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Alzheimer’s disease (AD) is a progressive neurodegenerative condition that causes cognitive impairment and other neuropsychiatric symptoms. Previously, little research has thus far investigated whether methamphetamine (MAMPH) can enhance cognitive function or ameliorate AD symptoms. This study examined whether a low dose of MAMPH can induce conditioned taste aversion (CTA) learning, or can increase plasma corticosterone levels, neural activity, and neural plasticity in the medial prefrontal cortex (mPFC) (responsible for cognitive function), the nucleus accumbens (NAc) and the amygdala (related to rewarding and aversive emotion), and the hippocampus (responsible for spatial learning). Furthermore, the excitations or lesions of the prelimbic cortex (PrL) can affect MAMPH-induced CTA learning, plasma corticosterone levels, and neural activity or plasticity in the mPFC [i.e., PrL, infralimbic cortex (IL), cingulate cortex 1 (Cg1)], the NAc, the amygdala [i.e., basolateral amygdala (BLA) and central amygdala (CeA)], and the hippocampus [i.e., CA1, CA2, CA3, and dentate gyrus (DG)]. In the experimental procedure, the rats were administered either saline or NMDA solutions, which were injected into the PrL to excite or destroy PrL neurons. Additionally, rats received 0.1% saccharin solution for 15 min, followed by intraperitoneal injections of either normal saline or 1 mg/kg MAMPH to induce CTA. A one-way ANOVA was performed to analyze the effects of saccharin intake on CTA, plasma corticosterone levels, and the expression of c-Fos and p-ERK. The results showed that the MAMPH induced CTA learning and increased plasma corticosterone levels. The mPFC, and particularly the PrL and IL and the DG of the hippocampus, appeared to show increased neural activity in c-Fos expression or neural plasticity in p-ERK expression. The excitation of the PrL neurons upregulated neural activity in c-Fos expression and neural plasticity in p-ERK expression in the PrL and IL. In summary, MAMPH may be able to improve cognitive and executive function in the brain and reduce AD symptoms. Moreover, the excitatory modulation of the PrL with MAMPH administration can facilitate MAMPH-induced neural activity and plasticity in the PrL and IL of the mPFC. The present data provide clinical implications for developing a possible treatment for AD in an animal model.

Memory extinction has been reported to be related to psychiatric disorders, such as post-traumatic stress disorder (PTSD). Secretion and synthesis of brain-derived neurotrophic factor (BDNF) have been shown to temporally regulate various memory processes via activation of tropomyosin-related kinase B (TrkB) receptors. However, whether memory extinction induces the synthesis and secretion of BDNF on the basis of its localization is not understood. In this study, we aim to investigate activity-dependent BDNF secretion and synthesis in the insular cortex (IC) in the setting of conditioned taste aversion (CTA) memory extinction. Rats were subjected to CTA memory extinction and BDNF antibody (or the equal volume of vehicle) was microinjected into the IC immediately after the extinction testing. Real-time polymerase chain reaction and in situ hybridization were used to detect the gene expression of BDNF, NGF and NT4. The protein levels of BDNF were determined through the enzyme-linked immunosorbent assay. In addition, the levels of phosphorylated TrkB normalized to total TrkB were evaluated using immunoprecipitation and immunoblotting. c-Fos, total extracellular signal-regulated kinase (Erk), phosphorylated Erk, and apoptosis-related protein (caspase-3), were detected by Western blotting. We found that blocking BDNF signaling within the IC disrupts CTA extinction, suggesting that BDNF signaling in the IC is necessary for CTA extinction. Increased expression levels of c-Fos indicate the induced neuronal activity in the IC during CTA extinction. In addition, temporal changes in the gene expression and protein levels of BDNF in the IC were noted during extinction. Moreover, we found that phosphorylation of TrkB increased prior to the enhanced BDNF expression, suggesting that CTA extinction induces rapid activity-dependent BDNF secretion in the IC. Finally, we found decreased expression of caspase-3 in the IC after CTA extinction. These results demonstrate that CTA memory extinction temporally induces the release and synthesis of BDNF in the IC and inhibits neuronal apoptosis.

Conditioned taste aversion (CTA) can be applied to study associative learning and its relevant underpinning molecular mechanisms in discrete brain regions. The present study examined, by immunohistochemistry and immunocytochemistry, the effects of acquisition and expression of lithium-induced CTA on activated Extracellular signal Regulated Kinase (p-ERK) in the prefrontal cortex (PFCx) and nucleus accumbens (Acb) of male Sprague-Dawley rats. The study also examined, by immunoblotting, whether acquisition and expression of lithium-induced CTA resulted in modified levels of phosphorylation of glutamate receptor subunits (NR1 and GluR1) and Thr(34)- and Thr(75-Dopamine-and-cAMP-Regulated) PhosphoProtein (DARPP-32). CTA acquisition was associated with an increase of p-ERK-positive neurons and phosphorylated NR1 receptor subunit (p-NR1) in the PFCx, whereas p-GluR1, p-Thr(34)- and p-Thr(75)-DARPP-32 levels were not changed in this brain region. CTA expression increased the number of p-ERK-positive neurons in the shell (AcbSh) and core (AcbC) but left unmodified p-NR1, p-GluR1, p-Thr(34)- and p-Thr(75-DARPP-32) levels. Furthermore, post-embedding immunogold quantitative analysis in AcbSh revealed that CTA expression significantly increased nuclear p-ERK immunostaining as well as p-ERK-labeled axo-spinous contacts. Overall, these results indicate that ERK and NR1, but not GluR1 and DARPP-32, are differentially phosphorylated as a consequence of acquisition and expression of aversive associative learning. Moreover, these results confirm that CTA represents an useful approach to study the molecular basis of associative learning in rats and suggest the involvement of ERK cascade in learning-associated synaptic plasticity.

The aversive action of the pharmacological properties of ethanol was studied in selectively bred Warsaw Alcohol High-Preferring (WHP) and Warsaw Alcohol Low-Preferring (WLP) rats. For this study, a conditioned-taste aversion test was used. Male WHP and WLP rats were submitted to daily 20-min sessions for 5 days, in which a saccharin solution (1.0 g/L) was available (pre-conditioning phase). Next, this drinking was paired with the injection of ethanol (0, 0.5, 1.0 g/kg), intraperitoneally [i.p.] immediately after removal of the saccharin bottle (conditioning phase). Afterward, the choice between the saccharin solution and water was extended for 18 subsequent days for 20-min daily sessions (post-conditioning phase). Both doses of ethanol did not produce an aversion to saccharin in WLP and WHP rats in the conditioning phase. However, injection of the 1.0 g/kg dose of ethanol produced an aversion in WLP rats that was detected by a decrease in saccharin intake at days 1, 3, 7, and 10 of the post-conditioning phase, with a decrease in saccharin preference for 16 days of the post-conditioning phase. Conditioned taste aversion, measured as a decrease in saccharin intake and saccharin preference, was only visible in WHP rats at day 1 and day 3 of the post-conditioning phase. This difference between WLP and WHP rats was apparent despite similar blood ethanol levels in both rat lines following injection of 0.5 and 1.0 g/kg of ethanol. These results may suggest differing levels of aversion to the post-ingestional effects of ethanol between WLP and WHP rats. These differing levels of aversion may contribute to the selected line difference in ethanol preference in WHP and WLP rats. •We measured conditioned taste aversion by saccharin intake and by preference.•We observe similar blood ethanol levels in WHP and WLP rats.•Conditioned taste aversion was visible only in WLP rats.

This chapter contains sections titled: Introduction Conservation measures and human‐wildlife conflicts Types of human‐wildlife conflict Regulation and management of human‐wildlife conflict Use of carbofuran in India Use of carbofuran in relation to other compounds Diagnosing carbofuran poisoning in India Forensic facilities and analyses in India Case studies: use of carbofuran for poisoning in relation to other compounds Potential short and long‐term solutions Mitigation of human‐wildlife conflicts Conclusion Acknowledgements References

Preclinical animal research has contributed greatly to our understanding of numerous human disease states and will continue to provide a method for investigating the various biochemical events, physiological processes, and behavioral implications of various diseases. For substance abuse and dependence, this research has enabled scientists to gain a greater understanding of the neurochemical events involved in the brain's response to drugs, both licit and illicit, and to provide a means by which to design and test novel pharmaco-therapeutic interventions. To enable these discoveries, scientists have developed numerous animal models that attempt to replicate human drug addiction. The current review explores two popular Pavlovian conditioning procedures, conditioned place preference and conditioned taste aversion, which are used to investigate the rewarding and aversive effects (respectively) of drugs of abuse. For each procedure, a brief history of the field is followed by the advantages of the procedures and a step-by-step explanation of each procedure's conditioning protocol.

Conditioned taste aversions (CTAs) are those that develop on the basis of experience with a food or drink. The experience on which such aversions are based is often the consumption of a food or drink prior to a bout of illness. In the laboratory, CTA is most commonly induced by administering a chemical agent (usually the agent lithium chloride (LiCl)) that produces some type of illness (unconditioned stimulus (US)), after consumption of a food or drink (usually a highly palatable solution such as sucrose or saccharin flavored water) that has a novel taste (conditioned stimulus (CS)). Estradiol is a member of a group of steroid hormones called estrogens. Substantial evidence unequivocally establishes estradiol as a hypophagic hormone. A number of theories, ranging from psychosocial to physiological, have been proposed to account for anorexia nervosa, but most theories remain unsubstantiated or inadequate.

Black bears (Ursus americanus) at Camp Ripley Military Reservation in central Minnesota regularly sought out, obtained, and consumed pre-packaged military foods, known as meals-ready-to-eat (MREs), making the bears a nuisance to personnel and a hindrance to military operations. Two adult females and 3 yearling (1-year-old) offspring of 1 of these females were responsible for most nuisance activity in the reserve. These bears were habituated to humans, enabling us to closely observe them and conduct taste-aversion experiments designed to reduce their attraction to MREs. Each of the 5 bears was given MREs containing thiabendazole (72-165 mg/kg bear). The bears eagerly consumed treatment baits, resulting in illness <90 minutes later. During the next 122 days, we conducted trials to test the response of these bears to MREs. They ignored 6 (15%), approached but did not taste 12 (29%), tasted but did not consume 14 (34%), partially consumed 9 (22%), and did not totally consume any of the 41 MREs that we offered. The bears rejected MREs even if they were not the same type of meal that was used in the treatment, but they continued to consume non-MRE foods (7/9=78%). Post-treatment avoidance of MREs also was unrelated to our method of presentation of the meal and presence or absence of thiabendazole in the food. We concluded that avoidance of MREs was from conditioned taste aversion. This aversion persisted in 2 bears that were retested >1 year later, but not in a bear tested 2 years later. Taste-aversion conditioning toward a specific food or class of food that attracts bears may be an effective component of a management strategy to diminish nuisance activity, if availability of alternate human-related foods also is reduced.