Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depressed patients exhibit an abnormal "supersensitive" increase in the plasma concentration of several pituitary hormones following intravenous injection of the acetyl cholinesterase inhibitor physostigmine (PHY). In the present study, we examined the effects of PHY treatments on the plasma concentrations of prolactin (PRL) and adrenocorticotrophic hormone (ACTH) in the rat. Physostigmine (0-0.6 mg/kg, s.c.) produced a dose-dependent increase in PRL and ACTH immunoreactivity in unoperated animals. Neurotoxin-induced depletion of brain dopamine (DA) or norepinephrine (NE) did not significantly alter baseline plasma PRL or ACTH values. Following depletion of brain DA, but not NE, animals exhibited a "supersensitive" increase in plasma ACTH values, which was evidenced by a sixfold left shift in the dose-response properties of PHY. These results suggest that there are intriguing parallels between the abnormal endocrine response to PHY demonstrated by depressed patients and that demonstrated by rats following depletion of central nervous system (CNS) DA levels.
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PMID:Supersensitive endocrine response to physostigmine in dopamine-depleted rats: a model of depression? 301 69

Patients with Alzheimer's disease participated in a trial of two sessions in which they received physostigmine and neostigmine in a double-blind crossover design. Most of these patients subsequently participated in a scopolamine vs saline double-blind crossover trial using a similar design. Physostigmine increased plasma cortisol relative to neostigmine, with the greatest difference at time points greater than 90 min post drug oral administration. Physostigmine also significantly decreased plasma cholinesterase (ChE). There was a significant positive correlation between the effects of physostigmine on increasing cortisol and decreasing ChE; there was no correlation between the increase in cortisol of cholinesterase inhibitor following neostigmine administration, but neither of these chemical parameters is related to the drug's effects on cognitive functioning.
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PMID:Cortisol responses to cholinergic drugs in Alzheimer's disease. 306 49

The histochemical distribution of cholinesterases in the cerebral cortex and their response to cholinesterase inhibitors such as physostigmine and tetrahydroaminoacridine (THA) were investigated in brains from patients with Alzheimer's disease and control subjects. In the temporal neocortex of the control subjects, most of the cholinesterase activity was located within axons and cell bodies belonging to cholinergic pathways. In keeping with their well-known cholinomimetic effects, physostigmine and THA effectively inhibited this cholinesterase activity. Cholinesterase-containing normal axons (and in some cases cells) were severely depleted in the cerebral cortex of patients with Alzheimer's disease. Although the cerebral cortex of these patients continued to display abundant cholinesterase activity, the location of this enzyme was largely shifted to the neuritic plaques and neurofibrillary tangles. In fact, the majority of these pathological structures demonstrated intense acetylcholinesterase and butyrylcholinesterase activities. Physostigmine and THA were potent inhibitors of these plaque- and tangle-bound cholinesterases as well. In patients with Alzheimer's disease, cholinesterase inhibitors would therefore appear to have a major and widespread effect directly upon the enzymatic activity of plaques and tangles. Consequently, the clinical effects of anticholinesterases in Alzheimer's disease may be based on mechanisms that are different from those that apply to the normal brain.
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PMID:Anatomy of cholinesterase inhibition in Alzheimer's disease: effect of physostigmine and tetrahydroaminoacridine on plaques and tangles. 343 78

The present study examined the effects of physostigmine, a cholinesterase inhibitor, on activity in young rats whose mothers consumed isocaloric liquid diets containing 35% or 0% ethanol-derived calories on days 6-20 of pregnancy. A pair-feeding procedure was utilized and an ad libitum lab chow group was included. Physostigmine was administered to 18-day-old offspring on 3 consecutive days with activity measures recorded for 30 min each day. Injections of physostigmine produced significant reductions in activity in alcohol-exposed offspring relative to control groups. These results provide support for a functional cholinergic deficit in offspring exposed to alcohol in utero and may have relevant clinical implications in the treatment of attentional deficit disorder which can occur following prenatal alcohol exposure.
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PMID:The effects of physostigmine on open-field behavior in rats exposed to alcohol prenatally. 351 92

Physostigmine (1.5 mg/kg, s.c.) and neostigmine (1.0 mg/kg, s.c.) injection into male mice produced signs of toxicosis characteristic of cholinesterase inhibition and evoked death in 95 and 94% of the animals respectively. Diphenhydramine injections (5-30 mg/kg, s.c.) 15 min before physostigmine or neostigmine significantly increased the latency period to onset of death and the percentage of survivors. Diphenhydramine injection (20 mg/kg, s.c.) between -30 and +2 min (but not at +5 and +10 min) relative to physostigmine prevented lethality in 100% of the animals. The data indicated that diphenhydramine which possesses anticholinergic effects protected mice against physostigmine- and neostigmine-induced toxicosis.
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PMID:Interaction of diphenhydramine with cholinesterase inhibitors in mice. 361 97

Ethylcholine aziridinium ion (AF64A), a putative cholinotoxin, was administered into the cerebroventricles of rats, and the effects on learning behaviors were observed. AF64A caused the impairment of learning acquisition in both passive and active avoidance responses. Physostigmine, a cholinesterase inhibitor, antagonized these changes at the doses of 0.03 to 0.1 mg/kg. Our behavioral study may indicate that the central cholinergic system might play a role in AF64A-induced impairment.
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PMID:Effects of physostigmine on AF64A-induced impairment of learning acquisition in rats. 368 13

The effectiveness of physostigmine and atropine pretreatment against the lethal effects of sarin was studied in rats given lethal subcutaneous injections (130 micrograms/kg) of the organophosphate. Pretreatment of these animals with physostigmine 30 min prior to injection of sarin reduced mortality to 28% and when the drug coadministered with atropine only 4% of the animals died. The latter treatment also reduced significantly the extent and duration of symptoms due to sarin; however, atropine, pyridostigmine, and neostigmine injected alone did not protect animals against the lethal effects of sarin. Physostigmine caused only slight inhibition of cholinesterase in blood and skeletal muscle. Cholinesterase activity in blood and muscle of rats pretreated with physostigmine before sarin administration was significantly higher than in tissues from rats injected with sarin alone. In rats receiving sarin following pretreatment with physostigmine, twitch potentiation of extensor muscles and maintenance of tension during tetanic stimulation of the nerve recovered to near control levels. Muscle function recovered despite significant inhibition of cholinesterase. Effective protection against lethality by physostigmine could be related to protection of cerebral cholinesterase since inhibition of this enzyme by sarin was lowered significantly after pretreatment with physostigmine. Alternatively, physostigmine may also interact with the nicotinic acetylcholine receptor ion-channel complex directly.
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PMID:Effectiveness of physostigmine as a pretreatment drug for protection of rats from organophosphate poisoning. 369 40

The relationship between physostigmine (Phy) concentration, acetylcholine (ACh), choline (Ch) and cholinesterase (ChE) activity was examined in whole rat brain after the administration of [3H]Phy (650 microgram/kg i.m.). Cholinesterase inhibition was found to be inversely related to Phy levels. Maximal inhibition (80%) was seen at 5 min and by 2 hrs ChE activity had returned to control levels. Acetylcholine levels in whole brain peaked at 30 min at a concentration (80 nmol/g) 2.3 times higher than controls (33 nmol/g). Choline levels were not significantly altered. The regional distribution of Phy concentration and ChE activity was studied in six areas of the brain following i.m. administration of three different dosages of ( 3H]Phy. Physostigmine concentration and ChE activity showed a dose dependency in each area examined except in SP (medial septum). Striatum (ST) showed the greatest relative increase of ACh up to 30 min, when compared to other areas. Choline levels were not changed in any area with the exception of ST at 5 min where a decrease was seen. There was a relationship between ChE activity, Phy concentration and ACh levels in all areas examined with exception of the medulla oblongata (MO). Our results indicate that even though ChE was inhibited practically uniformly in all brain areas, the percent increase with respect to control animals and the relative increase of ACh varied widely from area to area. This finding has clinical implications in cases in which cholinomimetic therapy is used to elevate ACh levels in specific brain areas which show a cholinergic deficit.
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PMID:Relation of brain regional physostigmine concentration to cholinesterase activity and acetylcholine and choline levels in rat. 374 73

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was observed in both areas. Administration of Physostigmine, a cholinesterase inhibitor, at a dose of 0.15 mg/Kg by intravenous route, induced an increase of CBF in the ischemic cortex. This change in CBF reached 120% of pre-occlusion level in the periphery and 80% of pre-occlusion value in the center of the area of distribution of the occluded artery. Although Physostigmine induced an increase in arterial blood pressure, the cerebral hyperemia observed both in normal and ischemic cortex could still be demonstrated after blockade of the pressor effect by bleeding or Phentolamine administration.
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PMID:Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat. 376 45

Alzheimer patients were treated with lecithin and gradually increasing doses of oral physostigmine during a drug trial to determine if these compounds would improve memory. Memory was measured using a selective reminding task. Of 16 patients, 10 showed improvement in total recall, retrieval from long-term storage and a decrease in intrusions. The optimal dose was 2.0 mg or 2.5 mg of physostigmine per dose for most patients. During a replication study, all 10 patients again responded. During long-term (4 to 20 months) treatment of five patients, most demonstrated continued drug response initially but then lost responsiveness to physostigmine and their dementia progressed. Physostigmine treatment appeared to improve memory with or without concomitant lecithin therapy. However, progressive dementia ensued despite physostigmine therapy. The degree of memory improvement correlated with increasing cerebrospinal fluid cholinesterase inhibition suggesting that memory improvement is associated with entry of physostigmine into the brain.
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PMID:Acute and chronic effects of oral physostigmine and lecithin in Alzheimer's disease. 379 88


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