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1.
Braz. J. Psychiatry (São Paulo, 1999, Impr.) ; 40(2): 128-137, Apr.-June 2018. tab, graf
Article in English | LILACS | ID: biblio-959226

ABSTRACT

Objective: To explore how a genetically-influenced characteristic (the level of response to alcohol [LR]), ethnicity, and sex relate to environmental and attitudinal characteristics (peer drinking [PEER], drinking to cope [COPE], and alcohol expectancies [EXPECT]) regarding future alcohol-related blackouts (ARBs). Methods: Structural equation models (SEMs) were used to evaluate how baseline variables related to ARB patterns in 462 college students over 55 weeks. Data were extracted from a longitudinal study of heavy drinking and its consequences at a U.S. university. Results: In the SEM analysis, female sex and Asian ethnicity directly predicted future ARBs (beta weights 0.10 and -0.11, respectively), while all other variables had indirect impacts on ARBs through alcohol quantities (beta weights ~ 0.23 for European American ethnicity and low LR, 0.21 for cannabis use and COPE, and 0.44 for PEER). Alcohol quantities then related to ARBs with beta = 0.44. The SEM explained 23% of the variance. Conclusion: These data may be useful in identifying college students who are more likely to experience future ARBs over a 1-year period. They enhance our understanding of whether the relationships of predictors to ARBs are direct or mediated through baseline drinking patterns, information that may be useful in prevention strategies for ARBs.


Subject(s)
Humans , Male , Female , Adolescent , Alcohol Drinking/adverse effects , Alcohol Drinking in College/ethnology , Amnesia/chemically induced , Socioeconomic Factors , Students/psychology , Students/statistics & numerical data , Universities , Alcohol Drinking/prevention & control , Alcohol Drinking/psychology , Marijuana Smoking/adverse effects , Marijuana Smoking/psychology , Ethnicity , Sex Factors , Risk Factors , Longitudinal Studies , Amnesia/psychology
2.
Acta cir. bras ; 31(8): 520-526, Aug. 2016. tab, graf
Article in English | LILACS | ID: lil-792414

ABSTRACT

ABSTRACT PURPOSE: To evaluated the long-term effect of scopolamine and sesame oil on spatial memory. METHODS: Memory impairment induced by Intracerebroventricular (ICV) injection of scopolamine hydrochloride (10 μg/ rat). Animals were gavaged for 4 weeks with saline, sesame oil (0.5, 1, or 2 mL/kg/day), or 3 weeks with memantine (30 mg/kg/day) in advance to induction of amnesia. Morris water maze (MWM) test was conducted 6 days after microinjection of scopolamine. Then, blood and brain samples were collected and evaluated for the malondialdehyde (MDA) levels, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities, and total antioxidant status (TAS) and ferric reducing ability of plasma (FRAP). RESULTS: Scopolamine significantly decreased traveled distance and time spent in target quadrant in probe test. Pretreatment of rats with sesame oil (0.5 mg/kg) mitigated scopolamine-induced behavioral alterations. Measurement of MDA, SOD, and GPX in brain tissue, and FRAP and TAS in blood showed little changes in animals which had received scopolamine or sesame oil. CONCLUSIONS: Intracerebroventricular injection of scopolamine has a residual effect on memory after six days. Sesame oil has an improving effect on spatial memory; however this effect is possibly mediated by mechanisms other than antioxidant effect of sesame oil.


Subject(s)
Animals , Male , Rats , Scopolamine/adverse effects , Sesame Oil/administration & dosage , Amnesia/drug therapy , Adjuvants, Anesthesia/adverse effects , Antioxidants/administration & dosage , Superoxide Dismutase/chemistry , Ferric Compounds/chemistry , Rats, Wistar , Oxidative Stress/drug effects , Maze Learning , Disease Models, Animal , Alzheimer Disease/prevention & control , Glutathione Peroxidase/chemistry , Amnesia/chemically induced , Injections, Intraventricular , Memory/drug effects , Antioxidants/chemistry
3.
Indian J Exp Biol ; 2013 Dec; 51(12): 1094-1100
Article in English | IMSEAR | ID: sea-150297

ABSTRACT

Chronic administration of aged garlic extract has been shown to prevent memory impairment in mice. Acute and chronic (21 days) effects of marketed formulation of crude garlic extract (Lasuna) were evaluated on learning and memory in mice using step down latency (SDL) by passive avoidance response and transfer latency (TL) using elevated plus maze. Scopolamine (0.4 mg/kg, ip) was used to induce amnesia in mice and piracetam (200 mg/kg, ip) served as positive control. In the acute study, Lasuna (65 mg/kg, po) partially reversed the scopolamine-induced amnesia but failed to improve learning and memory in untreated animals. Chronic administration of Lasuna (40 mg/kg/day for 21 days) significantly improved learning both in control and scopolamine induced amnesic animals. Influence of Lasuna on central cholinergic activity and its antioxidant properties were also studied by estimating the cortical acetylcholinesterase (AchE) activity and reduced glutathione (GSH) levels respectively. Chronic administration of Lasuna inhibited AchE, while increasing GSH levels. Thus the results indicate that long-term administration of crude garlic extract may improve learning and memory in mice while the underlying mechanism of action may be attributed to the anti-AchE activity and anti-oxidant property of garlic.


Subject(s)
Acetylcholinesterase/metabolism , Amnesia/chemically induced , Amnesia/drug therapy , Amnesia/metabolism , Amnesia/pathology , Animals , Antioxidants/administration & dosage , Antioxidants/chemistry , Avoidance Learning/drug effects , Brain/drug effects , Brain/metabolism , Garlic/chemistry , Glutathione/metabolism , Humans , Learning/drug effects , Maze Learning/drug effects , Memory/drug effects , Mice , Oxidative Stress , Plant Extracts/administration & dosage , Plant Extracts/chemistry , Scopolamine/toxicity
4.
Int. j. morphol ; 30(2): 388-393, jun. 2012. ilus
Article in English | LILACS | ID: lil-651801

ABSTRACT

As neuron­astrocyte interactions play a crucial role in the adult brain, it is thought that astrocytes support learning and memory through specific mechanisms. In this study, the effect of scopolamine based amnesia on the number of astrocytes in rats' hippocampus was studied. Adult male albino Wistar rats were bilaterally cannulated into the CA1 region and animals received saline or different doses of scopolamine (0.5, 1 and 2 mg/ rat, intra - CA1), immediately after training. Then all the rats were sacrificed and coronal sections were taken from the dorsal hippocampal formation of the right cerebral hemispheres and stained with PTAH. The area densities of the astrocytes in dentate gyrus were measured and compared in the all groups (p < 0.05). Data showed that post-training scopolamine (0.5, 1 and 2 ug/rat, intra-CA1) dose-dependently reduced the step-through latency in the inhibitory avoidance task, showing scopolamine-induced amnesia. Also we found different response of astrocytes in different subfields of hippocampal formation. In dentate gyrus the number of astrocytes was increased, but in other areas scopolamine can decreased the density of astrocytes. We concluded that scopolamine can cause amnesia and this phenomenon can have an effect on astrocyte numbers in the rats hippocampal formation.


Las interacciones neuronas-astrocitos desempeñan un papel crucial en el cerebro adulto, y se cree que los astrocitos apoyan el aprendizaje y la memoria a través de mecanismos específicos. Fue estudiado el efecto de amnesia inducida por escopolamina en el número de astrocitos del hipocampo de ratas. Ratas Wistar albinas macho adultas fueron canuladas bilateralmente en la región CA1 recibiendo solución salina o diferentes dosis de escopolamina (0,5, 1 y 2mg/rata, intra - CA1), inmediatamente después del entrenamiento. Luego, todas las ratas se sacrificaron y se tomaron secciones coronales de la formación del hipocampo dorsal del hemisferio cerebral derecho y se tiñeron con PTAH. Las densidades de área de los astrocitos en el giro dentado fueron medidas y comparadas en todos los grupos (p <0,05). Los datos mostraron que la escopolamina (0,5, 1 y 2 mg / rata, intra-CA1) dosis-dependiente post-entrenamiento redujo el paso de latencia de la tarea de evitación inhibitoria, mostrando amnesia inducida por escopolamina. También encontramos diferentes respuestas de los astrocitos en los distintos subcampos de la formación hipocampal. En el giro dentado, el número de astrocitos se incrementó, pero en otras áreas la escopolamina pudo disminuir la densidad de los astrocitos. Se concluye que la escopolamina puede causar amnesia y este fenómeno puede afectar el número astrocitos en la formación hipocampal de ratas.


Subject(s)
Animals , Rats , Amnesia/chemically induced , Astrocytes , Scopolamine/pharmacology , Hippocampus/pathology , Adjuvants, Anesthesia/pharmacology , Amnesia/pathology , Hippocampus , Rats, Wistar
5.
Indian J Biochem Biophys ; 2011 June; 48(3): 197-201
Article in English | IMSEAR | ID: sea-135320

ABSTRACT

The neuroprotective potential of ethanolic extract of roots of Pseudarthria viscida (L) Wight and Arn (EEPV) was investigated against -amyloid(25-35)-induced amnesia in mice which is a suitable animal model for Alzheimer’s disease (AD). The senile plaques of -amyloid (A) are major constituents accumulated during the progression of AD as a potent neurotoxicant. In our investigation, intracerebroventricular injection of A(25-35) in mice induced the neurodegeneration, exhibited the increased time of escape latency in behavioral pattern using water maze and decreased the levels of antioxidants namley superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and vitamin C with elevated level of acetylcholinesterase enzyme (AChE). The neuroprotective potential of EEPV was determined by behavioral pattern using water maze and biochemical parameters such as SOD, CAT and GPx and vitamin C content as well as AChE. Mice were treated with EEPV at 200 and 400 mg/kg doses for 21 days. Except control, all animals received a single injection of neurotoxicant A(25-35) on 14th day. In behavioural assessment, treatment with ethanolic extract improved the cognitive function in the water maze and attenuated the elevated levels of AChE with increase in antioxidant enzymes, indicating the neuroprotection with increased levels of vitamin C. These findings suggest that ethanolic extract of P. viscida exerts anti-amnesiac effects and enhances cognitive function.


Subject(s)
Acetylcholinesterase/drug effects , Acetylcholinesterase/metabolism , Alzheimer Disease/chemically induced , Alzheimer Disease/drug therapy , Alzheimer Disease/enzymology , Alzheimer Disease/pathology , Amnesia/chemically induced , Amnesia/drug therapy , Amnesia/enzymology , Amnesia/pathology , Amyloid beta-Peptides , Animals , Antioxidants/administration & dosage , Behavior, Animal/drug effects , Catalase/drug effects , Catalase/metabolism , Disease Models, Animal , Glutathione Peroxidase/drug effects , Glutathione Peroxidase/metabolism , Lipid Peroxidation/drug effects , Male , Maze Learning/drug effects , Mice , Neuroprotective Agents/administration & dosage , Plant Extracts/administration & dosage , Superoxide Dismutase/drug effects , Superoxide Dismutase/metabolism
6.
Archives of Iranian Medicine. 2010; 13 (3): 209-216
in English | IMEMR | ID: emr-105359

ABSTRACT

Repeated administration of certain drugs could result in an enhancement of the behavioral effects of those drugs. In the present study, the effect of repeated administration of histamine on amnesia induced by post-training administration of the drug was examined. A single trial step-down inhibitory [passive] avoidance task was used for memory assessment in male NMRI mice. The results showed that post-training administration of different doses of histamine [5, 10, and 20 micro g/mouse, i.c.v.] decreased the step-down latency on the test day. Repeated pretreatment of histamine [10 and 20 micro g/mouse] for three days followed by five days of no drug treatment prevented amnesia due to post-training histamine [20 micro g/mouse]. In contrast, repeated administration of histamine H1 receptor antagonist, pyrilamine [5, 10, and 20 mg/kg] or histamine H2 receptor antagonist, ranitidine [12.5 and 25 mg/kg] 10 minutes prior to histamine injections, decreased the effect of repeated histamine administration. Moreover, a similar pattern was seen in animals which received dopamine D1 receptor antagonist, SCH 23390 [0.025, 0.5, and 1 mg/kg] or dopamine D2 receptor antagonist, sulpiride [0.2, 1, and 5 mg/kg] 10 minutes prior to histamine injections during the repeated pretreatment. The results indicated that both the histamine and dopamine receptor mechanisms may be involved in the effects of repeated pretreatment of histamine on drug induced amnesia


Subject(s)
Male , Animals, Laboratory , Amnesia/prevention & control , Dopamine Antagonists/pharmacology , Behavior, Animal/drug effects , Amnesia/chemically induced , Avoidance Learning/drug effects , Statistics, Nonparametric , Mice, Inbred Strains , Disease Models, Animal , Probability , Random Allocation , Dose-Response Relationship, Drug
7.
Indian J Exp Biol ; 2006 Feb; 44(2): 133-6
Article in English | IMSEAR | ID: sea-61916

ABSTRACT

Dementia is one of the age related mental problems and a characteristic symptom of various neurodegenerative disorders including Alzheimer's disease. Certain drugs like diazepam, barbiturates and alcohol disrupt learning and memory in animals and man. However, a new class of drugs known as nootropic agents is now used in situations where there is organic disorder in learning abilities. The present work was undertaken to assess the potential of O. sanctum extract as a nootropic and anti-amnesic agent in mice. Aqueous extract of dried whole plant of O. sanctum ameliorated the amnesic effect of scopolamine (0.4 mg/kg), diazepam (1 mg/kg) and aging induced memory deficits in mice. Elevated plus maze and passive avoidance paradigm served as the exteroceptive behavioral models. O. sanctum extract decreased transfer latency and increased step down latency, when compared to control (piracetam treated), scopolamine and aged groups of mice significantly. O. sanctum preparations could of beneficial in the treatment of cognitive disorders such as dementia and Alzheimer's disease.


Subject(s)
Alzheimer Disease/drug therapy , Amnesia/chemically induced , Animals , Dementia/drug therapy , Diazepam , Dose-Response Relationship, Drug , Humans , Maze Learning/drug effects , Memory Disorders/chemically induced , Mice , Nootropic Agents/administration & dosage , Ocimum/chemistry , Phytotherapy , Piracetam/pharmacology , Plant Extracts/therapeutic use , Plants, Medicinal , Scopolamine/pharmacology
8.
Indian J Exp Biol ; 2005 Jul; 43(7): 640-5
Article in English | IMSEAR | ID: sea-55612

ABSTRACT

To investigate the effect of bacosides (alcoholic extract of brahmi) on scopolamine (3 mg kg(-1), ip), sodium nitrite (75 mg kg(-1), ip) and BN52021 (15 mg kg(-1), ip) induced experimental amnesia in mice, using Morris water maze test, all the agents were administered 30 min before the acquisition trials on each day and repeated for 4 consecutive days, and on 5th day during the retrieval trials. Bacosides on anterograde administration (before training) in mice, significantly decreased the escape latency time (ELT) during the acquisition trials for 4 consecutive days and increased the time spent (TS) in target quadrant during the retrieval trials on 5th day, and on retrograde administration (after training) bacosides were found not to affect TS significantly. Bacosides also significantly decreased the ELT and increased the TS in mice treated anterogradely with scopolamine and sodium nitrite. Bacosides did not exhibit any significant effect on TS of mice treated retrogradely with sodium nitrite. On the other hand, bacosides significantly increased the TS of mice treated retrogradely with BN52021. On the basis of the present results it can be concluded that bacosides facilitate anterograde memory and attenuate anterograde experimental amnesia induced by scopolamine and sodium nitrite possibly by improving acetylcholine level and hypoxic conditions, respectively. Beside this bacosides also reversed BN52021 induced retrograde amnesia, probably due to increase in platelet activating factor (PAF) synthesis by enhancing cerebral glutamate level.


Subject(s)
Amnesia/chemically induced , Animals , Bacopa , Diterpenes/toxicity , Female , Ginkgolides , Lactones/toxicity , Male , Maze Learning/drug effects , Memory/drug effects , Mice , Phytotherapy , Plant Extracts/pharmacology , Saponins/pharmacology , Scopolamine/toxicity , Sodium Nitrite/toxicity , Triterpenes/pharmacology
9.
Indian J Physiol Pharmacol ; 2003 Jul; 47(3): 318-24
Article in English | IMSEAR | ID: sea-108272

ABSTRACT

Sildenafil (Viagra) has been introduced recently in market to correct male impotency and has gained immense popularity for its dramatic effects all over the world. The present study was designed to investigate the effect of sildenafil on learning and memory in mice using elevated plus maze. A total of XV groups of animals were employed in the present study. Central cholinergic pathways play a crucial role in learning and memory processes. Physostigmine, an anticholinesterase agent (0.5 mg, 1.0 mg kg(-1), i.p) was employed for its memory enhancing property and alprazolam a benzodiazepine receptor agonist served as a memory-impairing agent. In the present study, alprazolam produced anterograde amnesia (at 0.5 mg kg(-1), i.p) and retrograde amnesia (at 0.25 mg, 0.5 mg, 0.75 mg kg(-1), i.p.) in separate groups of animals. Caffeine at 5 mg, 10 mg and 20 mg kg(-1), i.p. (an established psychostimulant) did not show any significant change in learning and memory of mice. Sildenafil (at 8 mg kg(-1), i.p.) administered 30 minutes prior to training on first day produced a marginal decrease in transfer latency time on first day; whereas, sildenafil (at 2 mg, 4 mg, 8 mg kg(-1), i.p.) administered immediately after training on first day produced a dose-dependent improvement of memory in mice. However, further studies need to be carried out to elucidate the underlying mechanism of sildenafil as a memory enhancer.


Subject(s)
Alprazolam/pharmacology , Amnesia/chemically induced , Animals , Caffeine/pharmacology , Cholinesterase Inhibitors/pharmacology , Dose-Response Relationship, Drug , Female , GABA Modulators/pharmacology , Learning/drug effects , Male , Maze Learning/drug effects , Memory/drug effects , Mice , Phosphodiesterase Inhibitors/pharmacology , Physostigmine/pharmacology , Piperazines/pharmacology , Purines , Receptors, GABA-A/antagonists & inhibitors , Sulfones , Transfer, Psychology/drug effects
10.
Rev. bras. anestesiol ; 52(1): 114-123, fev. 2002. ilus
Article in English, Portuguese | LILACS | ID: lil-311168

ABSTRACT

Justificativa e Objetivos - Estudos clínicos e experimentais têm sido desenvolvidos para identificar os locais onde os anestésicos (inalatórios) atuam e para determinar quais as alterações funcionais que esses fármacos produzem nas estruturas do sistema nervoso central determinantes do estado de anestesia que é observado clinicamente. O objetivo deste trabalho é descrever os resultados obtidos por vários autores em estudos clínicos e experimentais realizados recentemente na tentativa de esclarecer os mecanismos de ação dos anestésicos inalatórios no sistema nervoso central. Conteúdo - Para facilitar a compreensão dos complexos mecanismos de ação dos anestésicos inalatórios no sistema nervoso central, eles foram divididos em três níveis: o macroscópico, o microscópico e o molecular. Recentemente um grupo de autores descreveram estes mecanismos de ação em: orgânicos, celulares, e inibidores da entropia. Estes mecanismos tentariam explicar o estado de anestesia que teria como característica a capacidade de prover ao paciente duas ações principais: 1) imobilidade, inibição da resposta a estímulos nociceptivos; 2) amnésia. Outros efeitos (desejáveis) também são obtidos pela administração de anestésicos: analgesia e hipnose. Entretanto, tais efeitos seja isoladamente ou juntos, não definem o estado de anestesia. Embasados nestes conceitos, este grupo adota e divulga a classificação dos anestésicos em : 1) anestésicos completos, os que produzem imobilidade e amnésia; 2) incompletos ou não imobilizantes, os que não produzem imobilidade mas produzem amnésia. Conclusões - De acordo com os resultados de vários estudos realizados recentemente, provavelmente a amnésia e a inconsciência ocorrem pela ação do anestésico predominantemente no cérebro, enquanto a imobilidade, ou seja, a inibição da resposta ao estímulo nocicptivo por movimento, seria pela ação do anestésico preferencialmente e inicialmente na medula espinhal. Estas ações ocorrem por inibição da transformação de energia (entropia) que forma os potenciais de ação nas células (fibras) nervosas, especialmente nas sinapses


Subject(s)
Humans , Unconsciousness , Central Nervous System , Amnesia/chemically induced , Anesthetics, Inhalation/pharmacology
11.
Article in English | IMSEAR | ID: sea-47699

ABSTRACT

BACKGROUND: Whether the human brain is nothing but an advanced computer is a matter of inconclusive debate. This paper contributes to that debate. METHOD: Critical reasoning based on evidence provided by the history of a woman who complained of amnesia after each of two separate acts of attempted suicide. FINDINGS: A life-threatening tendency (suicidal impulses) may be countered by a functional imperfection (selective amnesia) or a feigned malfunction (malingering). INTERPRETATION: Some aspects of brain function may depend on operations that no hitherto invented computer can duplicate.


Subject(s)
Adult , Amnesia/chemically induced , Brain/physiopathology , Female , Humans , Drug Overdose , Pentobarbital/poisoning , Philosophy, Medical , Suicide, Attempted
12.
Odontol. chil ; 43(2): 113-6, dic. 1995. ilus, tab
Article in Spanish | LILACS | ID: lil-193888

ABSTRACT

Se realizó un estudio doble ciego, comparativo y prospectivo de la capacidad de producir amnesia anterógrada del flunitrazepam versus midazolam, administrados por vía oral, frente a percepciones visuales y auditivas, en 30 pacientes de ambos sexos, de edad promedio 27,9 años. Se concluye que la diferencia encontrada de los efectos amnésicos producidos por ambos medicamentos, medida en términos cuantitativos, utilizando el test T con un p menor 0,05, resultó no ser estadísticamente signiticativa


Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Amnesia/chemically induced , Dental Anxiety/drug therapy , Flunitrazepam/pharmacology , Midazolam/pharmacology , Eidetic Imagery
13.
Ciênc. cult. (Säo Paulo) ; 47(4): 252-6, jul.-ago. 1995. ilus
Article in English | LILACS | ID: lil-164746

ABSTRACT

Nitric oxide (NO), carbon monoxide (CO), the platelet-activating factor (PAF) and arachidonic acid are released by stimulated neurons, enhance glutamate release at nerve terminals and have been proposed as synaptic messengers involved in plastic phenomena, such as the long-term potentiation of glutamatergic synapses. Long-term potentiation has been suggested to be a basic mechanism of memory processes. The microinjection of inhibitors of the synthesis of NO and CO or of antagonists of the receptors to PAF into brain structures known to be involved in memory (hippocampus, amygdala, entorhinal cortex), during its early phases, causes amnesia. This indicates that NO, CO and PAF modulate the early phases of memory, perhaps by modulating long-term potentiation. In addition, microinjections of a NO releaser or of a soluble form of PAF into the hippocampus produce memory enhancement.


Subject(s)
Animals , Rats , Amygdala/drug effects , Entorhinal Cortex , Platelet Activating Factor/pharmacology , Hippocampus/drug effects , Memory/drug effects , Carbon Monoxide/pharmacology , Nitric Oxide/pharmacology , Amnesia/chemically induced , Synaptic Transmission
14.
Odontol. chil ; 43(1): 53-6, abr. 1995. ilus, tab
Article in Spanish | LILACS | ID: lil-193876

ABSTRACT

Se realizó un estudio comparativo prospectivo longitudinal de la capacidad de producir amnesia anterógrada del diazepam versus midazolam endovenoso, frente a percepciones visuales y auditivas en 30 pacientes ASA I de ambos sexos, edad promedio 24 años. Se utilizó el test estadístico Mann-Whitney y el arco del seno. Se concluye que existe una mayor potencia del efecto amnésico producido por midazolam en relación al diazepam


Subject(s)
Humans , Male , Female , Amnesia/chemically induced , Dental Anxiety/drug therapy , Diazepam/administration & dosage , Eidetic Imagery , Midazolam/administration & dosage , Molar, Third/surgery , Tooth, Impacted/surgery
15.
J. bras. psiquiatr ; 42(10): 517-27, nov.-dez. 1993.
Article in Portuguese | LILACS | ID: lil-154085

ABSTRACT

Neste artigo, o terceiro e último de uma série, nós descrevemos três síndromes dismnésticas associadas ao uso de benzodiazepínicos: esquecimento benigno, confabulaçöes e amnésia transitória global. Em seguida, apresentamos um levantamento de algumas modalidades de efeitos adversos encontradas em uma amostra de 70 pacientes com fobia social submetidos a tratamento prolongado com clonazepam


Subject(s)
Humans , Male , Female , Adult , Amnesia/chemically induced , Anti-Anxiety Agents/adverse effects , Clonazepam/adverse effects , Clonazepam/administration & dosage , Clonazepam/therapeutic use , Clonazepam/toxicity , Midazolam/adverse effects , Social Behavior Disorders/chemically induced , Phobic Disorders/drug therapy , Triazolam/adverse effects
16.
J. bras. psiquiatr ; 42(9): 463-8, out. 1993. ilus
Article in Portuguese | LILACS | ID: lil-154080

ABSTRACT

Neste artigo, o segundo de uma série de três, prosseguimos na revisäo da segurança e tolerância dos benzodiazepínicos, analisando seu potencial de induzir déficit cognitivo global - agudo, sob a forma de delirium e crônico, na demência - e seletivo - ao interferirem no funcionamento normal da memória


Subject(s)
Humans , Male , Middle Aged , Anti-Anxiety Agents/adverse effects , Delirium/chemically induced , Memory/drug effects , Amnesia/chemically induced , Dementia/chemically induced , Lorazepam/adverse effects , Memory Disorders/chemically induced
18.
Braz. j. med. biol. res ; 22(9): 1121-5, 1989. tab
Article in English | LILACS | ID: lil-83187

ABSTRACT

Rats were trained in a step-down inhibitory avoidance task and retrieval was measured during a test session conducted 24 h after training. The ip administration of a low dose of gamma-endorphin (0.2 microng/kg) immediately after training reduced retrieval time from 40.6 to 13.5 s (N = 15). Higher doses of gamma-endorphin given 5 min before testing (1.0 microng/kg) or immediately after training (5 microng/kg) enhanced retrieval time from 38.6 to 300 s (N = 15) and from 40.6 to 104.4 s (N = 15). All of these effects were either after training or before testing had no effect on retrieval. Since at least the amnestic effect of gamma-endorphin is similar to that of beta-endorphin, and gamma-endorphin is a possible metabolite of beta-endorphin by limited proteolysis of the carboxyl-terminal amino acid, it is suggested that at least some effects of beta-endorphin on memory may be mediated by its proteolysis product, gamma-endorphin


Subject(s)
Rats , Animals , Male , Avoidance Learning , Endorphins/pharmacology , Escape Reaction , Retention, Psychology , Amnesia/chemically induced , Analysis of Variance , Cerebrum/metabolism , Endorphins/biosynthesis , Rats, Inbred Strains
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