Modulation of Learning and Memory: Effects of Drugs Influencing Neurotransmitters

Hunter, Bruce E.; Zornetzer, Steven F.; Jarvik, Murray E.; McGaugh, James L.

doi:10.1007/978-1-4684-3180-3_11

Cited by 63 publications

(24 citation statements)

References 188 publications

(260 reference statements)

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“…Since we administered the drugs just before the acquisition trial, potential drug actions on cognitive function may be confounded by effects of the agent on non-specific processes, such as attention, arousal or sensory motor functions (Hunter et al 1988). To rule out this possibility, we evaluated the locomotor activity to determine any motor disability that might affect inhibitory avoidance performance.…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of ellagic acid against animal models of scopolamine- and diazepam-induced cognitive impairments

Mansouri

Farbood

Naghizadeh

et al. 2016

Pharmaceutical Biology

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(2016) Beneficial effects of ellagic acid against animal models of scopolamine-and diazepam-induced cognitive impairments, Pharmaceutical Biology, 54:10, 1947-1953, DOI: 10.3109/13880209.2015 PHARMACEUTICAL BIOLOGY, 2016 VOL. 54, NO. 10, 1947-1953 http://dx.doi.org/10.3109/13880209.2015 Context In a previous study, it has been shown that ellagic acid (EA), a polyphenolic compound found in pomegranate and different berries, prevents cognitive and hippocampal long-term potentiation (LTP) impairments induced by traumatic brain injury in rats through antioxidant and anti-inflammatory mechanisms.Objective The present study was conducted to assess the potential of EA as a memory enhancer. Materials and methodsThe elevated plus maze (EPM) and passive avoidance (PA) paradigm were used to evaluate learning and memory parameters. Three doses (10, 30 and 100 mg/kg, i.p.) of EA were administered to animals. Memory impairment was induced by scopolamine treatment (0.4 mg/kg, i.p.) and/or diazepam (1 mg/kg, i.p.). Acquisition trials were carried out 30 min after scopolamine treatment and retention trials were performed for 5 min 24 h after the acquisition trials.Results EA at doses 30 and 100 mg/kg significantly reversed the amnesia induced by scopolamine (0.4 mg/kg, i.p.) in the EPM and PA tests in mice. Also, EA at doses 30 and 100 mg/kg significantly antagonized the amnesia induced by diazepam (1 mg/kg, i.p.) in EPM test in rats. Moreover, chronic administration of EA at dose 30 mg/kg ameliorated the memory deficit induced by diazepam (1 mg/ kg, i.p.) in rats. Discussion and conclusion This study demonstrates that ellagic acid is effective in preventing scopolamine-and diazepam-induced cognitive impairments without altering the animals' locomotion. This suggests the potential of EA application as a useful memory restorative agent in the treatment of dementia seen in elderly persons.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Beneficial effects of ellagic acid against animal models of scopolamine- and diazepam-induced cognitive impairments

Mansouri

Farbood

Naghizadeh

et al. 2016

Pharmaceutical Biology

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“…Nicotine has been proposed for the potential treatment of Alzheimer's disease because of its ability to improve a variety of spatial memory and non-spatial avoidance tasks in animals and to enhance delayed recall, focused attention, and other memory-related behaviors in humans [ Henningfield and Goldberg, 1984;Hunter et al, 1977;Warburton, 1990;Levin, 19921. While the results of initial studies with nicotine in Alzheimer's disease have been promising [Newhouse et al, 1988;Sahakian et al, 19891, ing performance.…”

Section: Introductionmentioning

confidence: 99%

Effects of anabaseine‐related analogs on rat brain nicotinic receptor binding and on avoidance behaviors

Meyer

Fiebre

Hunter

et al. 1994

Drug Development Research

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Several novel anabaseine-derived compounds were investigated with respect to their ability to displace high affinity [3H]cytisine binding in rat brain membranes, as well as their ability to improve passive and active avoidance behaviors in nucleus basalis-lesioned rats. The avoidance behavior in bilaterally nucleus basalis-lesioned rats was improved by each of these drugs to an extent comparable to that observed with (-)-nicotine. The relative potencies of these compounds for improving this behavior exhibited a pattern very similar to their affinities for displacing[3H]cytisine binding (nicotine > anabaseine > DMXB > DMAB = DMAC > anabasine). Acquisition of active avoidance behavior was slower in unilaterally and bilaterally nucleus basalis-lesioned rats than unlesioned controls; (-)-nicotine improved acquisition behavior only in the former group. At doses that improved passive avoidance behavior, DMXB also improved acquisition of active avoidance behavior in unilaterally lesioned rats, while DMAB and DMAC did not. (-)Nicotine and DMXB had no effect on escape behavior in the active avoidance task at doses that improved retention of avoidance behavior itself. These results suggest that anabaseine and several of its analogs bind to brain a4p2 nicotinic receptors and mimic non-spatial, memory-related behaviors in a nicotine-like manner.

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“…A large body of evidence indicates that catechol amines may be involved in the modulation of learning and memory Hunter et al, 1977;McGaugh, 1983;Squire and Davis, 1981], Additionally, numerous age-related changes in catecholamines have been reported in human and animal studies [Kubanis and Zometzer, 1981;Zornetzer, 1985]. For example, norepinephrine and dopamine levels in specific regions of human and animal brains decline with aging.…”

Section: Catecholaminesmentioning

confidence: 99%

“…Numerous studies have shown that learning and memory are affected by treatments that influence var ious neurotransmitter, neuropeptide, and hormonal sys tems [Hunter et al, 1977;McGaugh, 1983;Squire and Davis, 1981]. Neurochemical evidence at many levels indicates that many of these systems are particularly sus ceptible to age-related disturbances [Algeri et al, 1983;Kubanis and Zometzer, 1981;Winblad et al, 1985].…”

Section: Neurotransmitter and Neuropeptidesmentioning

confidence: 99%

“…In young animals, an increasing number of drug studies has suggested that drugs which disrupt cat echolamine systems disrupt memory storage, while cate cholamine agonists produce dose-dependent facilitation or disruption [Gold et al, 1982;Hunter et al, 1977;McGaugh, 1983], For example, amphetamine shows no effect at low doses, improvement at a restricted range of doses, and impairment at higher doses.…”

Section: Catecholaminesmentioning

confidence: 99%

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Drug Influences on Learning and Memory in Aged Animals and Humans

Hock¹

1987

Neuropsychobiology

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In this article the effects of neurotransmitter systems or specific drugs on cognitive functions of aged animals and humans are reviewed. While there have been used many different pharmacologic and behavioral approaches to treat and test cognitive deficits in aged animals and geriatric or demented patients, there is still the question of the validity of animal models of human disorders. Attempts are made to show that there are parallels and similarities. These similarities suggest that the neurological and neurochemical changes observed may play common roles in similar behavioral deficits observed in aged animals and humans.

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Modulation of Learning and Memory: Effects of Drugs Influencing Neurotransmitters

Cited by 63 publications

References 188 publications

Beneficial effects of ellagic acid against animal models of scopolamine- and diazepam-induced cognitive impairments

Beneficial effects of ellagic acid against animal models of scopolamine- and diazepam-induced cognitive impairments

Effects of anabaseine‐related analogs on rat brain nicotinic receptor binding and on avoidance behaviors

Drug Influences on Learning and Memory in Aged Animals and Humans

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