The 5-HT syndrome in rats is composed of head weaving, body shaking, forepaw treading, flat body posture, hindlimb abduction, and Straub tail. The importance of the brainstem and spinal cord for the syndrome is underlined by findings of 5,7-dihydroxytryptamine (5,7-DHT)-induced denervation supersensitivity in response to 5-HT-stimulant drugs. For head weaving and Straub tail, supersensitivity occurred when the neurotoxin was injected into the cisterna magna or spinal cord, for forepaw treading in cisterna magna, and for hindlimb abduction in the spinal cord. Although 5,7- DHT-related body shaking increased in the spinal cord, the sign decreased when injected into the striatum, indicating the modulatory influence of the basal ganglia. Further details on body shaking are provided by its reduced response to harmaline after 5-HT depletion caused by intraventricular 5,7-DHT, electrolytic lesions of the medial or dorsal raphe, and lesions of the inferior olive caused by systemic injection of 3-acetylpyridine along with those found in Agtpbp1pcd or nr cerebellar mouse mutants. Yet the influence of the climbing fiber pathway on other signs of the 5-HT syndrome remains to be determined.

The distribution of the D2-like dopamine receptor (D2DR) in the cortex and striatum was compared between rats with absence, audiogenic, or combined genetically determined epilepsy and normal Wistar rats by autoradiography. A significantly lower D2DR binding density was observed in the dorsal and ventrolateral aspects of the nucleus accumbens in epileptic vs. non-epileptic rats. Rats with audiogenic epilepsy additionally showed a higher D2DR density in the dorsal striatum and motor and somatosensory cortex and a lower D2DR density in the ventrolateral part of the nucleus accumbens. The findings indicated that a common neuronal circuit is involved in the pathogenesis of both convulsive and nonconvulsive forms of generalized epilepsy.

Idiopathic pulmonary fibrosis (IPF) is the most widely studied interstitial lung disease. IPF eventually leads to respiratory insufficiency, lung cancer, and death. Carvedilol (CAR) is a third-generation β-adrenergic receptor antagonist with an α1-blocking effect. CAR demonstrates antifibrotic activities in various experimental models of organ fibrosis.
OBJECTIVE: This work is designed to explore the possible alleviating effects of CAR on bleomycin (BLM)-induced lung fibrosis in rats.
METHODS: The BLM rat model of lung fibrosis was achieved by intratracheal delivery of a single dose of 5 mg/kg of BLM. Seven days following BLM injection, either prednisolone or CAR was orally administered at doses of 10 mg/kg once daily for 21 days to the rats. The actions of CAR were evaluated by lung oxidant/antioxidant parameters, protein concentration and total leucocyte count (TLC) in bronchoalveolar lavage fluid (BALF), fibrosis regulator-related genes along with the coexistent lung histological changes.
RESULTS: CAR effectively decreased lung malondialdehyde level, increased superoxide dismutase activity, declined both protein concentration and TLC in BALF, downregulated TGF-β1/α-SMA/Smad2/3 and STAT3 gene expressions, and repaired the damaged lung tissues.
CONCLUSIONS: CAR conferred therapeutic potential against BLM-induced lung fibrosis in rats, at least in part, to its antioxidant, anti-inflammatory, and antifibrotic activities. CAR could be utilized as a prospective therapeutic option in patients with lung fibrosis in clinical practice.

We generated a genetically heterogenous rat model by a 4-way cross strategy using 4 inbred strains (Brown Norway [BN], Fischer 344 [F344], Lewis [LEW], and Wistar Kyoto [KY]) to provide investigators with a highly genetically diverse rat model from commercially available inbred rats. We made reciprocal crosses between males and females from the 2 F1 hybrids to generate genetically heterogeneous rats with mitochondrial genomes from either the BN (OKC-HETB, a.k.a \"B\" genotype) or WKY (OKC-HETW a.k.a \"W\" genotype) parental strains. These two mitochondrial genomes differ at 94 nucleotides, more akin to human mitochondrial genome diversity than that available in classical laboratory mouse strains. Body weights of the B and W genotypes were similar. However, mitochondrial genotype antagonistically affected grip strength and treadmill endurance in females only. In addition, mitochondrial genotype significantly affected multiple responses to a high-fat diet (HFD) and treatment with 17α-estradiol. Contrary to findings in mice in which males only are affected by 17α-estradiol supplementation, female rats fed a HFD beneficially responded to 17α-estradiol treatment as evidenced by declines in body mass, adiposity, and liver mass. Male rats, by contrast, differed in a mitochondrial genotype-specific manner, with only B males responding to 17α-estradiol treatment. Mitochondrial genotype and sex differences were also observed in features of brain-specific antioxidant response to a HFD and 17α-estradiol as shown by hippocampal levels of Sod2 acetylation, JNK, and FoxO3a. These results emphasize the importance of mitochondrial genotype in assessing responses to putative interventions in aging processes.

The aim of this study is to find out whether maternal methyl-enriched diet affects the content of monoamines and their metabolites in brain structures of adult WAG/Rij offspring. It has been shown for the first time that maternal methyl-enriched diet (choline, betaine, folic acid, vitamin B12, L-methionine, zink) during the perinatal period increases dopaminergic tone of the mesolimbic brain system in adult offspring of WAG/Rij rats, which is accompanied by the suppression of the symptoms of genetic absence epilepsy and comorbid depression. Results suggest that maternal methyl-enriched diet during the perinatal period may be served as a new therapeutic strategy to prevent the development of a hypofunction of the mesolimbic dopaminergic brain system and associated genetic absence epilepsy and comorbid depression in offspring.

Prepulse inhibition (PPI) allows assessing schizophrenia-like sensorimotor gating deficits in rodents. Previous studies indicate that PPI is modulated by the medial prefrontal cortex (mPFC), which is in agreement with our findings showing that PPI differences in the Roman rats are associated with divergences in mPFC activity. Here, we explore whether differences in PPI and mPFC activity in male Roman rats can be explained by (i) differences in the activation (c-Fos) of inhibitory neurons (parvalbumin (PV) interneurons); and/or (ii) reduced excitatory drive (PSD-95) to PV interneurons. Our data show that low PPI in the Roman high-avoidance (RHA) rats is associated with reduced activation of PV interneurons. Moreover, the RHA rats exhibit decreased density of both PV interneurons and PSD-95 puncta on active PV interneurons. These findings point to reduced cortical inhibition as a candidate to explain the schizophrenia-like features observed in RHA rats and support the role of impaired cortical inhibition in schizophrenia.

Throughout the reproductive cycle in rodents, prolactin levels are generally low. In some species, including rats, a prolactin surge occurs on proestrus with peak concentrations coinciding with the preovulatory luteinizing hormone (LH) surge. In mice, however, there are conflicting reports relating to the occurrence and timing of a proestrous prolactin surge. To gain further insight into the incidence and characteristics of this surge in mice, we have used serial tail tip blood sampling and trunk blood collection from both C57BL/6J (inbred) and Swiss Webster (outbred) mouse strains to build a profile of prolactin secretion during proestrus in individual mice. A clearly defined LH surge was detected in most animals, suggesting the blood sampling approach was suitable for detecting patterns of hormone secretion on proestrus. Despite this, levels of prolactin were quite variable between individuals. Overall both mouse strains showed a generalized rise in prolactin levels on the day of proestrus compared with levels seen in diestrus. This pattern is quite distinct from the discreet, circadian-entrained surge observed in rats.

BACKGROUND: The aim of this study was to evaluate protective effects of endurance exercise training against diabetic kidney disease (DKD) with muscle weakness by using male spontaneously diabetic Torii (SDT) fatty rats as type 2 diabetic animal models with obesity, hypertension, and hyperlipidemia.
METHODS: Eight-week-old SDT fatty rats (n = 12) and Sprague-Dawley (SD) rats (n = 10) were randomly divided into exercise (Ex; SDT-Ex: n = 6, SD-Ex: n = 5) and sedentary groups (SDT-Cont: n = 6, SD-Cont: n = 5), respectively. Each group underwent regular treadmill exercise 4 times a week from ages 8-16 weeks.
RESULTS: The exercise attenuated hypertension and hyperlipidemia and prevented increases in renal parameter levels without affecting blood glucose levels. In the SDT fatty rats, it prevented induction of renal morphological abnormalities in the interstitium of the superficial and intermediate layers of the cortex. Downregulated expression of endothelial nitric oxide synthase in the glomerulus of the SDT fatty rats was significantly upregulated by the exercise. The exercise upregulated the renal expressions of both medium-chain acyl-CoA dehydrogenase and peroxisome proliferator-activated receptor γ coactivator-1α related to fatty acid metabolism. It increased muscle strength and both muscle weight and cross-sectional area of type IIb muscle fibers in the extensor digitorum longus muscle in the SDT fatty rats.
CONCLUSIONS: Endurance exercise training in type 2 diabetes ameliorates DKD by improving endothelial abnormality and enhancing fatty acid metabolism in addition to attenuated hypertension, hyperlipidemia, and muscle weakness independently of blood glucose levels.

Sterculia tragacantha (ST) Lindl leaf is commonly used locally in the management of diabetes mellitus (DM) and its complications. This study was aimed at assessing the valuable effects of ST leaf on streptozotocin-diabetic cardiomyopathy (DCM). Streptozotocin was administered intraperitoneally to the experimental animals to induce DM, and hence, placed on different doses of ST for 14 days. Thereafter, on the 15th day of the experiment, the animals were euthanized, and a number of cardiomyopathy indices were investigated. The diabetic rats exhibited a momentous increase in hyperlipidemia, lipid peroxidation as well as a significant (p < 0.05) decline in antioxidant enzyme activities. The serum creatine kinase MB (CK-MB), C-reactive protein (CRP), cardiac troponin I, tumour necrosis factor-alpha (TNF-α) and urotensin II expression revealed a significant (p < 0.05) upsurge in diabetic rats. Also, the expression of GLUT4 and fatty acid-binding protein 3 (FABP3) were significantly (p < 0.05) reduced in diabetic rats. However, at the conclusion of the experimental trial ST significantly (p < 0.05) attenuated hyperlipidemia, oxidative stress biomarkers by augmenting the antioxidant enzyme activities and decrease in lipid peroxidation, ameliorated CK-MB, CRP, cardiac troponin I, TNF-α, and urotensin-II levels, and improved GLUT4 and FABP3 expressions. Similarly, the administration of ST prevented histological alterations in the heart of diabetic animals. Therefore, the obtained results suggest that ST could mitigate DCM in streptozotocin-induced diabetic rats.

Malnutrition can cause an increase in oxidative stress as it triggers the expression of heat shock protein70 (HSP70), a chaperon molecule that is needed to repair damaged cells within optimal levels. Honey is a source of feed that can stimulate HSP70 expression, which can be given to the malnourished in the animal trial.
The purpose of this study was to prove that Kaliandra honey can improve testosterone levels, diameter, and epithelial thickness of the seminiferous tubule of rat testes (Rattus norvegicus) due to malnutrition through stimulation of HSP70, which is expressed immunohistochemically.
This study used 40 male rats, which were divided into four treatment groups: T0 (negative control): normal rats and not given honey; T1 (positive control): malnourished rats and not given honey; T2 (treatment 2): malnourished rats and given 30% Kaliandra honey (v/v) for 10 days; T3 (treatment 3), malnourished rats and given 50% Kaliandra honey (v/v) for 10 days. The condition of malnutrition is carried out by fasting the feed for five consecutive days resulting in damage to the male reproductive organs, especially the testes.
The results showed that Kaliandra honey at a dose of 50% (v/v) had a significant effect in improving testosterone levels, diameter, and epithelial thickness of seminiferous tubule of malnourished male rats through stimulation of HSP70 expression. The HSP70 expression scores by IHC at T0, T1, T2, and T3 were 0.15a ± 0.5, 3.15c ± 0.4, 2.95c ± 0.35, and 1.75b ± 0.15, sequentially. enzyme-linked immunosorbent assay indirect testosterone levels at T0, T1, T2, and T3 (in μg/dl) were 36.39c ± 0.35, 6.12a ± 0.51, 7.45a ± 0.15, 25.27b ± 0.63, sequentially. The diameter and epithelial thickness of the seminiferous tubule of the testes (in μm) in the four treatments T0, T1, T2, and T3 were 362.40c ± 4.71, 248.46a ± 3.90, 255.22a ± 2.34, 318.37b ± 4.23 and 117.60d ± 11.30, 3.86a ± 1.57, 9.72b ± 3.96, 29.84c ± 4.02 sequentially.
The conclusion of the study showed that Kaliandra honey at a dose of 50% (v/v) had a significant effect in improving testosterone levels, diameter, and epithelial thickness of the seminiferous tubule of malnourished rats through stimulation of HSP70, although not significantly the same as negative control (T0).