OBJECTIVETo study the roles of protein synthesis inhibitors in long-term potentiation(LTP) and depotentiation(DP) in hippocampal CA1 region of adult rats.

METHODSStandard extracellular recording technique was used to record field EPSP(fEPSP) evoked by Schaffer collateral stimulation from the CA1 subfield of adult rat hippocampal slices. Paired-pulse low-frequency stimulation(PP-LFS) or high-intensity paired-pulse low-frequency stimulation(HI-PP-LFS) was delivered to induce depotentiation 2 h after LTP induction induced by six theta-burst stimulations. Protein synthesis inhibitors were applied before and after LTP induction to study their roles in LTP and DP in hippocampal CA1 region of adult rats.

RESULTSWhen HI-PP-LFS was applied at 2 h after LTP induction, the depotentiation was induced. The mean fEPSP slopes reduced from 346.2%±26.3% to 207.1%±21.6%. This depotentiation was named as partial LTP depotentiation and maintained at least for 30 min. The percentage of depotentiation was 59.81%. Application of protein synthesis inhibitors, anisomycin and cycloheximide prior to tetanus resulted in smaller LTP compared to control group, and almost complete depotentiation was induced by HI-PP-LFS. With application of protein synthesis inhibitors anisomycin and cycloheximide 90 min after LTP induction, HI-PP-LFS still induced partial LTP depotentiation. However, there was no significant difference in the percentage of depotentiation between this group and control group.

CONCLUSIONHI-PP-LFS partially reverses late phase LTP. When protein synthesis inhibitors are applied prior to tetanus, LTP amplitude is markedly reduced, and HI-PP-LFS completely reverses late-phase LTP. Application of protein synthesis inhibitors after LTP induction does not significantly affect either the amplitude or depotentiation of LTP.

Animals ; CA1 Region, Hippocampal ; drug effects ; In Vitro Techniques ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Protein Synthesis Inhibitors ; pharmacology ; Rats

Animals ; Corticosterone ; pharmacology ; Hippocampus ; drug effects ; physiology ; In Vitro Techniques ; Long-Term Potentiation ; drug effects ; physiology ; Male ; Rats ; Rats, Wistar

Animals ; Environmental Pollutants ; adverse effects ; Hippocampus ; physiopathology ; Humans ; Lead ; adverse effects ; Lead Poisoning ; physiopathology ; Long-Term Potentiation ; drug effects

Nicotine enhances the function of learning and memory, but the underlying mechanism still remains unclear. Hippocampal long-term potentiation (LTP) is assumed to be a cellular mechanism of learning and memory. Our previous experiments showed that with the single pulses evoking 80% of the maximal population spike (PS) amplitude, nicotine (10 μmol/L) induced LTP-like response in the hippocampal CA1 region. In the present study, the nicotinic acetylcholine receptor (nAChR) subtypes and relevant neurotransmitter releases involved in LTP-like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CA1 region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine (1 μmol/L) or κ-bungarotoxin (0.1 μmol/L), but not by dihydro-β-erythtroidine (DHβE, 10 μmol/L). Moreover, it was inhibited by propranolol (10 μmol/L), but not by phentolamine (10 μmol/L) or atropine (10 μmol/L). The results suggest that noradrenaline release secondary to the activation of κ-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CA1 region.
Animals ; Bungarotoxins ; CA1 Region, Hippocampal ; physiology ; Long-Term Potentiation ; drug effects ; Nicotine ; pharmacology ; Norepinephrine ; secretion ; Receptors, Nicotinic ; metabolism

OBJECTIVETo explore the changes in spatial learning performance and long-term potentiation (LTP) which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after administration of melatonin (MT) for two months.

METHODSExperiment was performed in adult male Wistar rats (12 controls, 12 exposed to melatonin treatment, 10 exposed to lead and 10 exposed to lead and melatonin treatment). The lead-exposed rats received 0.2% lead acetate solution from their birth day while the control rats drank tap water. Melatonin (3 mg/kg) or vehicle was administered to the control and lead-exposed rats from the time of their weaning by gastric gavage each day for 60 days, depending on their groups. At the age of 81-90 days, all the animals were subjected to Morris water maze test and then used for extracellular recording of LTP in the dentate gyrus (DG) area of the hippocampus in vivo.

RESULTSLow dose of melatonin given from weaning for two months impaired LTP in the DG area of hippocampus and induced learning and memory deficit in the control rats. When melatonin was administered over a prolonged period to the lead-exposed rats, it exacerbated LTP impairment, learning and memory deficit induced by lead.

CONCLUSIONMelatonin is not suitable for normal and lead-exposed children.

Animals ; Female ; Lead ; toxicity ; Learning ; drug effects ; Long-Term Potentiation ; drug effects ; Male ; Maze Learning ; drug effects ; Melatonin ; administration & dosage ; toxicity ; Rats ; Spatial Behavior ; drug effects

AIMTo study the effects of vitamin E on stress-induced impairments in hippocampus of rats.

METHODSTwenty four male Wistar rats were randomly allocated into four groups: control, stress, control+ VE, stress+ VE. The rat stress model was built by restraining for 6 h/d,21 d. The long-term potentiation was induced in rat hippocampal dentate gyrus (DG) by high-frequency test stimulation.

RESULTSCompared with control group, the rats suffered from restraint stress showed that the number of crossing in open-field test and the content of glucocorticoids in plasma was significantly increased, the changes of amplitude of population spike (PS) were significantly lower. After VE supplementation in stress rats, the indices mentioned above were significantly improved.

CONCLUSIONOpportune supplementation of vitamin E may improve the brain function under stress.

Animals ; Dentate Gyrus ; drug effects ; physiology ; Electric Stimulation ; Hippocampus ; drug effects ; physiology ; Long-Term Potentiation ; drug effects ; Male ; Rats ; Rats, Wistar ; Stress, Physiological ; Vitamin E ; pharmacology

AIMTo study the effect of melatonin on the induction of LTP in CA3 area of hippocampus and to investigated its possible mechanisms.

METHODSMelatonin and other drugs (Tacrine or DNQX) were microinjected into the CA3 area. By using extracellular electrophysiological recordings to observe the changes of the slope of fEPSP in the CA3 area.

RESULTS(1) Evoked potential and the induction of LTP were depressed by different concentration of melatonin (0.2 microg/microl, 1 microg/microl and 5 microg/microl). As the melatonin concentration increased, the induction of LTP was blocked more obviously. (2) Melatonin could attenuate the excitation effect of Tacrine (inhibitor of AChE) on LTP. (3) Inhibition of the melatonin-induced on LTP attenuated by DNQX.

CONCLUSIONThe application of melatonin in rats inhibits the induction of LTP in the hippocampal CA3 area. The action of melatonin on the induction of LTP may be through the modulation of not only non-NMDA receptors but also cholinergic system.

Animals ; CA3 Region, Hippocampal ; drug effects ; physiology ; Electric Stimulation ; Long-Term Potentiation ; drug effects ; Male ; Melatonin ; pharmacology ; Rats ; Rats, Sprague-Dawley

Long-term potentiation (LTP) is thought as a generative mechanism underlying learning and memory via storing information in central nervous system. Electro-neurophysiological assay for LTP is generally used in screening the drugs that can facilitate learning and memory. By using in vivo LTP technique, isolichenin was found to facilitate LTP induction by a tetanic stimulation (20 pulses/100 Hz) in dentate gyrus. This tetanic stimulation by itself, however, cannot induce LTP. Previous study showed the reagent being able to facilitate LTP-induction, like methanol extract of saffron (MES), usually can antagonize the inhibiting effect of 30% ethanol on LTP induction (30 pulses/60 Hz). Isolichenin may also fall into such kind of drugs. Interestingly, comparatively study showed that isolichenin failed to antagonize the inhibiting effect of 30% ethanol on LTP induction (30 pulses/60 Hz). This result indicates a different unknown mechanism existing in the effect of isolichenin on LTP or memory formation.
Animals ; Crocus ; chemistry ; Dentate Gyrus ; drug effects ; physiology ; Long-Term Potentiation ; drug effects ; physiology ; Male ; Plant Extracts ; pharmacology ; Polysaccharides ; pharmacology ; Rats ; Rats, Wistar

OBJECTIVEThe present study investigated the effects of rapamycin on Aβ1-42-induced deficits in working memory and synaptic plasticity.

METHODSAfter bilateral hippocampal injection of Aβ1-42 and rapamycinin rats, spontaneous alternation in Y-maze and in vivo hippocampal long-term potentiation (LTP) of rats were recorded. All data were analized by two-way repeated measures analysis of variance (ANOVA).

RESULTS(Hippocampal injection of Aβ1-42 alone impaired working memory of rats; (2) Rapamycin did not affect working memory of rats, but alleviated Aβ1-42-induced working memory deficits, compared with Aβ1-42 alone group; (Aβ1-42 remarkably suppressed in vivo hippocampal LTP of fEPSPs in the CA1 region; (4) Pretreatment with rapamycin prevented Aβ1-42-induced suppression of LTP.

CONCLUSIONThese data indicates that rapamycin could protect against Aβ1-42-induced impairments in working memory and synaptic plasticity in rats.

Amyloid beta-Peptides ; adverse effects ; Animals ; Hippocampus ; drug effects ; Long-Term Potentiation ; Maze Learning ; Memory, Short-Term ; drug effects ; Neuronal Plasticity ; drug effects ; Peptide Fragments ; adverse effects ; Rats ; Sirolimus ; pharmacology

Animals ; Dementia, Vascular ; drug therapy ; physiopathology ; Hippocampus ; physiopathology ; Isoflavones ; pharmacology ; therapeutic use ; Long-Term Potentiation ; physiology ; Male ; Memory ; drug effects ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission ; physiology