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Biomedical subjects

F Amenta

Publications and source records attributed to F Amenta.

At least 127 records · Page 7Linked to original sources
PubMed1994

Long term choline alfoscerate treatment counters age-dependent microanatomical changes in rat brain.

1. The density of nerve cells and of silver-gold impregnated fibres were evaluated in the hippocampus and in the cerebellar cortex in adult (12-month-old) and old (24-month-old) Sprague-Dawley rats. 2. The effects of long-term choline alfoscerate (GFC) treatment (100 mg/Kg/day for 6 months) on the above parameters were investigated in old rats. 3. The number of nerve cell profiles and the area occupied by silver-gold impregnated fibres were decreased both in the hippocampus and in the cerebellar cortex in old in comparison with adult rats. 4. GFC treatment countered the age-dependent reduction of nerve cells and silver-gold impregnated fibres. The hippocampus was more sensitive than the cerebellar cortex to the activity of GFC. 5. These results suggest that GFC treatment is effective in slowing down the expression of structural changes occurring in aging brain.

Aging↗
PubMed1994

Microanatomical changes in the frontal cortex of aged rats: effect of L-deprenyl treatment.

The present study was designed to assess whether treatment with L-deprenyl has any effect on the age-related microanatomical changes in the rat frontal cortex. Male Sprague-Dawley rats of 19 months of age were treated until the 24th month with an oral daily dose of 1.25 mg/kg or of 5 mg/kg of L-deprenyl. Eleven-month-old untreated rats were used as an adult reference group. The density of nerve cell profiles and of glial fibrillary acidic protein-(GFAP) immunoreactive astroglial profiles, lipofuscin accumulation within the cytoplasm of pyramidal neurons, and MAO-B reactivity were assessed. A decreased density of nerve cell profiles and an increased density of astroglial profiles as well as augmented lipofuscin deposition and MAO-B reactivity were observed in the frontal cortex of rats of 24 months in comparison with 12-month-old animals. In the frontal cortex of rats treated with 5 mg/kg/day L-deprenyl, which is a dose inhibiting MAO-B activity, the density of nerve cell and GFAP-immunoreactive astrocyte profiles is increased and decreased respectively in comparison with age-matched untreated subjects. Lipofuscin deposition is reduced. The lower dose of L-deprenyl (1.25 mg/kg/day) which did not affect MAO-B activity, decreased lipofuscin deposition but was without effect on the density of nerve cell or GFAP-immunoreactive astrocyte profiles. The above findings suggest that treatment with L-deprenyl is able to counter some microanatomical changes occurring in the frontal cortex of aged rats. Some of these effects are probably not related to the inhibitory MAO-B activity of the compound.

Aging↗
PubMed1994

Dopamine D1 and D2 receptors in the human ureter and urinary bladder: a radioligand binding and autoradiographic study.

OBJECTIVE: To analyse the pharmacological profile and the anatomical localization of the dopamine D1 and D2 receptors in sections of the pelvic part of the ureter and of the fundus of the urinary bladder. PATIENTS, MATERIALS AND METHODS: Samples of the pelvic part of the ureter and of the fundus of the urinary bladder were taken in men (age range 61 +/- 4 years) who were undergoing lower urinary tract surgery. Biochemical characterization and autoradiographical techniques were used on frozen sections of the ureter or the urinary bladder. [3H]-SCH 23390 was used as a ligand of dopamine D1 receptors and [3H]-spiroperidol as a ligand of dopamine D2 receptors. RESULTS: [3H]-SCH 23390 and [3H]-spiroperidol were bound by specific sections of the ureter and of the urinary bladder. The pharmacological profile of the binding was consistent with the labelling of D1 and D2 receptors respectively. Light microscope analysis of the localization of D1 and D2 receptors revealed the accumulation of the two radioligands in the tunica muscularis of the ureter or of the urinary bladder. CONCLUSION: A possible role of the dopaminergic system in the control of urine flow and of some dysfunctions of the lower urinary tract is suggested.

Aged↗
PubMed1994

Pharmacological characterization and autoradiographic localization of dopamine receptors in the portal vein.

1. Dopamine (DA) and DA receptor agonists exert a variety of effects on the cardiovascular system through interaction with specific DA receptors, including decreases in blood pressure and heart rate. 2. The decrease in blood pressure is due primarily to arterial vasodilation. This phenomenon is due to the stimulation of both postjunctional (D1-like or DA1) and prejunctional (D2-like or DA2) receptors causing respectively relaxation of arterial smooth muscle and decrease of the sympathetic vasoconstriction tone. 3. In view of the lack of detailed information on the existence of DA receptors in venous tissue, we have analysed D1-like and D2-like receptors in the rat portal vein using radioligand binding techniques associated with light microscope autoradiography. 4. No D1-like receptors were demonstrated in sections of the rat portal vein, whereas the D2-like receptor ligand, [3H]-spiroperidol, was bound to sections of the vein in a manner consistent with the labelling of D2-like sites. Anatomically, D2-like sites were located within the tunica adventitia, including the adventitia-media border, and in the endothelium. 5. These findings suggest the existence of D2-like but not D1-like receptor sites in the rat portal vein. D2-like sites of the tunica adventitia are probably prejunctional and involved in the modulation of sympathetic outflow. The functional significance of endothelial D2-like sites, if any, should be clarified in future studies.

Animals↗
PubMed1994

Interactions between calcium channel blockers and alpha-adrenoceptors in the human coronary and mammary arteries: a radioligand binding study.

The study was designed to assess whether Ca2+ channel blockers of the dihydropyridine family (felodipine, nicardipine, nifedipine, nimodipine, nitrendipine and nisoldipine), and of the phenylalkylamine family (verapamil) have any effect on alpha-adrenoceptor binding to sections of the human right coronary and mammary arteries, measured using [3H]-dihydroergocryptine (DHT) as a ligand. Increasing concentrations of nicardipine, verapamil and nitrendipine competed with [3H]-DHT binding to sections of the human coronary and mammary arteries. The other compounds tested were without effect. Among the competitors of [3H]-DHT binding, nicardipine was the most powerful, with a 50% inhibition (IC50) value of approximately 10 nM. The pharmacological profile of competition with [3H]-DHT binding by nicardipine, in the presence or in the absence of guanosine triphosphate and NaCl, is consistent with antagonist activity of the dihydropyridine derivative at the alpha-adrenoceptor. This property may account for the lower sympathetic stimulatory activity elicited by nicardipine, in comparison with other Ca2+ channel blockers used in cardiovascular therapy.

Adolescent↗
PubMed1994

Interactions between endothelin and the dihydropyridine-type calcium antagonist nicardipine in the human renal artery: a radioligand and autoradiographic study.

The interactions between dihydropyridine Ca2+ channels and endothelin were analysed using combined radioligand binding and autoradiographic techniques. Endothelin is a potent constrictor peptide of arterial smooth muscle. Endothelin-induced vasoconstriction is attenuated by dihydropyridine-type Ca2+ antagonists such as nicardipine. However, the molecular mechanisms of this effect are not yet understood. Sections of the human renal artery bound [3H]-nicardipine in a manner consistent with the labelling of dihydropyridine-type Ca2+ channels. The highest density of [3H]-nicardipine binding sites occurred within the tunica media of the renal artery, probably over smooth muscle. A lower density of [3H]-nicardipine binding sites was noticeable in the tunica adventitia, whereas no specific binding occurred in the tunica intima. Endothelin-1, from a concentration of 1 pM l-1, reduced [3H]-nicardipine binding as a function of concentration. A 10 nM endothelin concentration reduced [3H]-nicardipine binding by about 85%. The isoform, endothelin-3, had little effect on [3H]-nicardipine binding. The above findings suggest the occurrence of an interaction, probably at the receptor level, between [3H]-nicardipine binding and endothelin-1. This interaction probably accounts for the attenuation of endothelin-1-elicited vasoconstriction induced by nicardipine.

Aged↗
PubMed1994

Loss of dopamine D1-like receptors in the umbilical artery of pre-eclamptic subjects.

1. The influence of pre-eclampsia on the density and pattern of dopamine D1-like receptors was studied in frozen samples of the placental end of the umbilical artery by using radioligand binding and autoradiographic techniques in combination. 2. Analysis was performed on normotensive (n = 10) and pre-eclamptic subjects (n = 9) undergoing caesarean delivery, using [3H]-SCH 23390 as a ligand. Pre-eclamptic patients received a low salt diet and were treated with magnesium sulphate and hydralazine. The possibility that this treatment may cause changes in the density of dopamine D1-like receptors was evaluated by treating male Wistar rats in the same way and by determining [3H]-SCH 23390 binding in sections of the kidney which represents an organ containing dopamine D1-like receptors. 3. The density of dopamine D1-like receptors of the umbilical artery, which are probably vasodilatory, was decreased in pre-eclamptic compared with normotensive subjects. In contrast, the affinity of the radioligand for dopamine D1-like receptors was not statistically different between normotensive and pre-eclamptic subjects. Low salt diet, magnesium sulphate and hydralazine treatment did not affect [3H]-SCH 23390 binding to sections of rat kidney. This suggests that changes in the density of dopamine D1-like receptors in pre-eclamptic patients are a specific phenomenon not dependent upon antihypertensive measures. 4. Analysis of the pharmacological profile of [3H]-SCH 23390 binding to sections of the umbilical artery both in normotensive and pre-eclamptic subjects indicates the labelling of dopamine D5 receptors. 5. These findings collectively suggest that the dopaminergic vasodilatory tone in the umbilical artery is impaired in pre-eclampsia. The possible significance of these data should be clarified in future studies.

Adult↗
PubMed1994

Pharmacological characterization and anatomical localization of prejunctional beta-adrenoceptors in the rat kidney.

1. The subtype and anatomical localization of beta-adrenoceptors mediating facilitation of stimulus-induced overflow of noradrenaline ('prejunctional beta-adrenoceptors') are not conclusively known to date. The present study was undertaken to characterize these receptors by use of pharmacological methods as well as to define their localization (prejunctional or postjunctional) with radio-ligand binding and autoradiography techniques combined with surgical denervation of the sympathetic innervation to the rat kidney. 2. Exposure of the kidney to (-)-isoprenaline, the nonselective beta-adrenoceptor agonist, resulted in a dose-dependent facilitation of stimulus-induced neurotransmitter overflow. This response was inhibited by propranolol, the beta 1- and beta 2-adrenoceptor antagonist, with a pA2 of 9.20 suggesting that the prejunctional beta-adrenoceptors are not of the beta 3-subtype. 3. The rank order of potency and potency ratios of beta-adrenoceptor agonists at renal prejunctional beta-adrenoceptors (EC50 for agonist/EC50 for (-)-isoprenaline) were: (-)-isoprenaline (1) > procaterol (2) > salbutamol (3) > adrenaline (10) > (+)-isoprenaline (25). However, dobutamine, the beta 1-adrenoceptor agonist, failed to enhance stimulus-induced overflow of noradrenaline. These results are indicative of the presence of beta 2-adrenoceptors as prejunctional beta-adrenoceptors. 4. Facilitation elicited by (-)-isoprenaline and procaterol, the selective beta 2-adrenoceptor agonist, was inhibited by ICI 118,551, the selective beta 2-adrenoceptor antagonist, with pKb values of 9.20 and 9.35, respectively at renal prejunctional beta-adrenoceptors. Similarly, the pKb values of metoprolol, the selective beta 1-adrenoceptor antagonist, at renal prejunctional beta-adrenoceptors were determined to be 6.25 and 6.18 against (-)-isoprenaline and procaterol, respectively. These results suggest the presence of a homogeneous population of beta 2-adrenoceptors as prejunctional beta-adrenoceptors. 5. Radio-ligand binding analysis of renal beta-adrenoceptors revealed the prevalence of the beta 1-subtype as compared to the beta 2-subtype (63% vs 37%). However, surgical denervation of the rat kidney, resulting in more than 90% reduction in renal noradrenaline content, selectively reduced the beta 2-adrenoceptor population by 80%, implying the presence of beta 2-adrenoceptors on renal sympathetic nerve terminals. 6. Autoradiographic analysis demonstrated the presence of beta 1-adrenoceptors on cortical structures such as glomeruli and tubules. beta-Adrenoceptors were found to be present on tubules (minor population), collecting tubules in outer medulla and the adventitia and adventitial-medial border of intraparenchymal branches of the renal artery. Surgical denervation of the rat kidney resulted in the disappearance of Beta2-adrenoceptors associated with the intraparenchymal branches, without affecting the Beta-adrenoceptor populations at other sites. These results support the notion that the Beta2-subtype is present on renal sympathetic nerve terminals and demonstrate that these prejunctional Beta2-adrenoceptors are associated with the renal vasculature and not with renal tubules.7. The results of the present investigation demonstrate that renal prejunctional Beta-adrenoceptors are of the Beta2-subtype in nature. These receptors are present on sympathetic nerve terminals which are associated with the renal vasculature.

Animals↗
PubMed1994

Pharmacological characterization and autoradiographic localization of dopamine receptors in the human adrenal cortex.

The pharmacological characteristics and the anatomical localization of dopamine D1-like and D2-like receptors were studied in sections of the human adrenal cortex using radioligand binding and autoradiographic techniques. [3H]SCH 23390 was used as a ligand of D1-like receptors, whereas [3H]spiroperidol was used to label D2-like receptors. No specific [3H]SCH 23390 binding was detectable in sections of the human adrenal cortex. On the other hand, [3H]spiroperidol was bound to sections of the adrenal gland in a manner consistent with the labelling of dopamine D2-like receptor sites. The binding was time, temperature and concentration dependent, belonging in the range of concentrations of the radioligand used for a single class of high-affinity sites. The dissociation constant (Kd) averaged 2.7 nmol/l, whereas the maximum density of binding sites (Bmax) was 160 nmol/mg tissue. Experiments on the pharmacological specificity of [3H]spiroperidol binding to sections of the human adrenal cortex revealed that clozapine was the most powerful displacer of [3H]spiroperidol from sections of the human adrenal cortex. This suggests the presence in the human adrenal cortex of dopamine receptors of the D4 subtype. Light microscope autoradiography showed the highest density of specific [3H]spiroperidol binding sites in the zona glomerulosa and to a lesser extent in the zona reticularis. Only sparse [3H]spiroperidol binding sites were localized in the zona fasciculata. The possible functional consequences of this localization of dopamine D2-like receptor sites in the human adrenal cortex are discussed.

Adrenal Cortex↗
PubMed1994

Protective effect of nicardipine treatment on renal microanatomical changes in spontaneously hypertensive rats.

The effects of nicardipine administration on kidney morphology were studied in spontaneously hypertensive rats (SHR). Male 12-week-old SHR received an oral dose of 1 mg/Kg/day of nicardipine or vehicle for 8 weeks Age-matched Wistar-Kyoto rats were used as normotensive reference animals. At 20 weeks, the non treated SHR exhibited hypertension, albuminuria, decreased urinary sodium excretion and renal microanatomical changes. These changes were characterized by vascular alterations consisting in hypertrophy of the tunica media accompanied by a decrease of luminal surface. Glomerular changes consisting primarily in signs of glomerulosclerosis of varying degrees were noticeable in the kidneys of SHR. Treatment with nicardipine significantly reduced blood pressure and albuminuria and increased urinary sodium excretion. Moreover, hypertrophy of the tunica media and the luminal surface were decreased and increased respectively in nicardipine-treated SHR. The above results suggest that treatment with nicardipine reduces blood pressure in SHR and counteracts hypertension-dependent changes in the morphology of the kidney. The protective effect of the drug on hypertensive changes of renal microanatomy probably have functional relevance given of the influence of nicardipine treatment on albuminuria and urinary sodium excretion in SHR.

Albuminuria↗
PubMed1994

Influence of isradipine treatment on left ventricular and coronary vascular hypertrophy in spontaneously hypertensive rats.

The purpose of this study was to ascertain if Isradipine treatment in spontaneously hypertensive rats (SHR) decreased hypertension-dependent left ventricular and coronary vascular hypertrophy. Twelve week male SHR were used in this study; one group of SHR was treated with Isradipine while the control group of SHR was left untreated. Age-matched normotensive Wistar-Kyoto rats (WKY) were utilized as a reference group. After 12 weeks of treatment rats were sacrificed. The hearts were removed and morphometric analysis was performed on the left ventricles. Isradipine treatment reduced systolic blood pressure in SHR. The heart/body weight ratio significantly increased in SHR and in Isradipine-treated SHR in comparison with WKY rats. Isradipine treatment decreased the left ventricular muscle fibre diameter and decreased the amount of focal necrosis in SHR. Different sized coronary arteries were also examined using a light microscope and an image analyzer. We found that the area occupied by the medial layer and the media-to-lumen ratio were significantly increased in comparison with WKY rats. In Isradipine-treated SHR the area of the medial layer and the media-to-lumen ratio in small and medium sized but not in large sized coronary arteries were significantly reduced in comparison with untreated SHR. The above results suggest that long term Isradipine treatment is not only able to reduce high blood pressure in SHR but is also able to counter the development of certain morphological changes often seen in the hypertensive heart and coronary arteries.

Animals↗
PubMed1994

Influence of treatment with the calcium channel blocker darodipine (PY 108-068) on the morphology of pial and coronary arteries in spontaneously hypertensive rats.

The present study was designed to assess the influence of treatment with the calcium channel blocker darodipine (PY 108-068) on the morphology of pial and coronary arteries in spontaneously hypertensive rats (SHR). Twelve week male SHR were used in this study. One group was treated with a daily dose of 5 mg/Kg of darodipine, while the control group of SHR was treated with placebo. Age-matched normotensive Wistar Kyoto (WKY) rats were used as a reference group. After 12 weeks of treatment the rats were sacrificed. The brains and the hearts were removed, embedded in resin, cut and used for light microscope analysis. Darodipine treatment reduced blood pressure in SHR. Morphometric analysis of different sized pial and coronary arteries revealed decreased arterial lumen in SHR in comparison with WKY rats. The area occupied by the tunica media and the media-to-lumen ratio were increased in SHR in comparison with WKY rats. In darodipine-treated rats the area occupied by the arterial lumen was increased in comparison with control SHR, whereas the area occupied by the tunica media and the media-to-lumen ratio were decreased. Pial arteries were more sensitive than coronary arteries to darodipine treatment. Medium and small sized pial and coronary arteries were most sensitive to darodipine treatment. Large-sized coronary artery branches were unaffected by pharmacological treatment. The above results suggest that treatment of SHR with darodipine is able to reduce high blood pressure and to counter the development of structural changes of pial and coronary arteries noticeable in SHR. The higher sensitivity of the cerebral vasculature to darodipine treatment is discussed.

Animals↗
PubMed1994

Quantitative image analysis study of the cerebral vasodilatory activity of nicardipine in spontaneously hypertensive rats.

The effect of the Ca2+ channel blocker nicardipine on the circle of Willis and the different sized pial arteries was assessed in 20-week-old spontaneously hypertensive rats (SHR) using quantitative image analysis techniques. Normotensive Wistar Kyoto (WKY) rats were also used as a normotensive reference group. In SHR a significant increase of systolic blood pressure (SBP) is noticeable in comparison with WKY rats. The media-to-lumen ratio was increased in the circle of Willis arteries, large sized (diameter > than 150 microns), medium sized (diameter between 150 and 50 microns) and small sized (diameter < than 50 microns), pial artery branches. An increase in the thickness of the tunica media and a luminal narrowing was also seen in medium and small sized pial arteries of SHR in comparison with WKY rats. Treatment with an oral dose of 10 mg/Kg of nicardipine 3 h before the sacrifice significantly reduced SBP in SHR. The drug was without effect on circle of Willis and on large sized pial arteries. Moreover, treatment with nicardipine reduced the thickness of the tunica media, the media-to-lumen ratio and increased the luminal area in medium and small sized pial artery branches. These findings show that treatment of SHR with nicardipine significantly reduces SBP and causes a moderate vasodilatation of arteries regulating cerebrovascular resistance. This property may be useful in avoiding generalized or exaggerated cerebrovascular dilatation which could be accompanied by impaired brain perfusion in hypertension.

Animals↗
PubMed1994

Effect of long term isradipine treatment on the morphology of the endothelium in the aorta of spontaneously hypertensive rats.

The influence of hypertension and of treatment with the dihydropyridine calcium channel blocker isradipine on the morphology of the thoracic aorta and of the aortic tunica intima were studied. Three experimental groups of male spontaneously hypertensive rats (SHR) of 10 weeks of age were used. Two groups were treated with a daily oral dose of 0.01 mg/kg or of 0.1 mg/Kg of isradipine respectively. A third group of SHR was left untreated and served as control. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as a reference group. Animals were allowed to survive for 12 weeks and were killed at 22 weeks of age. Systolic pressure values which did not change in WKY rats, significantly increased in SHR as a function of age. The dose of 0.1 mg/Kg/day isradipine reduced systolic pressure to normotensive values after the first week of treatment, whereas the lower one was ineffective. The area of the wall, the area of the tunica media and the wall-to-lumen ratio of the aorta significantly increased in SHR and decreased either with the antihypertensive and non-antihypertensive doses of isradipine. Transmission and scanning electron microscope analysis of the tunica intima revealed hypertrophy of the endothelial cells with an increase in sub endothelial space in SHR. An improvement of the endothelial morphology and a decrease in sub endothelial space was noticeable in isradipine-treated SHR. Although the hypotensive dose of the compound was the most effective, the non-hypotensive dose was active was well. The above results suggest that isradipine treatment may counter structural changes of the aorta of SHR and has a protective action on the hypertension-dependent modifications of the endothelium. The endothelial effects are probably dependent only in part by the hypotensive activity of the compound.

Animals↗
PubMed1994

Influence of isradipine treatment on the morphology of the aorta in spontaneously hypertensive rats.

OBJECTIVE: To investigate the influence of hypertension and of treatment with the vasodilator hydralazine or with the dihydropyridine calcium antagonist isradipine on the morphology of the thoracic aorta in spontaneously hypertensive rats (SHR). DESIGN: The systolic blood pressure (SBP), body weight and morphology of the thoracic aorta were evaluated. The ultrastructure of the smooth muscle component of the aorta and of the tunica intima were analysed by transmission and scanning electron microscopy. METHODS: The SHR were divided into three groups: a control group, which was left untreated, and two treatment groups, one with 1 mg/kg per day hydralazine and the other with 0.1 mg/kg per day isradipine. Three age-matched groups of Wistar-Kyoto (WKY) rats were included in the study: one group was left untreated and was used as a normotensive reference group, the other two groups were treated with 1 mg/kg per day hydralazine or with 0.1 mg/kg per day isradipine. RESULTS: The SBP did not change in the WKY rats treated with hydralazine, with isradipine or untreated, but was significantly increased in the SHR as a function of age. Both hydralazine and isradipine significantly reduced the SBP in the SHR after the second week of treatment. Light microscopy analysis of the thoracic aorta revealed thickening of the wall of the tunica media as well as an increase in the wall: lumen ratio in the SHR. Treatment with hydralazine had no effect on the morphometric parameters evaluated, whereas isradipine administration significantly reduced the thickening of both the wall and the tunica media of the aorta, and reduced the wall: lumen ratio. No significant modifications in the structure of the thoracic aorta were noticed in the hydralazine- or isradipine-treated WKY rats compared with untreated WKY rats. Transmission and scanning electron microscopy analysis demonstrated in control SHR hypertrophy of smooth muscle cells of the tunica media, an increased size and impairment of the internal elastic lamina, and a widening of the subendothelial space. Hypertrophy of the endothelium was also noticeable in the SHR. Treatment with isradipine reduced the hypertrophy of smooth muscle cells of the tunica media and the structural impairment of the tunica intima. No effect of isradipine treatment on the morphology of the aorta was noticed in the WKY rats. CONCLUSION: The present results show that the effect of isradipine was different from that of hydralazine. Both compounds lowered the SBP, but only isradipine countered the structural changes of the aorta in the SHR. The effect of isradipine administration is particularly pronounced on the hypertension-dependent changes of endothelium. This suggests that isradipine may have a protective effect on the endothelium.

Animals↗
PubMed1993

Effect of ipsilateral lesioning of the nucleus basalis magnocellularis and of L-alpha-glyceryl phosphorylcholine treatment on choline acetyltransferase and acetylcholinesterase in the rat fronto-parietal cortex.

The present study assesses the effect of unilateral lesions of the nucleus basalis magnocellularis (NBM) and of treatment with L-alpha-glyceryl phosphorylcholine (GFC, choline alfoscerate) on the acetylcholine-synthesizing (choline acetyltransferase (ChAT)), and acetylcholine-degradating (acetylcholinesterase (AChE)) enzymes in the rat fronto-parietal cortex ipsilateral to the lesion. Ibotenic acid injections in the right NBM area caused a significant decrease of both ChAT and AChE activities as well as of histochemically reactive stores of AChE in the right fronto-parietal cortex. Treatment with GFC restored in part the loss of ChAT and AChE activities. Moreover, AChE reactivity is restored in the fronto-parietal cortex of NBM-lesioned rats treated with GFC. GFC is a precursor in the biosynthesis of brain phospholipids which increases the bioavailability of acetylcholine in the nervous tissue. The possible relevance of the restoration of the marker enzymes of cholinergic neurotransmission by GFC in an animal model of cholinergic hypofunction is considered.

Acetylcholinesterase↗
PubMed1993

Cholinergic neurotransmission in the hippocampus of aged rats: influence of L-alpha-glycerylphosphorylcholine treatment.

The influence of aging and of L-alpha-glycerylphosphorylcholine (GFC) treatment on the acetylcholine synthesizing and degradating enzymes choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) and on cholinergic muscarinic M-1 and M-2 receptors were assessed in the hippocampus using immunocytochemical, histochemical and radioligand binding techniques, respectively. The investigation was performed on male Wistar rats of 2 months (young), 12 months (adult), and 27 months (old). Oral GFC was given at the dose of 100 mg/Kg/day from the 21st to the 27th month of age. ChAT revealed the highest immunostaining in the hippocampus of adult rats followed by young and old animals. The highest expression of AChE reactivity was noticeable in the hippocampus of adult rats followed by old and young animals. Treatment with GFC restored in part ChAT immunoreactivity and AChE reactivity in the hippocampus of aged rats. Muscarinic M-1 and M-2 receptors were labeled with [3H]-pirenzepine and [3H]-AF-DX-116 respectively. The density of M-1 muscarinic receptors decreased with age, whereas M-2 muscarinic receptors did not change. GFC treatment countered in part the loss of M-1 receptors in old rats and was without effect on M-2 receptors.

Acetylcholine↗