ABSTRACT
The electrochemical behavior of neural implants with 50 microm-diameter platinum electrodes was tested during acute implantations in the motor cortex of anesthetized rats. Custom Ag|AgCl reference electrodes were prepared that could be co-implanted with the probes. The results obtained in vivo are compared with in vitro measurements performed in buffered saline solution (PBS) with and without the addition of bovine serum albumin (BSA). The presence of BSA clearly altered the performance of the electrodes which was studied by means of cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), voltage transient measurements (VT) and monitoring of the open circuit potential (OCP). We found that hydrogen gas evolved at 1.22 A/cm(2) in BSA-free PBS whereas in BSA-containing PBS it occurred already at 0.51 A/cm(2).
Subject(s)
Electrodes, Implanted , Microelectrodes , Motor Cortex/physiology , Motor Cortex/surgery , Animals , Biomedical Engineering , Cattle , Electrochemical Techniques , Equipment Design , In Vitro Techniques , Rats , Serum Albumin, Bovine , Silver , Silver Compounds , Sodium ChlorideABSTRACT
Transient forebrain ischaemia is widely observed in clinical practice. We have examined the effect of a single administration of the cholinesterase inhibitor galanthamine (2mg kg(-1) i.p.) 25 min after reperfusion in male Sprague-Dawley rats (180 +/- 20 g) after a 20-min common carotid artery occlusion. Twenty-four-hours post-ischaemia there was no difference in motor co-ordination or muscle tonus of the rats treated with or without galanthamine as assessed by the rota-rod test. Learning ability was examined using the shuttle-box test, evaluating the latency time and the number of errors for six days in succession. The performance of the ischaemic saline-injected rats was significantly impaired on days 4, 5, 6 (latency time) compared with the non-ischaemic rats and with the ischaemic animals administered galanthamine (P < 0.05). Similar results were obtained when counting the number of errors (failure to cross the cage during conditioned or unconditioned stimulus). The monitoring of body temperature during the first 12-h post-ischaemia did not show any significant difference between the groups. The data showed a beneficial effect of galanthamine on the recovery of learning ability when administered once only post-ischaemia. This suggests a direct effect on the early pathologic mechanisms of CNS damage. Cholinesterase inhibitors may prove useful in the early clinical treatment of ischaemic conditions.
Subject(s)
Cholinesterase Inhibitors/therapeutic use , Galantamine/therapeutic use , Ischemic Attack, Transient/drug therapy , Learning/drug effects , Animals , Male , Rats , Rats, Sprague-DawleyABSTRACT
Different cholinomimetics are used in conditions of CNS acetylcholine (ACh) deficit. In this study, we examined the effect of the acetylcholinesterase inhibitor galanthamine in a prolonged alcohol intake model of ACh deficit in male Wistar rats. After 16 weeks of alcohol intake and a 2-week pause, rats administered galanthamine (2.5 mg/kg/day i.p.) showed an improved speed of learning and short-term memory in the shuttle box test as compared to the saline-injected alcoholic group (p < 0.05). Four weeks later, significant improvement in the passive avoidance memory of alcoholic galanthamine-treated rats was noted in the eight-arm radial maze (14 day test duration) as compared to the saline-injected alcoholic group (p < 0.05). During the first week in the shuttle box test, the nonalcoholic galanthamine-treated animals exhibited significantly impaired performance as compared to the untreated nonalcoholic control, while four weeks later, in the eight-arm radial maze, both groups did not differ. Our results show that galanthamine improves the speed of learning, short-term memory and spatial orientation of rats in conditions of prolonged alcohol intake.
Subject(s)
Acetylcholine/deficiency , Cholinesterase Inhibitors/pharmacology , Ethanol/adverse effects , Galantamine/pharmacology , Learning/drug effects , Memory, Short-Term/drug effects , Animals , Avoidance Learning/drug effects , Behavior, Animal/drug effects , Drug Antagonism , Male , Rats , Rats, Wistar , Spatial Behavior/drug effects , Time FactorsABSTRACT
In this study the effect of dexamethasone on the motoneuronal cell death and the nuclear and somatic morphology changes occurring after peripheral nerve transection in the neonatal rats has been determined. The study was performed on 3 day old Wistar rats. Animals were divided into 3 groups--control, axotomised, and axotomised and dexamethasone-treated. The nerve transection was performed bilaterally. A dose of 0.5 mg/kg/24h dexamethasone, administered i.p., was used. On day 7 after the operation the animals were sacrificed and the motoneurons in segments L4 and L5 in the spinal cord were counted and their morphology was analysed. 25. 88% cell loss was found in the axotomised group (p<0.001 vs. control) versus 43.33% cell loss in the dexamethasone-treated and axotomised animals (p<0.01 vs. control). Dexamethasone significantly decreased the number of the surviving motoneurons (p<0.05 vs. axotomised). The axotomised group showed enlargement of the somatic area and the maximal and minimal diameters of the cell while the dexamethasone-treated and axotomised group showed soma shrinkage and decrease in the minimal cell diameter. Our results propose a possible hazard towards the application of dexamethasone in the treatment of new-borns with concomitant nerve injuries.
