the specific role of LK is not yet known. This review summarizes Drosophila data on embryonic lineages of LK neurons, functional roles of individual LK neuron types, interactions with other peptidergic systems, and orchestrating functions of LK.
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Noble, Emily E., Charles J. Billington, Catherine M. Kotz, and ChuanFeng Wang. "The lighter side of BDNF." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 5 (May 2011): R1053—R1069. http://dx.doi.org/10.1152/ajpregu.00776.2010.
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Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that “faulty” circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity.
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Dissel, Stephane, Markus K. Klose, Bruno van Swinderen, Lijuan Cao, Melanie Ford, Erica M. Periandri, Joseph D. Jones, Zhaoyi Li, and Paul J. Shaw. "Sleep-promoting neurons remodel their response properties to calibrate sleep drive with environmental demands." PLOS Biology 20, no. 9 (September 29, 2022): e3001797. http://dx.doi.org/10.1371/journal.pbio.3001797.
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Falling asleep at the wrong time can place an individual at risk of immediate physical harm. However, not sleeping degrades cognition and adaptive behavior. To understand how animals match sleep need with environmental demands, we used live-brain imaging to examine the physiological response properties of the dorsal fan-shaped body (dFB) following interventions that modify sleep (sleep deprivation, starvation, time-restricted feeding, memory consolidation) in Drosophila. We report that dFB neurons change their physiological response-properties to dopamine (DA) and allatostatin-A (AstA) in response to different types of waking. That is, dFB neurons are not simply passive components of a hard-wired circuit. Rather, the dFB neurons intrinsically regulate their response to the activity from upstream circuits. Finally, we show that the dFB appears to contain a memory trace of prior exposure to metabolic challenges induced by starvation or time-restricted feeding. Together, these data highlight that the sleep homeostat is plastic and suggests an underlying mechanism.
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Shien Wee, Ryan Wei, and Andrew MacAskill. "Hippocampal Circuits for the Hunger-Dependent Control of Feeding Behaviour." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A540. http://dx.doi.org/10.1210/jendso/bvab048.1100.
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Abstract Background: Feeding behavior is a complex motivated behavior that requires organisms to integrate features of the environment, such as food availability and value, and internal states, such as hunger, in deliberating over the decision to eat. The hippocampus - a brain region classically thought to support spatial cognition and episodic memory - is increasingly recognised to contribute to such decision-making processes. This function makes the hippocampus a likely candidate in supporting the higher-order decisions that underpin motivated behaviors such as feeding. However, the role of the hippocampus during free-feeding behavior has not been examined. Methods and Results: To address this question, we used in vivo calcium imaging during feeding behavior in mice to monitor the neural activity of the ventral subiculum (vS) - one of the main output structures of the ventral hippocampus. In a free-feeding task, we found that the vS encoded the investigative approach phase of feeding behavior and that activity during this period correlated with the probability of transitioning from food investigation to consumption. Calcium imaging during an operant task confirmed the specific encoding of preparatory behaviour preceding food consumption. Furthermore, the sensitivity of vS to the hunger state could be mapped to vS neurons projecting to the nucleus accumbens (vS-NAc). Ghrelin - a hormone signalling the hunger state - altered synaptic transmission specifically in vS-NAc neurons, and molecular knockdown of the ghrelin receptor was required for the hunger sensitivity of vS-NAc. Consequently, both reducing ghrelin signalling in vS-NAc neurons through molecular knockdown and artificially elevating vS-NAc activity through optogenetics were sufficient to shift the feeding strategy of animals, effectively curtailing overall food consumption. Conclusion: In summary, these results provide evidence for a hippocampal circuit that integrates hunger state signals to regulate the decision to eat.
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Acevedo-Triana, Cesar A., Manuel J. Rojas, and Fernando Cardenas P. "Running wheel training does not change neurogenesis levels or alter working memory tasks in adult rats." PeerJ 5 (May 9, 2017): e2976. http://dx.doi.org/10.7717/peerj.2976.
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BackgroundExercise can change cellular structure and connectivity (neurogenesis or synaptogenesis), causing alterations in both behavior and working memory. The aim of this study was to evaluate the effect of exercise on working memory and hippocampal neurogenesis in adult male Wistar rats using a T-maze test.MethodsAn experimental design with two groups was developed: the experimental group (n = 12) was subject to a forced exercise program for five days, whereas the control group (n = 9) stayed in the home cage. Six to eight weeks after training, the rats’ working memory was evaluated in a T-maze test and four choice days were analyzed, taking into account alternation as a working memory indicator. Hippocampal neurogenesis was evaluated by means of immunohistochemistry of BrdU positive cells.ResultsNo differences between groups were found in the behavioral variables (alternation, preference index, time of response, time of trial or feeding), or in the levels of BrdU positive cells.DiscussionResults suggest that although exercise may have effects on brain structure, a construct such as working memory may require more complex changes in networks or connections to demonstrate a change at behavioral level.
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Ubaldi, Massimo, Nazzareno Cannella, Anna Maria Borruto, Michele Petrella, Maria Vittoria Micioni Di Bonaventura, Laura Soverchia, Serena Stopponi, Friedbert Weiss, Carlo Cifani, and Roberto Ciccocioppo. "Role of Nociceptin/Orphanin FQ-NOP Receptor System in the Regulation of Stress-Related Disorders." International Journal of Molecular Sciences 22, no. 23 (November 30, 2021): 12956. http://dx.doi.org/10.3390/ijms222312956.
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Nociceptin/orphanin FQ (N/OFQ) is a 17-residue neuropeptide that binds the nociceptin opioid-like receptor (NOP). N/OFQ exhibits nucleotidic and aminoacidics sequence homology with the precursors of other opioid neuropeptides but it does not activate either MOP, KOP or DOP receptors. Furthermore, opioid neuropeptides do not activate the NOP receptor. Generally, activation of N/OFQ system exerts anti-opioids effects, for instance toward opioid-induced reward and analgesia. The NOP receptor is widely expressed throughout the brain, whereas N/OFQ localization is confined to brain nuclei that are involved in stress response such as amygdala, BNST and hypothalamus. Decades of studies have delineated the biological role of this system demonstrating its involvement in significant physiological processes such as pain, learning and memory, anxiety, depression, feeding, drug and alcohol dependence. This review discusses the role of this peptidergic system in the modulation of stress and stress-associated psychiatric disorders in particular drug addiction, mood, anxiety and food-related associated-disorders. Emerging preclinical evidence suggests that both NOP agonists and antagonists may represent a effective therapeutic approaches for substances use disorder. Moreover, the current literature suggests that NOP antagonists can be useful to treat depression and feeding-related diseases, such as obesity and binge eating behavior, whereas the activation of NOP receptor by agonists could be a promising tool for anxiety.
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Kim, Woosuk, Hyun Jung Kwon, Hyo Young Jung, Soon-Sung Lim, Beom-Goo Kang, Yong-Bok Jo, Dong-Sool Yu, Soo Young Choi, In Koo Hwang, and Dae Won Kim. "Extracts from the Leaves of Cissus verticillata Ameliorate High-Fat Diet-Induced Memory Deficits in Mice." Plants 10, no. 9 (August 31, 2021): 1814. http://dx.doi.org/10.3390/plants10091814.
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We investigated the effects of Cissus verticillata leaf extract (CVE) on a high-fat diet (HFD)-induced obesity and memory deficits. Male mice (5 weeks of age) were fed vehicle (distilled water), or 30, 100, or 300 mg/kg of CVE once a day for 8 weeks with an HFD. Treatment with CVE resulted in lower body weight and glucose levels in a concentration- and feeding time-dependent manner. LDL cholesterol and triglyceride levels were significantly lower in the CVE-treated HFD group than in the vehicle-treated HFD group. In contrast, high-density lipoprotein cholesterol levels did not show any significant changes. Lipid droplets and ballooning were reduced depending on the concentration of CVE treatment compared to the HFD group. Treatment with CVE ameliorated the increase in glucagon and immunoreactivities in the pancreas, and novel object recognition memory was improved by 300 mg/kg CVE treatment compared to the HFD group. More proliferating cells and differentiated neuroblasts were higher in mice treated with CVE than in vehicle-treated HFD-fed mice. Brain-derived neurotrophic factor (BDNF) levels were significantly decreased in the HFD group, which was facilitated by treatment with 300 mg/kg CVE in hippocampal homogenates. These results suggest that CVE ameliorates HFD-induced obesity and memory deficits in mice, associated with increased BDNF levels in the hippocampus.
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Gottsch, Michelle L., Hongkui Zeng, John G. Hohmann, David Weinshenker, Donald K. Clifton, and Robert A. Steiner. "Phenotypic Analysis of Mice Deficient in the Type 2 Galanin Receptor (GALR2)." Molecular and Cellular Biology 25, no. 11 (June 1, 2005): 4804–11. http://dx.doi.org/10.1128/mcb.25.11.4804-4811.2005.
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ABSTRACT Galanin is a neuropeptide implicated in the regulation of feeding, reproduction, cognition, nociception, and seizure susceptibility. There are three known galanin receptor (GALR) subtypes (GALR1, GALR2, and GALR3), which bind to galanin with different affinities and have their own unique distributions, signaling mechanisms, and putative functions in the brain and peripheral nervous system. To gain further insight into the possible physiological significance of GALR2, we created mutant mice that were deficient in GALR2 and compared their phenotype to that of wild-type (WT) littermate or age-matched controls, with respect to basic motor and sensory function, feeding behavior, reproduction, mood, learning and memory, and seizure susceptibility. Phenotypic analysis revealed that animals bearing a deletion of GALR2 did not differ significantly from their WT controls in any of the measured variables. We conclude that either GALR2 plays no role in these physiological functions or through redundancy or compensation these mutant animals can adapt to the congenital absence of GALR2. It is also conceivable that GALR2 plays only a subtle role in some of these functions and that the impact of its loss could not be detected by the analytical procedures used here.
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Kelberman, Michael A., Claire R. Anderson, Eli Chlan, Jacki M. Rorabaugh, Katharine E. McCann, and David Weinshenker. "Consequences of Hyperphosphorylated Tau in the Locus Coeruleus on Behavior and Cognition in a Rat Model of Alzheimer’s Disease." Journal of Alzheimer's Disease 86, no. 3 (April 5, 2022): 1037–59. http://dx.doi.org/10.3233/jad-215546.
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Background: The locus coeruleus (LC) is one of the earliest brain regions to accumulate hyperphosphorylated tau, but a lack of animal models that recapitulate this pathology has hampered our understanding of its contributions to Alzheimer’s disease (AD) pathophysiology. Objective: We previously reported that TgF344-AD rats, which overexpress mutant human amyloid precursor protein and presenilin-1, accumulate early endogenous hyperphosphorylated tau in the LC. Here, we used TgF344-AD rats and a wild-type (WT) human tau virus to interrogate the effects of endogenous hyperphosphorylated rat tau and human tau in the LC on AD-related neuropathology and behavior. Methods: Two-month-old TgF344-AD and WT rats received bilateral LC infusions of full-length WT human tau or mCherry control virus driven by the noradrenergic-specific PRSx8 promoter. Rats were subsequently assessed at 6 and 12 months for arousal (sleep latency), anxiety-like behavior (open field, elevated plus maze, novelty-suppressed feeding), passive coping (forced swim task), and learning and memory (Morris water maze and fear conditioning). Hippocampal microglia, astrocyte, and AD pathology were evaluated using immunohistochemistry. Results: In general, the effects of age were more pronounced than genotype or treatment; older rats displayed greater hippocampal pathology, took longer to fall asleep, had reduced locomotor activity, floated more, and had impaired cognition compared to younger animals. TgF344-AD rats showed increased anxiety-like behavior and impaired learning and memory. The tau virus had negligible influence on most measures. Conclusion: Effects of hyperphosphorylated tau on AD-like neuropathology and behavioral symptoms were subtle. Further investigation of different forms of tau is warranted.
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Shebl, Ghada Mostafa, Hanan Ibrahim Sayed-Ahmed, Mohamed Bassuony Hamza, and Ashraf Salah El-Din Haider. "Phenylalanine Rich Diet (Vicia faba L.) Enhances the Expression of Dopamine Receptor D3 (DRD3) Gene in Rabbits." European Journal of Biology and Biotechnology 2, no. 5 (October 24, 2021): 81–85. http://dx.doi.org/10.24018/ejbio.2021.2.5.297.
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Dopamine is a neurotransmitter hormone for pleasure and reward. It is synthesized only in the brain cells of human and animals and responsible for the regulation of behavior, mood, memory, cognitive, flexible movement, the body weight, and other important functions. The Dopamine Receptor D3 (DRD3) is the most important receptor for dopamine. In this investigation, expression of DRD3 gene was studied in rabbits fed on supplemented diet of dry and fresh faba bean (Vicia faba L. Sakha 3). DRD3 gene (≈ 1200 bp) in control and treated rabbits were PCR amplified, sequenced and aligned with reference gene (Acc. No XM_017346708.1). High genetic similarity values were detected among all sequences. DRD3 gene sequences of control, fresh and dry faba bean fed rabbits were deposited in the GenBank with accession numbers MZ714134, MZ714135 and MZ714136 respectively. Direct estimation of blood phenylalanine (Phe) amino acid indicated that feeding rabbits on dry faba bean reflected the highest level of Phe in the rabbit’s blood. Quantitative RT-qPCR analysis showed that DRD3 gene was over expressed after feeding rabbits on dry faba bean form compared with feeding on green form and control. Thus, diet rich with phenylalanine like Sakha3 (dry and fresh forms) enhance gene expression of DRD3 gene. However, diet doesn't affect the DRD3 gene sequence and structure. In a conclusion, our findings indicated a direct effect of faba bean supplemented diet on increasing DRD3 expression levels which improve the life quality for human.
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Shin, Mimi, and B. Jill Venton. "(Digital Presentation) In Vivo Electrochemical Measurement of Dopamine in Adult Drosophila Mushroom Body." ECS Meeting Abstracts MA2022-01, no. 53 (July 7, 2022): 2197. http://dx.doi.org/10.1149/ma2022-01532197mtgabs.
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Dopamine is a neuromodulator that is secreted to the synapse to relay chemical signals to target neurons. Abnormal levels of dopamine release leads to various neurodegenerative diseases. Therefore, measuring dopamine is essential to understand how dopamine is regulated under normal and pathological conditions. Drosophila melanogaster, the fruit fly, is an ideal model system for studying fundamental neurological processes and diseases because of the availability of sophisticated genetic tools and well conserved neurological processes between mammals and flies. Majority of neuroscience studies involved in modifying a gene and measure the effect of genetic mutation on output behaviors. However, dopamine release is highly dynamic because of the complex activity of dopamine transporters and autoreceptors. Therefore, to understand how dopamine signaling controls the behavior, a direct measurement of changes in dopamine release is necessary. Fast-scan cyclic voltammetry (FSCV) at a carbon-fiber microelectrode is an electrochemical technique that trace concentration changes in dopamine release on the sub-second time scale. Our lab pioneered directly measuring various endogenous neuromodulators in the fly central nervous system with FSCV. Initially, these studies were performed in ex vivo preparations, where brains were isolated from larvae and adult fly, and thus could not monitor neuromodulators during behavior. In this study, we developed in vivo FSCV method to measure phasic dopamine in the mushroom body (MB) during behavior for the first time. The MB in fly has been extensively studied as an associative center for regulating olfactory learning and memory. First, acetylcholine stimulation was applied to the MB heel and medial tip to characterize dopamine signaling and to demonstrate the feasibility of in vivo FSCV in intact fly brain. Application of 0.2 pmol acetylcholine released 0.36 ± 0.06 µM dopamine in the medial tip, which is slightly higher than 0.22 ± 0.06 µM dopamine in the heel. Compartmental differences in evoked release suggest heterogeneity of dopamine regulation in the MB. Nisoxetine, a dopamine transporter inhibitor, and flupentixol, a D2 antagonist, increased stimulated dopamine release. We then applied the in vivo method to monitor changes in behaviorally evoked dopamine release during sugar feeding. Sugar feeding evoked 0.31 ± 0.09 µM dopamine in the medial tip of MB. Flupentixol significantly increased sugar evoked release implying D2 receptor acts as autoreceptor and regulates dopamine signaling during sugar feeding. Therefore, this developed in vivo FSCV method is a great addition to the existing tools to measure endogenous neuromodulators in the fly and valuable for studying real-time dopamine signaling during behavior. This in vivo method also can be further extended to better understand how dopamine and other neuromodulators regulate complex behaviors, such as reward associated learning and memory formation.
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Hsieh, Hsin-Yi, Yu-Chieh Chen, Mei-Hsin Hsu, Hong-Ren Yu, Chung-Hao Su, You-Lin Tain, Li-Tung Huang, and Jiunn-Ming Sheen. "Maternal Iron Deficiency Programs Offspring Cognition and Its Relationship with Gastrointestinal Microbiota and Metabolites." International Journal of Environmental Research and Public Health 17, no. 17 (August 20, 2020): 6070. http://dx.doi.org/10.3390/ijerph17176070.
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Iron is an essential micronutrient for the brain development of the fetus. Altered intestinal microbiota might affect behavior and cognition through the so-called microbiota-gut-brain axis. We used a Sprague-Dawley rat model of a maternal low-iron diet to explore the changes in cognition, dorsal hippocampal brain-derived neurotrophic factor (BDNF) and related pathways, gut microbiota, and related metabolites in adult male offspring. We established maternal iron-deficient rats by feeding them a low-iron diet (2.9 mg/kg), while the control rats were fed a standard diet (52.3 mg/kg). We used a Morris water maze test to assess spatial learning and long-term memory. Western blot (WB) assays and a quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to detect the BDNF concentration and related signaling pathways. We collected fecal samples for microbiota profiling and measured the concentrations of plasma short-chain fatty acids. The adult male offspring of maternal rats fed low-iron diets before pregnancy, during pregnancy and throughout the lactation period had (1) spatial deficits, (2) a decreased BDNF mRNA expression and protein concentrations, accompanied by a decreased TrkB protein abundance, (3) a decreased plasma acetate concentration, and (4) an enrichment of the Bacteroidaceae genus Bacteroides and Lachnospiraceae genus Marvinbryantia. Maternal iron deficiency leads to an offspring spatial deficit and is associated with alternations in gastrointestinal microbiota and metabolites.
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Eschment, Melanie, Hanna R. Franz, Nazlı Güllü, Luis G. Hölscher, Ko-Eun Huh, and Annekathrin Widmann. "Insulin signaling represents a gating mechanism between different memory phases in Drosophila larvae." PLOS Genetics 16, no. 10 (October 26, 2020): e1009064. http://dx.doi.org/10.1371/journal.pgen.1009064.
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The ability to learn new skills and to store them as memory entities is one of the most impressive features of higher evolved organisms. However, not all memories are created equal; some are short-lived forms, and some are longer lasting. Formation of the latter is energetically costly and by the reason of restricted availability of food or fluctuations in energy expanses, efficient metabolic homeostasis modulating different needs like survival, growth, reproduction, or investment in longer lasting memories is crucial. Whilst equipped with cellular and molecular pre-requisites for formation of a protein synthesis dependent long-term memory (LTM), its existence in the larval stage of Drosophila remains elusive. Considering it from the viewpoint that larval brain structures are completely rebuilt during metamorphosis, and that this process depends completely on accumulated energy stores formed during the larval stage, investing in LTM represents an unnecessary expenditure. However, as an alternative, Drosophila larvae are equipped with the capacity to form a protein synthesis independent so-called larval anaesthesia resistant memory (lARM), which is consolidated in terms of being insensitive to cold-shock treatments. Motivated by the fact that LTM formation causes an increase in energy uptake in Drosophila adults, we tested the idea of whether an energy surplus can induce the formation of LTM in the larval stage. Suprisingly, increasing the metabolic state by feeding Drosophila larvae the disaccharide sucrose directly before aversive olfactory conditioning led to the formation of a protein synthesis dependent longer lasting memory. Moreover, formation of this memory component is accompanied by the suppression of lARM. We ascertained that insulin receptors (InRs) expressed in the mushroom body Kenyon cells suppresses the formation of lARM and induces the formation of a protein synthesis dependent longer lasting memory in Drosophila larvae. Given the numerical simplicity of the larval nervous system this work offers a unique prospect to study the impact of insulin signaling on the formation of protein synthesis dependent memories on a molecular level.
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Jensen, Nanna H., Thomas I. Cremers, and Florence Sotty. "Therapeutic Potential of 5-HT2CReceptor Ligands." Scientific World JOURNAL 10 (2010): 1870–85. http://dx.doi.org/10.1100/tsw.2010.180.
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Serotonin 2C receptors are G protein-coupled receptors expressed by GABAergic, glutamatergic, and dopaminergic neurons. Anatomically, they are present in various brain regions, including cortical areas, hippocampus, ventral midbrain, striatum, nucleus accumbens, hypothalamus, and amygdala. A large body of evidence supports a critical role of serotonin 2C receptors in mediating the interaction between serotonergic and dopaminergic systems, which is at the basis of their proposed involvement in the regulation of mood, affective behavior, and memory. In addition, their expression in specific neuronal populations in the hypothalamus would be critical for their role in the regulation of feeding behavior. Modulation of these receptors has therefore been proposed to be of interest in the search for novel pharmacological strategies for the treatment of various pathological conditions, including schizophrenia and mood disorders, as well as obesity. More precisely, blockade of serotonin 2C receptors has been suggested to provide antidepressant and anxiolytic benefit, while stimulation of these receptors may offer therapeutic benefit for the treatment of psychotic symptoms in schizophrenia and obesity. In addition, modulation of serotonin 2C receptors may offer cognitive-enhancing potential, albeit still a matter of debate. In the present review, the most compelling evidence from the literature is presented and tentative hypotheses with respect to existing controversies are outlined.
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Kasatkina, Ludmila A., Sonja Rittchen, and Eva M. Sturm. "Neuroprotective and Immunomodulatory Action of the Endocannabinoid System under Neuroinflammation." International Journal of Molecular Sciences 22, no. 11 (May 21, 2021): 5431. http://dx.doi.org/10.3390/ijms22115431.
Full textAbstract:
Endocannabinoids (eCBs) are lipid-based retrograde messengers with a relatively short half-life that are produced endogenously and, upon binding to the primary cannabinoid receptors CB1/2, mediate multiple mechanisms of intercellular communication within the body. Endocannabinoid signaling is implicated in brain development, memory formation, learning, mood, anxiety, depression, feeding behavior, analgesia, and drug addiction. It is now recognized that the endocannabinoid system mediates not only neuronal communications but also governs the crosstalk between neurons, glia, and immune cells, and thus represents an important player within the neuroimmune interface. Generation of primary endocannabinoids is accompanied by the production of their congeners, the N-acylethanolamines (NAEs), which together with N-acylneurotransmitters, lipoamino acids and primary fatty acid amides comprise expanded endocannabinoid/endovanilloid signaling systems. Most of these compounds do not bind CB1/2, but signal via several other pathways involving the transient receptor potential cation channel subfamily V member 1 (TRPV1), peroxisome proliferator-activated receptor (PPAR)-α and non-cannabinoid G-protein coupled receptors (GPRs) to mediate anti-inflammatory, immunomodulatory and neuroprotective activities. In vivo generation of the cannabinoid compounds is triggered by physiological and pathological stimuli and, specifically in the brain, mediates fine regulation of synaptic strength, neuroprotection, and resolution of neuroinflammation. Here, we review the role of the endocannabinoid system in intrinsic neuroprotective mechanisms and its therapeutic potential for the treatment of neuroinflammation and associated synaptopathy.
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Sidorova, Yuliia S., Nikita A. Petrov, Oksana A. Vrzhesinskaya, Vera M. Kodentsova, Nina A. Beketova, Olga V. Kosheleva, Svetlana N. Leonenko, Sergey N. Zorin, and Petr S. Gromovyh. "Influence of multiple deficiency of vitamins, calcium, magnesium and iodine on cognitive function in growing rats." Vestnik Tomskogo gosudarstvennogo universiteta. Biologiya, no. 54 (2021): 64–82. http://dx.doi.org/10.17223/19988591/54/4.
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Due to the prevalence of multiple deficiency of vitamins and some minerals among the population, as well as the role of micronutrients in maintaining cognitive functions, the aim of the research was to study the effect of combined deficit of vitamins and/or calcium, magnesium and iodine in the diet of growing Wistar male weaning rats on the manifestation of an unconditioned reflex and ability to learn in response to an electric shock. Mice for the experiment were obtained from Stolbovaya nursery, Federal State Budgetory Scientific Institution Scientific Center of Biomedical Technologies of the Federal Medical-Biological Agency (Moscow region, Russia). After a 5-day feeding on a complete semi-synthetic diet, rats with an initial body weight of 51.4 ± 0.5 g were randomly (according to body weight and the results of the “Elevated Plus Maze” test) divided into four groups (10-12 animals in each group). Subsequently, within 23 days, the animals of the control group (I) received a complete semi-synthetic diet, the rats of Group II (- Ca, Mg, I) were fed on the same diet, but with a 50% reduction in the amount of calcium, magnesium and iodine in the mineral mixture, the rats of Group III (- Vit) received a diet containing 100% of minerals with a reduced amount of vitamin mixture up to 20% with the complete elimination of vitamin E from it. The animals of Group IV (- Vit, Ca, Mg, I) were kept on a diet simultaneously deficient in vitamins and mineral substances. The manifestation of the unconditioned reflex was studied in the “Elevated plus maze” test before feeding the animals on experimental diets and on the 21st day of feeding. The behavior and memory of animals were evaluated in the test “Conditioned reflex of passive avoidance” on the 7th day of feeding on experimental diets in response to electrocutaneous irritation of paws (current 0.4 mA, not more than 8 sec.) when entering the dark compartment (development of a conditioned reflex), on the 8th day - a test of training (a memorable trace), and on the 21st day - an assessment of longterm memory. Pre-anesthetized with ether, the rats were taken out of the experiment by decapitation, and the content of vitamin E (α-tocopherol) was determined by HPLC, vitamins B1 and B2 were measured fluorimetrically in the whole lyophilized brain. In this research, we revealed, that throughout the experiment, the general condition of all animals (appearance and fur) and the body weight did not differ. Reducing the content of vitamins in the diet led to a significant decrease (p < 0.001) in the brain content of selectively measured vitamins B1 and E at the end of the experiment (See Table 1), that indicated the development of micronutrient deficiency in them. Micronutrient deficiencies for 21 days did not affect the degree of anxiety of the growing rats, assessed in the “Elevated Plus Maze” test. However, the rats from the groups deficient in vitamins (group - Vit and group - Vit, Ca, Mg and I) had a higher motor activity than the animals of the control group and the animals fed on a diet deficient in calcium, magnesium and iodine (group - Ca, Mg and I), which significantly less moved through the maze (See Table 2). In this research, we found out that on the 7th day of the development of micronutrient deficiency in rats the reproduction of the unconditioned reflex (photophobia) worsened (See Fig. 1). In the rats with vitamin deficiency (group - Vit), the time spent in the open compartments increased 3.0 times compared to the control, whereas in the rats with mineral deficiency (group - Ca, Mg and I) and combined deficiency (group - Vit, Ca, Mg and I) it increased 1.85 and 1.95 times, correspondingly (p < 0.05), while no differences were detected when playing a conditioned reflex 24 hours after training (See Fig. 1). In this research, a significant (p < 0.05) decrease in long-term memory have been discovered in the animals fed on a vitamin-deficient diet (group - Vit) and in the rats fed on a diet with simultaneously reduced levels of vitamins, calcium, magnesium and iodine (group - Vit, Ca, Mg and I). On the basis of the latent time of entry into the dark compartment after 24 hours and 2 weeks, we established that the memory deterioration was due to a decrease in the vitamin content in the diet, whereas the deficit of mineral substances did not affect these parameters (See Fig. 2). In this research, we revealed that multivitamin deficiency in rats exerted an amnestic effect and made a major contribution to impaired learning and long-term memory. This findings suggest the importance of adequate provision of the organism with all vitamins and mineral substances to maintain cognitive functions and memory.
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Fernández-Gayol, Olaya, Paula Sanchis, Kevin Aguilar, Alicia Navarro-Sempere, Gemma Comes, Amalia Molinero, Mercedes Giralt, and Juan Hidalgo. "Different Responses to a High-Fat Diet in IL-6 Conditional Knockout Mice Driven by Constitutive GFAP-Cre and Synapsin 1-Cre Expression." Neuroendocrinology 109, no. 2 (2019): 113–30. http://dx.doi.org/10.1159/000496845.
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Background/Aims: Interleukin-6 (IL-6) is a major cytokine controlling body weight and metabolism, at least in part through actions in the central nervous system (CNS) from local sources. Methods: We herewith report results obtained in conditional IL-6 KO mice for brain cells (Il6ΔGfap and Il6ΔSyn). Results: The reporter RiboTag mouse line demonstrated specific astrocytic expression of GFAP-dependent Cre in the hypothalamus but not in other brain areas, whereas that of synapsin 1-dependent Cre was specific for neurons. Feeding a high-fat diet (HFD) or a control diet showed that Il6ΔGfap and Il6ΔSyn mice were more prone and resistant, respectively, to HFD-induced obesity. Energy intake was not altered in HFD experiments, but it was reduced in Il6ΔSyn male mice following a 24-h fast. HFD increased circulating insulin, leptin, and cholesterol levels, decreased triglycerides, and caused impaired responses to the insulin and glucose tolerance tests. In Il6ΔGfap mice, the only significant difference observed was an increase in insulin levels of females, whereas in Il6ΔSyn mice the effects of HFD were decreased. Hypothalamic Agrp expression was significantly decreased by HFD, further decreased in Il6ΔGfap, and increased in Il6ΔSyn female mice. Hypothalamic Il-6 mRNA levels were not decreased in Il6ΔSyn mice and even increased in Il6ΔGfapmale mice. Microarray analysis of hypothalamic RNA showed that female Il6ΔGfap mice had increased interferon-related pathways and affected processes in behavior, modulation of chemical synaptic transmission, learning, and memory. Conclusion: The present results demonstrate that brain production of IL-6 regulates body weight in the context of caloric excess and that the cellular source is critical.
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Kouhnavardi, Shima, Alev Ecevitoglu, Vladimir Dragačević, Fabrizio Sanna, Edgar Arias-Sandoval, Predrag Kalaba, Michael Kirchhofer, et al. "A Novel and Selective Dopamine Transporter Inhibitor, (S)-MK-26, Promotes Hippocampal Synaptic Plasticity and Restores Effort-Related Motivational Dysfunctions." Biomolecules 12, no. 7 (June 24, 2022): 881. http://dx.doi.org/10.3390/biom12070881.
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Dopamine (DA), the most abundant human brain catecholaminergic neurotransmitter, modulates key behavioral and neurological processes in young and senescent brains, including motricity, sleep, attention, emotion, learning and memory, and social and reward-seeking behaviors. The DA transporter (DAT) regulates transsynaptic DA levels, influencing all these processes. Compounds targeting DAT (e.g., cocaine and amphetamines) were historically used to shape mood and cognition, but these substances typically lead to severe negative side effects (tolerance, abuse, addiction, and dependence). DA/DAT signaling dysfunctions are associated with neuropsychiatric and progressive brain disorders, including Parkinson’s and Alzheimer diseases, drug addiction and dementia, resulting in devastating personal and familial concerns and high socioeconomic costs worldwide. The development of low-side-effect, new/selective medicaments with reduced abuse-liability and which ameliorate DA/DAT-related dysfunctions is therefore crucial in the fields of medicine and healthcare. Using the rat as experimental animal model, the present work describes the synthesis and pharmacological profile of (S)-MK-26, a new modafinil analogue with markedly improved potency and selectivity for DAT over parent drug. Ex vivo electrophysiology revealed significantly augmented hippocampal long-term synaptic potentiation upon acute, intraperitoneally delivered (S)-MK-26 treatment, whereas in vivo experiments in the hole-board test showed only lesser effects on reference memory performance in aged rats. However, in effort-related FR5/chow and PROG/chow feeding choice experiments, (S)-MK-26 treatment reversed the depression-like behavior induced by the dopamine-depleting drug tetrabenazine (TBZ) and increased the selection of high-effort alternatives. Moreover, in in vivo microdialysis experiments, (S)-MK-26 significantly increased extracellular DA levels in the prefrontal cortex and in nucleus accumbens core and shell. These studies highlight (S)-MK-26 as a potent enhancer of transsynaptic DA and promoter of synaptic plasticity, with predominant beneficial effects on effort-related behaviors, thus proposing therapeutic potentials for (S)-MK-26 in the treatment of low-effort exertion and motivational dysfunctions characteristic of depression and aging-related disorders.
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Sakata, Ichiro, and Takafumi Sakai. "Ghrelin Cells in the Gastrointestinal Tract." International Journal of Peptides 2010 (March 14, 2010): 1–7. http://dx.doi.org/10.1155/2010/945056.
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Ghrelin is 28-amino-acid peptide that was discovered from the rat and human stomach in 1999. Since the discovery of ghrelin, various functions of ghrelin, including growth hormone release, feeding behavior, glucose metabolism, memory, and also antidepressant effects, have been studied. It has also been reported that ghrelin in the gastrointestinal tract has an important physiological effect on gastric acid secretion and gastrointestinal motility. Ghrelin has a unique structure that is modified by O-acylation with n-octanoic acid at third serine residues, and this modification enzyme has recently been identified and named ghrelin O-acyl transferase (GOAT). Ghrelin is considered to be a gut-brain peptide and is abundantly produced from endocrine cells in the gastrointestinal mucosa. In the gastrointestinal tract, ghrelin cells are most abundant in the stomach and are localized in gastric mucosal layers. Ghrelin cells are also widely distributed throughout the gastrointestinal tract. In addition, abundance of ghrelin cells in the gastric mucosa is evolutionally conserved from mammals to lower vertebrates, indicating that gastric ghrelin plays important roles for fundamental physiological functions. Ghrelin cells in the gastrointestinal tract are a major source of circulating plasma ghrelin, and thus understanding the physiology of these cells would reveal the biological significance of ghrelin.
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Parande, Falguni, Asim Dave, Eun-Jung Park, Christopher McAllister, and John M. Pezzuto. "Effect of Dietary Grapes on Female C57BL6/J Mice Consuming a High-Fat Diet: Behavioral and Genetic Changes." Antioxidants 11, no. 2 (February 18, 2022): 414. http://dx.doi.org/10.3390/antiox11020414.
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(1) Background: Adverse effects of a chronic high-fat diet (HFD) on murine behavior, cognition, and memory are well established. Polyphenols such as resveratrol, anthocyanins, and flavonoids, that are known for antioxidative and anti-inflammatory properties, are present in grapes. The objective of this work was to determine if the dietary intake of grapes has the potential of alleviating HFD-induced deficiencies. (2) Methods: The effect of dietary grape intake was studied using behavioral assays and high throughput genome-wide RNA transcriptome analyses with female C57BL6/J mice. (3) Results: Mice that were fed a HFD from 3-weeks of age showed anxiety-like behaviors compared with the standard diet (STD). This HFD-induced effect was attenuated by supplementing the HFD with 1% grape powder (HF1G) (open field test). Similar results were observed with the novel object recognition test; there was a significant difference in time spent exploring a novel object between the HFD and the HF1G groups. There was no significant difference between the HFD1G and the STD groups. Based on the RNA-Seq analysis, genetic expression in the brain varied as a result of diet, with 210, 360, and 221 uniquely expressed genes in the STD, HFD, and HF1G groups, respectively. Cluster analysis revealed that the HFIG group mapped more closely with the STD group than the HFD group. Focusing on some specific areas, based on genetic expression, Dopamine receptor 2 (Drd2) was increased in the HFD group and normalized in the HF1G group, relative to the STD group. In addition, as judged by cluster hierarchy, the expression of genes that are associated with the dopamine receptor 2 pathway were increased in the HFD group, whereas the pattern that was derived from mouse brain from the HF1G group showed greater similarity to the STD group. KEGG pathway analyses were consistent with these results. For example, neuroactive ligand-receptor interaction (KEGG ID: mmu04080) was altered due to HFD compared with STD, but normalized by grape supplementation or the HFD; there was no significant difference between the STD and HF1G groups. In addition, the expression of genes related to feeding behavior, such as Adora2a, Th, and Trh, were also increased in the HFD group compared with the STD group, and attenuated by grape supplementation. (4) Conclusions: Dietary grape consumption has positive effects on behavior and cognition that are impaired by a HFD. Attenuation of these effects correlates with global transcriptional changes in mouse brain.
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Wei, Juntong, He Qi, Keke Liu, Changsheng Zhao, Yan Bian, and Guorong Li. "Effects of Metformin on Life Span, Cognitive Ability, and Inflammatory Response in a Short-Lived Fish." Journals of Gerontology: Series A 75, no. 11 (May 3, 2020): 2042–50. http://dx.doi.org/10.1093/gerona/glaa109.
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Abstract Metformin, an oral antidiabetic drug, prolongs the life span in nematode, silkworm, and other transgenic rodents, but its effects on longevity and aging-related cognitive ability using natural aging vertebrate models remain poorly understood. The genus of annual fish Nothobranchius show accelerated growth and expression of aging biomarkers. Here, using the short-lived fish Nothobranchius guentheri, we investigated effects of metformin on life span and aging-related cognitive ability and inflammation. Total of 145 fish, 72 fish were fed with metformin in the concentration of 2 mg/g food and 73 fish without metformin from 16 weeks of age until the end of their lives. The chronic feeding with metformin prolonged the life span of the fish and delayed aging with retarded accumulation of lipofuscin in liver, senescence-associated beta-galactosidase (SA-β-gal) activity in skin and serum levels of cholesterol and triglyceride significantly in the 10-month-old fish. Furthermore, metformin improved motor, learning, and memory skills by behavior tests accompanying with reduction of SA-β-gal activity and neurofibrillary degeneration and inhibition of inflammatory response including downregulated NF-κB and proinflammatory cytokines IL-8, TNF-α, and IL-1β expression and enhanced anti-inflammatory cytokine IL-10 level in brain. These findings demonstrate that metformin prolongs the life span and exerts neuroprotective and anti-inflammation function to improve cognitive ability in annual fish. It might be an effective strategy by using metformin to raise the possibility of promoting healthy aging of old population in aging process.
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Rosikon, Katarzyna D., Megan C. Bone, and Hakeem O. Lawal. "Regulation and modulation of biogenic amine neurotransmission in Drosophila and Caenorhabditis elegans." Frontiers in Physiology 14 (February 16, 2023). http://dx.doi.org/10.3389/fphys.2023.970405.
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Neurotransmitters are crucial for the relay of signals between neurons and their target. Monoamine neurotransmitters dopamine (DA), serotonin (5-HT), and histamine are found in both invertebrates and mammals and are known to control key physiological aspects in health and disease. Others, such as octopamine (OA) and tyramine (TA), are abundant in invertebrates. TA is expressed in both Caenorhabditis elegans and Drosophila melanogaster and plays important roles in the regulation of essential life functions in each organism. OA and TA are thought to act as the mammalian homologs of epinephrine and norepinephrine respectively, and when triggered, they act in response to the various stressors in the fight-or-flight response. 5-HT regulates a wide range of behaviors in C. elegans including egg-laying, male mating, locomotion, and pharyngeal pumping. 5-HT acts predominantly through its receptors, of which various classes have been described in both flies and worms. The adult brain of Drosophila is composed of approximately 80 serotonergic neurons, which are involved in modulation of circadian rhythm, feeding, aggression, and long-term memory formation. DA is a major monoamine neurotransmitter that mediates a variety of critical organismal functions and is essential for synaptic transmission in invertebrates as it is in mammals, in which it is also a precursor for the synthesis of adrenaline and noradrenaline. In C. elegans and Drosophila as in mammals, DA receptors play critical roles and are generally grouped into two classes, D1-like and D2-like based on their predicted coupling to downstream G proteins. Drosophila uses histamine as a neurotransmitter in photoreceptors as well as a small number of neurons in the CNS. C. elegans does not use histamine as a neurotransmitter. Here, we review the comprehensive set of known amine neurotransmitters found in invertebrates, and discuss their biological and modulatory functions using the vast literature on both Drosophila and C. elegans. We also suggest the potential interactions between aminergic neurotransmitters systems in the modulation of neurophysiological activity and behavior.
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Chen, Zhong, Lingyu Xu, Wenkai Lin, Yanrong Zheng, and Yi Wang. "The Diverse Network of Brain Histamine in Feeding: Dissect its Functions in a Circuit-specific Way." Current Neuropharmacology 21 (November 17, 2022). http://dx.doi.org/10.2174/1570159x21666221117153755.
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Abstracts: Feeding is an intrinsic and important behavior regulated by complex molecular, cellular and circuit-level mechanisms, one of which is the brain histaminergic network. In the past decades, many studies have provided a foundation of knowledge about the relationship between feeding and histamine receptors, which are deemed to have therapeutic potential but are not successful in treating feeding- related diseases. Indeed, the histaminergic circuits underlying feeding are poorly understood and characterized. This review describes current knowledge of histamine in feeding at the receptor level. Further, we provide insight into putative histamine- involved feeding circuits based on the classic feeding circuits. Understanding the histaminergic network in a circuit-specific way may be therapeutically relevant for increasing the drug specificity and precise treatment in feeding-related diseases.
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Tackenberg, Michael C., Manuel A. Giannoni-Guzmán, Erik Sanchez-Perez, Caleb A. Doll, José L. Agosto-Rivera, Kendal Broadie, Darrell Moore, and Douglas G. McMahon. "Neonicotinoids disrupt circadian rhythms and sleep in honey bees." Scientific Reports 10, no. 1 (October 21, 2020). http://dx.doi.org/10.1038/s41598-020-72041-3.
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Abstract Honey bees are critical pollinators in ecosystems and agriculture, but their numbers have significantly declined. Declines in pollinator populations are thought to be due to multiple factors including habitat loss, climate change, increased vulnerability to disease and parasites, and pesticide use. Neonicotinoid pesticides are agonists of insect nicotinic cholinergic receptors, and sub-lethal exposures are linked to reduced honey bee hive survival. Honey bees are highly dependent on circadian clocks to regulate critical behaviors, such as foraging orientation and navigation, time-memory for food sources, sleep, and learning/memory processes. Because circadian clock neurons in insects receive light input through cholinergic signaling we tested for effects of neonicotinoids on honey bee circadian rhythms and sleep. Neonicotinoid ingestion by feeding over several days results in neonicotinoid accumulation in the bee brain, disrupts circadian rhythmicity in many individual bees, shifts the timing of behavioral circadian rhythms in bees that remain rhythmic, and impairs sleep. Neonicotinoids and light input act synergistically to disrupt bee circadian behavior, and neonicotinoids directly stimulate wake-promoting clock neurons in the fruit fly brain. Neonicotinoids disrupt honey bee circadian rhythms and sleep, likely by aberrant stimulation of clock neurons, to potentially impair honey bee navigation, time-memory, and social communication.
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Stamatakis, Alice M., Shanna L. Resendez, Kai-Siang Chen, Morgana Favero, Jing Liang-Guallpa, Jonathan J. Nassi, Shay Q. Neufeld, Koen Visscher, and Kunal K. Ghosh. "Miniature microscopes for manipulating and recording in vivo brain activity." Microscopy, August 2, 2021. http://dx.doi.org/10.1093/jmicro/dfab028.
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Abstract Here we describe the development and application of miniature integrated microscopes (miniscopes) paired with microendoscopes that allow for the visualization and manipulation of neural circuits in superficial and subcortical brain regions in freely behaving animals. Over the past decade the miniscope platform has expanded to include simultaneous optogenetic capabilities, electrically-tunable lenses that enable multi-plane imaging, color-corrected optics, and an integrated data acquisition platform that streamlines multimodal experiments. Miniscopes have given researchers an unprecedented ability to monitor hundreds to thousands of genetically-defined neurons from weeks to months in both healthy and diseased animal brains. Sophisticated algorithms that take advantage of constrained matrix factorization allow for background estimation and reliable cell identification, greatly improving the reliability and scalability of source extraction for large imaging datasets. Data generated from miniscopes have empowered researchers to investigate the neural circuit underpinnings of a wide array of behaviors that cannot be studied under head-fixed conditions, such as sleep, reward seeking, learning and memory, social behaviors, and feeding. Importantly, the miniscope has broadened our understanding of how neural circuits can go awry in animal models of progressive neurological disorders, such as Parkinson’s disease. Continued miniscope development, including the ability to record from multiple populations of cells simultaneously, along with continued multimodal integration of techniques such as electrophysiology, will allow for deeper understanding into the neural circuits that underlie complex and naturalistic behavior.
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"Mild cognitive impairment: animal models." Dialogues in Clinical Neuroscience 6, no. 4 (December 2004): 369–77. http://dx.doi.org/10.31887/dcns.2004.6.4/gpepeu.
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Mild cognitive impairment (MCI) is an aspect of cognitive aging that is considered to be a transitional state between normal aging and the dementia into which it may convert. Appropriate animal models are necessary in order to understand the pathogenic mechanisms of MCI and develop drugs for its treatment. In this review, we identify the features that should characterize an animal model of MCI, namely old age, subtle memory impairment, mild neuropathological changes, and changes in the cholinergic system, and the age at which these features can be detected in laboratory animals. These features should occur in aging animals with normal motor activity and feeding behavior. The animal models may be middle-aged rats and mice, rats with brain ischemia, transgenic mice overexpressing amyloid precursor protein and presenilin 1 (tested at an early stage), or aging monkeys. Memory deficits can be detected by selecting appropriately difficult behavioral tasks, and the deficits can be associated with neuropathological alterations. The reviewed literature demonstrates that, under certain conditions, these animal species can be considered to be MCI models, and that cognitive impairment in these models responds to drug treatment.
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Kacířová, Miroslava, Blanka Železná, Michaela Blažková, Martina Holubová, Andrea Popelová, Jaroslav Kuneš, Blanka Šedivá, and Lenka Maletínská. "Aging and high-fat diet feeding lead to peripheral insulin resistance and sex-dependent changes in brain of mouse model of tau pathology THY-Tau22." Journal of Neuroinflammation 18, no. 1 (June 22, 2021). http://dx.doi.org/10.1186/s12974-021-02190-3.
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Abstract Background Obesity leads to low-grade inflammation in the adipose tissue and liver and neuroinflammation in the brain. Obesity-induced insulin resistance (IR) and neuroinflammation seem to intensify neurodegeneration including Alzheimer’s disease. In this study, the impact of high-fat (HF) diet-induced obesity on potential neuroinflammation and peripheral IR was tested separately in males and females of THY-Tau22 mice, a model of tau pathology expressing mutated human tau protein. Methods Three-, 7-, and 11-month-old THY-Tau22 and wild-type males and females were tested for mobility, anxiety-like behavior, and short-term spatial memory in open-field and Y-maze tests. Plasma insulin, free fatty acid, cholesterol, and leptin were evaluated with commercial assays. Liver was stained with hematoxylin and eosin for histology. Brain sections were 3′,3′-diaminobenzidine (DAB) and/or fluorescently detected for ionized calcium-binding adapter molecule 1 (Iba1), glial fibrillary acidic protein (GFAP), and tau phosphorylated at T231 (pTau (T231)), and analyzed. Insulin signaling cascade, pTau, extracellular signal-regulated kinase 1/2 (ERK1/2), and protein phosphatase 2A (PP2A) were quantified by western blotting of hippocampi of 11-month-old mice. Data are mean ± SEM and were subjected to Mann-Whitney t test within age and sex and mixed-effects analysis and Bonferroni’s post hoc test for age comparison. Results Increased age most potently decreased mobility and increased anxiety in all mice. THY-Tau22 males showed impaired short-term spatial memory. HF diet increased body, fat, and liver weights and peripheral IR. HF diet-fed THY-Tau22 males showed massive Iba1+ microgliosis and GFAP+ astrocytosis in the hippocampus and amygdala. Activated astrocytes colocalized with pTau (T231) in THY-Tau22, although no significant difference in hippocampal tau phosphorylation was observed between 11-month-old HF and standard diet-fed THY-Tau22 mice. Eleven-month-old THY-Tau22 females, but not males, on both diets showed decreased synaptic and postsynaptic plasticity. Conclusions Significant sex differences in neurodegenerative signs were found in THY-Tau22. Impaired short-term spatial memory was observed in 11-month-old THY-tau22 males but not females, which corresponded to increased neuroinflammation colocalized with pTau(T231) in the hippocampi and amygdalae of THY-Tau22 males. A robust decrease in synaptic and postsynaptic plasticity was observed in 11-month-old females but not males. HF diet caused peripheral but not central IR in mice of both sexes.
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Gómez-Moracho, Tamara, Tristan Durand, and Mathieu Lihoreau. "The gut parasite Nosema ceranae impairs olfactory learning in bumblebees." Journal of Experimental Biology, June 21, 2022. http://dx.doi.org/10.1242/jeb.244340.
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Pollinators are exposed to numerous parasites and pathogens when foraging on flowers. These biological stressors may affect critical cognitive abilities required for foraging. Here, we tested whether exposure to Nosema ceranae, one of the most widespread parasites of honey bees also found in wild pollinators, impacts cognition in bumblebees. We investigated different forms of olfactory learning and memory using conditioning of the proboscis extension reflex. Seven days after feeding parasite spores, bumblebees showed lower performances in absolute, differential, and reversal learning than controls. The consistent observations across different types of olfactory learning indicates a general negative effect of N. ceranae exposure that did not specifically target particular brain areas or neural processes. We discuss the potential mechanisms by which N. ceranae impairs bumblebee cognition and the broader consequences for populations of pollinators.
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Bo, Tingbei, Jing Wen, Wenting Gao, Liqiu Tang, Min Liu, and Dehua Wang. "Influence of HFD-induced precocious puberty on neurodevelopment in mice." Nutrition & Metabolism 18, no. 1 (September 16, 2021). http://dx.doi.org/10.1186/s12986-021-00604-w.
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Abstract Background Precocious puberty is frequently associated with obesity, which will lead to long-term effects, especially on growth and reproduction. However, the effect of precocious puberty on children's neurodevelopment is still unknown. Objectives Here we evaluated the effect of High fat diet (HFD)-induced precocious puberty on neurodevelopment and behaviors of animals. Methods Ovaries sections were stained with hematoxylin–eosin (H&E) using standard techniques. Behavioral tests included elevated plus maze (EPM), open field exploration, Y-Maze, marble burying test, and novelty- suppressed feeding. The expression of genes related to puberty and neural development was detected by immunohistochemistry and Western blot. Results Our results showed HFD-induced precocious puberty increased the risk-taking behavior and decreased memory of mice. The content of Tyrosine hydroxylase (TH) and Arginine vasopressin (AVP) in hypothalamus were higher in HFD group than control group. Although the recovery of normal diet will gradually restore the body fat and other physiological index of mice, the anxiety increases in adult mice, and the memory is also damaged. Conclusions These findings describe the sensitivity of mice brain to HFD-induced precocious puberty and the irrecoverability of neural damage caused by precocious puberty. Therefore, avoiding HFD in childhood is important to prevent precocious puberty and neurodevelopmental impairment in mice. Graphic abstract
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Guo, Yingxue, Yan Qu, Wenpeng Li, Hongkuan Shen, Jiwen Cui, Jiguang Liu, Jinlian Li, and Dongmei Wu. "Protective effect of Monarda didymaL. essential oil and its main component thymol on learning and memory impairment in aging mice." Frontiers in Pharmacology 13 (August 29, 2022). http://dx.doi.org/10.3389/fphar.2022.992269.
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The aging process of human beings is accompanied by the decline of learning and memory ability and progressive decline of brain function, which induces Alzheimer’s Disease (AD) in serious cases and seriously affects the quality of patient’s life. In recent years, more and more studies have found that natural plant antioxidants can help to improve the learning and memory impairment, reduce oxidative stress injury and aging lesions in tissues. This study aimed to investigate the effect of Monarda didymaL. essential oil and its main component thymol on learning and memory impairment in D-galactose-induced aging mice and its molecular mechanism. The composition of Monarda didymaL. essential oil was analyzed by Gas Chromatography-Mass Spectrometer (GC-MS). A mouse aging model was established by the subcutaneous injection of D-galactose in mice. The behavior changes of the mice were observed by feeding the model mice with essential oil, thymol and donepezil, and the histopathological changes of the hippocampus were observed by HE staining. And the changes of acetylcholinesterase (AchE), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities, and the content of malondialdehyde (MDA) in hippocampal tissues were detected by corresponding kits. The expression of mitogen activated protein kinase (MAPK) and nuclear factor E2 related factor 2 (Nrf2) pathways related proteins were detected by western blot. Animal experimental results showed that compared with model group, the above indexes in Monarda didymaL. essential oil and thymol groups improved significantly in a dose-dependent manner. Monarda didymaL. essential oil and its main active component thymol can improve the learning and memory impairment of aging mice to some extent, and Nrf2 and MAPK pathways may be involved in its action process.
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Li, Xue, Shuling Zhang, and Lu Wang. "PO-216 The Effects of Aerobic Exercise on Spatial Learning and Memory and Expression of PDE-4 in Hippocampus of the Aging Rats." Exercise Biochemistry Review 1, no. 5 (October 3, 2018). http://dx.doi.org/10.14428/ebr.v1i5.9463.
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Objective To discuss the effect of aerobic exercise intervention before aging rats and on aging rats, the spatial learning and memory abilities and the expression of PDE-4 in hippocampus.
Methods 64 male SD rats were divided into 4 groups at random (n=16): control group(group C), D-galactose aging model group (group A), Pre-aging aerobic exercise intervention group (group S1), Aerobic exercise intervention on aging group (group S2). After 6 weeks, each group was randomly divided into Morris water maze behavior training group (M group) and natural feeding group (N group), record as CM, AM, S1M, S2M, CN, AN, S1N, S2N. At the end of 7th week, all rats were killed and the cerebral cortex SOD, GSH-PX and MDA content were tested; The expression of PDE-4 gene in hippocampus was detected by Real-time PCR and Western blotting.
Results 1) The general state: When compared to the rats in C group, which in A group show obvious symptoms of aging, such as lethargy, loss of appetite, slow, yellow curly hair color, even off signs and so on; but S2 group were similar to C group; S1 group were a little worse than S2 group. 2) HE staining: When compared to the rats in C group, the hippocampus neurons in A group were disordered, the cells staining were deepened, the cytoplasm were edema, most of the interstitial cells were loose, and other morphological structure in aging state;S2 group were similar to C group; S1 group were a little worse than S2 group.3) The free radical detection: Almost no difference in each corresponding M group and N group. The activities of the cerebral cortex SOD and GSH-PX in were consistent: C group and S2group were significantly or very significantly higher than others (P<0.05/0.01); The cerebral cortex MDA content: C group was the lowest, S2 group followed, and all significantly lower than those in A group and S1 group (P<0.05). 4)The Morris water maze test: the Positioning navigation experiment results showed that the spatial memory was preliminarily formed on the day 2, CM group, S1M group and S2M group formed stable spatial learning and memory on day 3,but that of AM group formed on day 4; The space exploration test results showed that the maximum number of times of through the site was CM group, the percentage of the original site quadrant of CM group was the highest, and there was a very significant difference with the other groups (P<0.01); S2 group followed, but AM group and S1M were relatively low. 5)The results of Real-time PCR and Western blotting: When compared to the rats in C group, which in A group and S1group were very significantly higher(P<0.01),but which in S2 group was very significantly lower (P<0.01); When compared to the rats in A group, which in S2 group was very significantly lower (P<0.01),but S1group were significantly higher(P<0.01/0.05); When compared to the rats in S1 group, which in S2 group was very significantly lower (P<0.01).
Conclusions 1)Aerobic exercise can improve the antioxidant capacity of the brain, protect and repair the hippocampal neurons, change the morphological structure of hippocampal neurons, improve and maintain the brain's spatial learning and memory, and thus delay brain aging. 2)Aerobic exercise intervention can down-regulate the expression of PDE-4 gene, may directly activate the cAMP/PKA/CREB signal transduction pathway to promote the synthesis of some learning memory proteins, thereby improving the learning and memory ability of aging rats and delay brain aging. 3)The different periods of aerobic exercise on brain aging intervention were different. Aerobic exercise intervention in the aging process performed relatively well. Tip: sustained aerobic exercise need to better play its role.
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Best, Janet, William Duncan, Farrah Sadre-Marandi, Parastoo Hashemi, H. Frederik Nijhout, and Michael Reed. "Autoreceptor control of serotonin dynamics." BMC Neuroscience 21, no. 1 (September 23, 2020). http://dx.doi.org/10.1186/s12868-020-00587-z.
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Abstract Background Serotonin is a neurotransmitter that has been linked to a wide variety of behaviors including feeding and body-weight regulation, social hierarchies, aggression and suicidality, obsessive compulsive disorder, alcoholism, anxiety, and affective disorders. Full understanding involves genomics, neurochemistry, electrophysiology, and behavior. The scientific issues are daunting but important for human health because of the use of selective serotonin reuptake inhibitors and other pharmacological agents to treat disorders. This paper presents a new deterministic model of serotonin metabolism and a new systems population model that takes into account the large variation in enzyme and transporter expression levels, tryptophan input, and autoreceptor function. Results We discuss the steady state of the model and the steady state distribution of extracellular serotonin under different hypotheses on the autoreceptors and we show the effect of tryptophan input on the steady state and the effect of meals. We use the deterministic model to interpret experimental data on the responses in the hippocampus of male and female mice, and to illustrate the short-time dynamics of the autoreceptors. We show there are likely two reuptake mechanisms for serotonin and that the autoreceptors have long-lasting influence and compare our results to measurements of serotonin dynamics in the substantia nigra pars reticulata. We also show how histamine affects serotonin dynamics. We examine experimental data that show very variable response curves in populations of mice and ask how much variation in parameters in the model is necessary to produce the observed variation in the data. Finally, we show how the systems population model can potentially be used to investigate specific biological and clinical questions. Conclusions We have shown that our new models can be used to investigate the effects of tryptophan input and meals and the behavior of experimental response curves in different brain nuclei. The systems population model incorporates individual variation and can be used to investigate clinical questions and the variation in drug efficacy. The codes for both the deterministic model and the systems population model are available from the authors and can be used by other researchers to investigate the serotonergic system.