Decreased Memory Retention Research Articles

Effect of vitamin E on memory retention in rats: Possible involvement of cholinergic system

This study concerned effects of vitamin E and the cholinergic system on memory retention of passive avoidance learning in rats. Post-training intracerebroventricular (i.c.v.) injections were carried out in all experiments. Administrations of vitamin E (10, 25 and 50 μg/rat), nicotine (0.1 μg/rat) and pilocarpine (0.5 μg/rat), the muscarinic receptor agonist increased memory retention, while mecamylamine (0.01, 0.1 and 0.5 μg/rat), the nicotinic receptor antagonist and scopolamine (0.1, 1 and 5 μg/rat), the muscarinic receptor antagonist decreased memory retention. The combination of vitamin E with nicotine or pilocarpine showed potentiation. Effects of mecamylamine or scopolamine were attenuated by vitamin E. It is concluded that vitamin E has a close interaction with cholinergic system in memory retention process.

Involvement of the ventral tegmental area (VTA) in morphine-induced memory retention in morphine-sensitized rats

In the present study, the effects of intra-ventral tegmental area (VTA) injections of morphine on memory retention of a one-trial passive avoidance task have been investigated in morphine-sensitized rats. Retrieval was examined 24 h after training and used as memory retention. Sensitization was obtained by subcutaneous (s.c.) injections of morphine, once daily for 3 and 5 days free of the opioid before training. Post-training administration of the both systemic (2.5, 5 and 7.5 mg/kg, s.c.) and intra-VTA (5 and 7.5 μg/rat) of morphine, dose-dependently decreased memory retention. The response induced by post-training administration of intra-VTA morphine (7.5 μg/rat) was significantly reversed in morphine-sensitized rats. The inhibition of morphine-induced amnesia in morphine-sensitized rats was decreased by once daily injections of naloxone (0.5, 1 and 2 mg/kg, s.c.), SCH 23390 (0.025, 0.05 and 0.1 mg/kg, s.c.) or sulpiride (25, 50 and 100 mg/kg, s.c.), during the sensitization. The results suggest that VTA has an important role in morphine-induced amnesia and morphine sensitization affects this process through opioid and dopamine receptors.

GABAergic system and imipramine-induced impairment of memory retention in rats

In this study, the influence of GABAergic agents, imipramine and their interactions on memory retention have been investigated. Intracerebroventricular (i.c.v.; 1–6 μg/rat) or intraperitoneal (i.p.; 5–40 mg/kg) injection of imipramine decreased memory retention. i.c.v. administration of GABA receptor agonists baclofen and muscimol also reduced memory retention. The combination of i.p. or i.c.v. injection of imipramine with a low dose of muscimol (1 μg/rat, i.c.v.) induced a higher decrease in memory retention. The higher dose of GABA B receptor antagonist CGP35348 [ p-(3-aminopropyl)- p-diethoxymethyl-phosphinic acid] (10 μg/rat) increased memory retention by itself, and decreased the response induced by baclofen or imipramine. Bicuculline (1, 2 and 4 μg/rat, i.c.v.) tends to increase memory retention by itself. Furthermore, bicuculline in same doses reduced the response induced by muscimol or imipramine, but it did not show interaction with the latter drugs. It is concluded that the GABA B receptor mechanism is involved in memory impairment induced by imipramine.

Effects of histamine and cholinergic systems on memory retention of passive avoidance learning in rats

In the present study, the effects of the histamine and cholinergic systems on memory retention in adult male rats were investigated. Post-training intracerebroventricular injections were carried out in all the experiments. Cholinoceptor agonist, acetylcholine (1–10 μg/rat) or nicotine (1–10 μg/rat), increased, while a cholinoceptor antagonist, scopolamine (5–20 μg/rat), decreased memory retention. The response to acetylcholine was attenuated by scopolamine. Administration of histamine (5–20 μg/rat) reduced, but the histamine H 1 receptor antagonist, pyrilamine (10–50 μg/rat), and the histamine H 2 receptor antagonist, cimetidine (1–50 μg/rat), increased memory retention in rats. The histamine receptor antagonists attenuated the response to histamine. Histamine reduced the acetylcholine- or nicotine-induced enhancement. The histamine receptor antagonists enhanced the nicotine- or acetylcholine-induced response. Histamine potentiated the inhibitory effect induced by scopolamine. It is concluded that histaminergic and cholinergic systems have opposing effects on memory retention. Also, the histaminergic system elicits an interaction with the cholinergic system in memory retention.

Effects of intrahippocampal injection of GABAergic drugs on memory retention of passive avoidance learning in rats.

The effect of post-training intrahippocampal injection of gamma-aminobutyric acid (GABA) receptor agonists and antagonists, immediately after a training session on memory retention of passive avoidance learning in rats, was measured in the presence and absence of physostigmine. Post-training treatments were carried out in all the experiments. The different doses of the GABAA receptor agonist muscimol (2, 4 and 6 microg/rat) decreased memory retention in rats dose-dependently. The higher response was obtained with 6 microg/rat of the drug. When the GABAA receptor antagonist bicuculline (0.5, 1, 2 and 4 microg/rat) was administered, only one dose of the drug (1 microg/rat) increased memory retention; however, the antagonist reduced the effect of muscimol. The GABAB receptor agonist, baclofen (0.25, 0.5, 1 and 2 microg/rat) also reduced memory retention in the animals. Intrahippocampal injection of lower doses of the GABAB receptor antagonist CGP35348 (P-[3-aminopropyl]-p-diethoxymethyl-phosphinic acid) (2.5, 5, 10 microg/rat) did not effect memory retention, although the higher doses of the drug (25 and 50 microg/rat) decreased memory retention. The doses of antagonist (2.5, 5 and 10 microg/rat), which did not elicit any response alone, reduced the effect of baclofen. The inhibitory response of CGP35348 was also decreased by bicuculline. In another series of experiments, physostigmine improved memory retention. The GABA receptor agonists, muscimol and baclofen, as well as the GABA receptor antagonists bicuculline and CGP35348, decreased the effect of physostigmine. Atropine decreased memory retention by itself and potentiated the response of muscimol and baclofen. It is concluded that GABAA and GABAB receptor activation may be involved in the impairment of memory retention.

Baclofen-impairment of memory retention in rats: possible interaction with adrenoceptor mechanism(s)

This study concerned the influence of adrenoceptor agonists and antagonists on baclofen-induced impairment of memory retention. Intracerebroventricular injection of baclofen (0.25–2 μg/rat) reduced memory retention in rats. The combination of different doses of baclofen with a low dose of clonidine (0.5 μg/rat) elicited a greater decrease in memory retention. Yohimbine (1 μg/rat) potentiated the response to a low dose, but decreased the response to higher doses of baclofen. Single administration of clonidine (0.5–2 μg/rat) but not yohimbine (1–4 μg/rat) itself decreased memory retention. The combination of clonidine with yohimbine did not show any interaction. The low dose of phenylephrine (0.5 μg/rat) or prazosin (0.5 μg/rat) also potentiated the inhibition of memory retention by baclofen. Phenylephrine (0.5–3 μg/rat) increased, while prazosin (0.5–2 μg/rat) decreased memory retention. The combination of the two drugs showed an interaction. It may be concluded that an adrenoceptor mechanism may interact with the memory retention impairment induced by baclofen.