Pharmacological protection against hypoxia induced amnesia in rats

Giurgea, C.; Lefevre, D.; Lescrenier, C.; David-Remacle, M.

doi:10.1007/bf00404369

Cited by 78 publications

(19 citation statements)

References 13 publications

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“…The results are at variance with studies reporting facilitation of avoidance acquisition following treatment with piracetam (Giurgea et al, 1971;Sara & David-Remacle, 1974 ;Wolthuis, 1971). The most obvious explanation of the fact that pirace tam did not partially reverse the DMT lesion-induced deficit is that the mechanism of piracetam facilitation is unrelated to the disruptive anatomical and biochemical effects of DMT lesions.…”

Section: Discussioncontrasting

confidence: 82%

“…The most obvious explanation of the fact that pirace tam did not partially reverse the DMT lesion-induced deficit is that the mechanism of piracetam facilitation is unrelated to the disruptive anatomical and biochemical effects of DMT lesions. It has been suggested that piracetam increases oxygen availabilit y (Giurgea et al, 1971 ;Pede , Schimpfessel, & Crokaert , 1971 ;Sara & David-Rernacle , 1974) and thus protects subjects from hypoxia-induced amnesia or facilitates acquisition. Why lesions of the DMT produce deficits on learning tasks is not understood, but this may be due to changes in attentional processes.…”

Section: Discussionmentioning

confidence: 99%

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Effect of piracetam on one-way active avoidance in rats with medial thalamic lesions

Abbott

Means

1979

Bull. Psychon. Soc.

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Rats sustaining either medial thalamic electrolytic lesions or sham operations were injected with either piractam (100 mg/kg), a drug previously shown to enhance acquisition, or saline for 3 consecutive days prior to being tested for shock-flinch threshold and one-way active avoidance. The animals with medial thalamic lesions were found to make fewer avoidances than the sham-operated animals. Piracetam was shown neither to alleviate the lesion-induced avoidance deficit nor to facilitate acquisition in the sham-operated animals. No differences were observed in shock-flinch threshold. 158Rats with relatively large lesions centered in the dorsomedial nucleus of the thalamus (DMT) have been found to be deficient on acquisition of one-way active avoidance (Tigner, 1972;Vanderwolf, 1964Vanderwolf, , 1966Vanderwolf, , 1967 Wuensch & Means, 1976). Several treatments, including septal lesions (Vanderwolf, 1964), warm-up period (Vanderwolf, 1966), electroconvulsive shock (Vanderwolf, 1968), and chlorpromazine injections (Wuensch & Means, 1976) have been found to partially alleviate the DMT lesion-induced active avoidance deficit. It has been suggested that all of the above treatments improve the performance of DMT-lesioned rats in avoidance conditioning by decreasing the tendency to behaviorally freeze when shocked. Further, it has been shown that amphetamine injections decrease the freezing behavior of DMT-lesioned rats in a two-choice discrimination task, but they do not improve choice performance (Wuensch, Broom, Means, & Harris, 1978). Thus, several treatments have been found to decrease the freezing behavior of DMT-Iesioned rats, but no treatment has been found that directly affects the acquisition process.Piracetam (2-pyrrolidone acetamide) has been proposed as a learning-facilitation drug (Giurgea, Note 1). In humans, it has been shown to alleviate some of the symptoms of senility (Stegnik, 1972). In rats, piracetam has been found to facilitate acquisition of a lightsignaled active avoidance in a Y maze (Wolthuis, 1971) and to reduce errors and escape latency in a four-choice water-filled maze (Giurgea & Mouravieff-Lesiusse, 1972). It has also been shown to protect against the amnestic effects of electroconvulsive shock (Sara & David-Remacle, 1974) and hypoxia (Giurgea, Lefevre, & Lescrenier, 1971;Sara & Lefevre, 1972 METHOD SubjectsA total of 41 individually housed , male, Long-Evans rats from the East Carolina University colony were used. All rats were given food and water ad lib.The study involved four groups. Eight rats received lesions centered on the DMT and were treated with piracetam (Group D-P). Group SoP (n =12) received sham operations and treatment with piracetam . Group D-S (n =9) received lesions centered on the DMT and saline. Group S-S (n =12) received sham operations and saline. ProcedureSurgery. Surgery was done under clean conditions ; sodium pentobarbital was used as anesthesia (Nembutal, 50 mg/kg) and .2 cc of BicilIin was administered to prevent infection. Subjects in Group D-P and Group D-...

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Section: Discussioncontrasting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Effect of piracetam on one-way active avoidance in rats with medial thalamic lesions

Abbott

Means

1979

Bull. Psychon. Soc.

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“…The following compounds, for example, have been reported to reduce amnesia: amitriptyline [4]; Piracetam [7] ; pentylenetetrazol [20] and strychnine [ 11] ; a-methyl-para-tyrosine, propranolol and chlorpromazine [10]. This group of compounds is so pharmacologically heterogeneous that a uniform mechanism of action seems to be excluded.…”

Section: Discussionmentioning

confidence: 99%

The effects of ACTH- and vasopressin-analogues on CO2-induced retrograde amnesia in rats

Rigter¹,

Riezen²,

Wied

1974

Physiology & Behavior

218

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RIGTER, H., H. VAN R1EZEN AND D. DE WIED. The effects of ACTH-and vasopressin-analogues on C02-induced retrograde amnesia in rats. PHYSIOL. BEHAV. 13(3) [381][382][383][384][385][386][387][388] 1974. -Amnesia for a one-trial step-through passive avoidance response was induced in rats by application of CO 2 until respiratory arrest occurred. The ACTH-analogue ACTH4-1 o alleviated the amnesia when administered 1 hr prior to the retrieval test but not when given 1 hr prior to the acquisition trial. The behaviourally inert ACTH-analogue ACTH 11-24 appeared to have no effect on the amnesia. The vasopressin-analogue desglycinamide lysine vasopressin (DG-LVP) antagonized the amnesia when administered 1 hr prior to the acquisition trial or 1 hr prior to the test trial. The relevance of these date to present theories on amnesia is discussed. ACTH4_I0Amnesia Desglycinamide lysine vasopressin CO 2 " Memory consolidation Memory retrieval FLEXNER and Flexner [6] reported that amnesia in mice induced by the intracerebral injection of puromycin was almost completely reversed when the animals were treated with an ACTH-preparation before or within 16 hr of the acquisition of an avoidance response. In a later investigation from the same laboratory [9], in which a chemically pure ACTH-preparation was used, no anti-amnesic effect could be detected; the originally observed anti-amnesic effect of ACTH was attributed to a vasopressin impurity. This assumption was validated by the finding that desglycinamine lysine vasopressin (DG-LVP) caused a reduction of the amnesia under the same circumstances as the crude ACTH-preparation used by Flexner and Flexner [6]. DG-LVP almost completely lacks the endocrine effects of vasopressin but exerts the same effects on learning behaviour in rats [25]. These results do not exclude an effect of ACTH on amnesia. Firstly, puromycin like other inhibitors of protein synthesis affects the function of the pituitaryadrenal axis [16], thereby possibly contaminating the effects of administration of exogeneous ACTH. Secondly, Flexner and Flexner [6] and Lande, Flexner and Flexner [9] administered ACTH prior to the amnesic treatment but not prior to the retrieval test. Furthermore, these investigators used ACTH, which apart from exerting an effect on the 381 central nervous system also stimulates the production of corticosteroids from the adrenals. These corticosteroids may exert effects on behaviour which are opposite to those of ACTH [3,21]. Moreover, surgical removal of the adrenals, which causes increased ACTH release, results in a reduction of amnesia [5]. Although it is possible that adrenalectomy also causes an increased release of vasopressin [17], further studies on the possible anti-amnesic effect on ACTH seem justified. In the present investigation we compared the anti-amnesic effects of the ACTHanalogue ACTH4.1o with the effects of DG-LVP. ACTH4.1o lacks virtually all corticotrophic activities but possesses the same effects with respect to acquisition and extinction of avoidance behaviour as ...

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“…Piracetam (2-oxo-1-pyrrolidine acetamide), a drug shown to protect against hypoxic brain damage and used as a psychotropic agent, 1 has been shown to have beneficial effects in sickle cell anemia (SCA). [2][3][4][5][6] Its exact role, however, still remains controversial.…”

Section: Introductionmentioning

confidence: 99%

A Preliminary Report on Piracetam in Sickle Cell Anemia: A Double-Blind Crossover Clinical Trial and Effects on Erythrocyte Survival

et al. 1983

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Nine subjects with sickle cell disease were treated with Piracetam in the dosage of 80mg/kg p.o. divided into four doses per day for a period of 5 months and with placebo for a similar period on a double-blind crossover basis. The number of pain crises during the treatment period was significantly less than the number of attacks during the placebo period. Red blood cell survival measured in seven patients failed to show any significant change during the administration of Piracetam. These results suggest that Piracetam may be a useful drug in the amelioration of pain crises in sickle cell anemia.

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Pharmacological protection against hypoxia induced amnesia in rats

Cited by 78 publications

References 13 publications

Effect of piracetam on one-way active avoidance in rats with medial thalamic lesions

Effect of piracetam on one-way active avoidance in rats with medial thalamic lesions

The effects of ACTH- and vasopressin-analogues on CO2-induced retrograde amnesia in rats

A Preliminary Report on Piracetam in Sickle Cell Anemia: A Double-Blind Crossover Clinical Trial and Effects on Erythrocyte Survival

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