Publications by authors named "Fernando Mauricio Francis Abdalla"

Here, we investigate the effects of obesity induced by monosodium glutamate (MSG) on cognitive impairment and whether this model induces any alteration in the affinity, density, and subtypes of muscarinic acetylcholine receptors (mAChRs) in rat hippocampus. Healthy rats were used as controls, and MSG-obese rats were selected via the Lee index > 0.300.

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Background: Here, we described the presence of a neurotoxin with phospholipase A activity isolated from venom (Mlx-8) with affinity for muscarinic acetylcholine receptors (mAChRs).

Methods: The purification, molecular mass determination, partial amino acid sequencing, phospholipase A activity determination, inhibition of the binding of the selective muscarinic ligand [H]QNB and inhibition of the total [H]inositol phosphate accumulation in rat hippocampus of the Mlx-8 were determined.

Results: Thirty-one fractions were collected from HPLC chromatography, and the Mlx-8 toxin was used in this work.

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Here, we described the effects of obesity induced by high-calorie diet and its treatment with exenatide, an anti-diabetogenic and potential anti-obesogenic drug derived from the venom of the Gila monster Heloderma suspectum, on the affinity, density, subtypes and intracellular signaling pathways linked to activation of muscarinic acetylcholine receptors (mAChRs) in rat hippocampus. Male Wistar rats were divided into three groups: control (CT), obese induced by high-calorie diet (DIO) and DIO treated with exenatide (DIO + E). [H]Quinuclidinyl benzilate specific binding analysis showed that the equilibrium dissociation constant (K) did not differ among CT, DIO and DIO + E, indicating that affinity is not affected by high-calorie diet or its treatment with exenatide.

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Introduction: Glucagon-like peptide-1 (GLP-1) receptor (R) agonists are a class of incretin mimetic drugs that have been used for the treatment of type 2 diabetes mellitus and also considered strong candidates for the treatment of obesity. The original prototypical drug in this class is the exenatide, a synthetic peptide with the same structure as the native molecule, exendin-4, found in the saliva of the Gila monster (Heloderma suspectum suspectum lizard).

Objectives: To identify and compare the anti-obesogenic, antidyslipidemic and antidiabetogenic effects of agonism in GLP-1R by exenatide on two distinct models of obesity: induced by hypothalamic injury (MSG) or high-calorie diet (DIO).

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Article Synopsis
  • The smoke from crack cocaine contains both cocaine and AEME, a compound that is more neurotoxic than cocaine and can have additive effects when combined.
  • AEME interacts with muscarinic cholinergic receptors (mAChRs), and atropine can block its neurotoxic effects, suggesting a potential link to these receptors.
  • Experiments show AEME increases cellular calcium and causes DNA fragmentation in neurons, particularly affecting mAChR subtypes M1 and M3, leading to neuronal death through apoptosis.
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The aim of the present study was to investigate the effects of different periods of ovariectomy and 17β-estradiol (E2) replacement on the expression of Cytochrome C, apoptosis inducing factor (AIF) and Endonuclease-G (Endo-G) in mitochondrial and cytosolic fractions obtained from hippocampus of the adult female rats. In addition, the expression of phosphorylated CREB (phospho-CREB) was also analyzed in hippocampus. Ovariectomy or E2 treatment did not change the expression of Cytochrome C and AIF.

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Smoking crack cocaine involves the inhalation of cocaine and its pyrolysis product, anhydroecgonine methyl ester (AEME). Although there is evidence that cocaine is neurotoxic, the neurotoxicity of AEME has never been evaluated. AEME seems to have cholinergic agonist properties in the cardiovascular system; however, there are no reports on its effects in the central nervous system.

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Aims: We have isolated a new muscarinic protein (MT-Mlα) from the venom of the Brazilian coral snake Micrurus lemniscatus.

Main Methods: This small protein, which had a molecular mass of 7,048Da, shared high sequence homology with three-finger proteins that act on cholinergic receptors. The first 12 amino acid residues of the N-terminal sequence were determined to be: Leu-Ile-Cys-Phe-Ile-Cys-Phe-Ser-Pro-Thr-Ala-His.

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Aims: The aim of the present study was to investigate the effects of different periods of ovariectomy and 17beta-estradiol replacement on apoptotic cell death and expression of members of the Bcl-2 family in the rat hippocampus.

Main Methods: Hippocampi were obtained from rats in proestrus, ovariectomized (15 days, 21 days and 36 days), ovariectomized for 15 days and then treated with 17beta-estradiol for 7 or 21 days, and rats ovariectomized and immediately treated with 17beta-estradiol for 21 days. The expression of Bcl-2 and Bax and the number of apoptotic cells were determined.

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The aim of the present study was to investigate the effects of 17beta-estradiol on expression of muscarinic acetylcholine receptor subtypes (M1 to M5) and estrogen receptor alpha, in the rat hippocampus. Hippocampi were obtained from rats in proestrus, rats ovariectomized for 15 days, rats ovariectomized for 15 days and then treated with 17beta-estradiol for 7 days, and rats ovariectomized and immediately treated with 17beta-estradiol for 21 days. Expression of M1 to M5 was increased in hippocampi of rats ovariectomized for 15 days compared to rats in proestrus.

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The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [3H]inositol phosphate ([3H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17beta-estradiol for 7 days (E7) and ovariectomized and immediately treated with 17beta-estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [3H]IP in the hippocampus.

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Article Synopsis
  • The study investigated heart rate responses and the effects of vagal electrical stimulation in rats after sinoaortic denervation, looking at both acute (1 day) and chronic (20 days) phases.
  • In the acute phase, rats exhibited hypertension and tachycardia, while in the chronic phase, heart rate and blood pressure normalized, but blood pressure variability remained high.
  • Chronic phase rats showed increased binding and affinity of muscarinic acetylcholine receptors, indicating that adaptations in the cardiac parasympathetic pathway occur as a response to baroreceptor disruption.
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