[ effect of hydro-alcoholic extract of licorice [Glycyrrhiza glabra] rhizome on the mechanical activity of the isolated colon of male rats and its interaction with cholinergic system]

Background: Glycyrrhiza glabra [Licorice] has been traditionally used as a medicinal plant in Iran for treatment of diseases such as gastric ulcer and relieve intestinal spasms

Objective: In the present study, the effect of hydro-alcoholic extract of licorice rhizome on mechanical activity of isolated colon of male rats has been studied

Methods: In this experimental study, the colon tissue of 10 adult male rats were dissected and separated into two groups: experimental and control. Each group including ten strips of tissue. The segments were connected to a force transducer longitudinally and inserted to an organ bathe contained oxygenated Tyrode solution [37 [degree]C, pH=7.4]. Their mechanical activity were recorded by power lab AD instrument in basal condition, and after administration of acetylcholine [4x10-6M] and Atropine [10-6M] in the presence and absence of licorice rhizome extract [0.036 mg/ml]. Also, the mechanical activity of control group segments were recorded at the same condition with extract solvent [ethanol %70]

Results: A significant decrease in mechanical activity was found after administration of hydroalcoholic extract of licorice compared with the control group. Also, a significant decrease of mechanical activity was seen in the presence of extract and acetylcholine compared to the control group. While the mechanical activity of tissue didn't significant changed in the presence of Atropine and extract between experimental and control groups

Conclusion: We can conclude that hydro-alcoholic extract of licorice has modifying effect on colon motility, and this activity maybe occurred independent of the cholinergic system

Basal Forebrain Cholinergic Deficits Reduce Glucose Metabolism and Function of Cholinergic and GABAergic Systems in the Cingulate Cortex

PURPOSE: Reduced brain glucose metabolism and basal forebrain cholinergic neuron degeneration are common features of Alzheimer's disease and have been correlated with memory function. Although regions representing glucose hypometabolism in patients with Alzheimer's disease are targets of cholinergic basal forebrain neurons, the interaction between cholinergic denervation and glucose hypometabolism is still unclear. The aim of the present study was to evaluate glucose metabolism changes caused by cholinergic deficits. MATERIALS AND METHODS: We lesioned basal forebrain cholinergic neurons in rats using 192 immunoglobulin G-saporin. After 3 weeks, lesioned animals underwent water maze testing or were analyzed by 18F-2-fluoro-2-deoxyglucose positron emission tomography. RESULTS: During water maze probe testing, performance of the lesioned group decreased with respect to time spent in the target quadrant and platform zone. Cingulate cortex glucose metabolism in the lesioned group decreased, compared with the normal group. Additionally, acetylcholinesterase activity and glutamate decarboxylase 65/67 expression declined in the cingulate cortex. CONCLUSION: Our results reveal that spatial memory impairment in animals with selective basal forebrain cholinergic neuron damage is associated with a functional decline in the GABAergic and cholinergic system associated with cingulate cortex glucose hypometabolism.

Cardiovascular effects of the intracerebroventricular injection of adrenomedullin: roles of the peripheral vasopressin and central cholinergic systems

Our objective was to investigate in conscious Sprague-Dawley (6-8 weeks, 250-300 g) female rats (N = 7 in each group) the effects of intracerebroventricularly (icv) injected adrenomedullin (ADM) on blood pressure and heart rate (HR), and to determine if ADM and calcitonin gene-related peptide (CGRP) receptors, peripheral V1 receptors or the central cholinergic system play roles in these cardiovascular effects. Blood pressure and HR were observed before and for 30 min following drug injections. The following results were obtained: 1) icv ADM (750 ng/10 µL) caused an increase in both blood pressure and HR (DMAP = 11.8 ± 2.3 mmHg and ΔHR = 39.7 ± 4.8 bpm). 2) Pretreatment with a CGRP receptor antagonist (CGRP8-37) and ADM receptor antagonist (ADM22-52) blocked the effect of central ADM on blood pressure and HR. 3) The nicotinic receptor antagonist mecamylamine (25 µg/10 µL, icv) and the muscarinic receptor antagonist atropine (5 µg/10 µL, icv) prevented the stimulating effect of ADM on blood pressure. The effect of ADM on HR was blocked only by atropine (5 µg/10 µL, icv). 4) The V1 receptor antagonist [β-mercapto-β-β-cyclopentamethylenepropionyl¹, O-me-Tyr²,Arg8]-vasopressin (V2255; 10 µg/kg), that was applied intravenously, prevented the effect of ADM on blood pressure and HR. This is the first study reporting the role of specific ADM and CGRP receptors, especially the role of nicotinic and muscarinic central cholinergic receptors and the role of peripheral V1 receptors in the increasing effects of icv ADM on blood pressure and HR.