Single-trial Passive Avoidance Task Research Articles

Similar effects of a monoamine oxidase inhibitor and a sympathomimetic amine on memory formation

Amnesia resulting from inhibition of cerebral protein synthesis by cycloheximide can be prevented by subcutaneous injection of the monoamine oxidase inhibitor pargyline (25 mg/kg) or the sympathomimetic amine metaraminol (3.0 mg/kg) administered up to 30 min following learning of a single trial passive avoidance task in day-old chickens. The injection has to be made during the life time of labile memory for the prevention of cycloheximide-induced amnesia. On the other hand amnesia induced by the Na/K ATP'ase inhibitor ouabain can only be prevented if these two agents are administered up to 5 min after learning, i.e. during the life time of short-term memory. In addition, both agents produce a retrieval deficit 90 min after the injection, but only when memory is in long-term storage. These results are compared to those obtained with administration of norepinephrine, d-amphetamine and diphenylhydantoin.

Memory formation for an appetitive visual discrimination task in young chicks

The three-phase model of memory formation in young chicks proposed by Gibbs and Ng [7] was based on a single trial passive avoidance task. Some methodological and interpretative problems associated with this task are not encountered in appetitive visual discrimanation tasks. Using such a task, it is shown that 2 mM KCl induces amnesia at 10 min, ouabain at 30 min and cycloheximide at 60 min after learning. These findings are consistent with those for the single trial passive avoidance task and confirm the generality of a model of memory formation in young chicks entailing a short-term phase, a sodium pump-dependent labile phase, and a long-term, protein synthesis-dependent phase.

Counteractive effects of norepinephrine and amphetamine on ouabain-induced amnesia

Ouabain, administered 5 min prior to learning induces amnesia for a single-trial passive avoidance task in day-old chickens by inhibiting memory formation during the labile sodium-pump dependent phase. Amphetamine and norepinephrine (NE) successfully counteract ouabain-induced amnesia when administered immediately after learning. The actions of these drugs on ouabain-induced amnesia parallel that of diphenylhydantoin (DPH), and within similar time constraints. It is concluded that amphetamine (through release of NE) and norepinephrine exert their effects through stimulation of Na +/K + ATP'ase activity. This conclusion is supported by the observation that these drugs do not overcome potassium chloride (KCI) inhibition of memory formation in the short-term phase prior to formation of labile sodium-pump dependent memory, and the fact that the noradrenergic blockers, propranolol and piperoxane do not alter the couteractive influence of DPH on cycloheximide (CXM) inhibition of the protein synthesis dependent long term memory phase which follows the labile phase.

Amino acid uptake required for long-term memory formation

α-Amino-iso-butyrate (AIB) inhibits long-term, protein synthesis-dependent memory formation by reducing labelled leucine uptake in vivo without affecting leucine incorporation into protein. Unlike the antibiotic cycloheximide, AIB does not block long-term memory formation through inhibition of protein synthesis per se. The behavioural effect of AIB is restricted to times of administration between 5 min before and 5 min after learning a single trial passive avoidance task by day-old chickens. It is concluded that (1) AIB competes with normal amino acids for uptake into cells, and (2) the uptake of amino acids for protein synthesis specific to long-term memory formation takes place in the first few minutes following learning.

Comparative study of retrograde amnesia in rats on active and passive avoidance tasks and spontaneous recovery of memory

Naive and pretrained rats were trained in two active avoidance paradigms using a pole-climbing box and in a single-trial passive avoidance task using a T-maze. They were then subjected to amnestic treatments with electroshock, leptazol, pentobarbitone, or ether anesthesia. Single retention tests were given at 20-24, 44-48, or 68-96 h posttreatment. Electroshock and leptazol seizures produced retrograde amnesia in all three paradigms, provided that seizures were maximal and retention was tested before 48 h. Prior treatment with anticonvulsant drugs prevented amnesia. Ether and pentobarbitone anesthesia failed to produce amnesia in all three tasks. A trend of recovery from amnesia was observed in the electroshock and leptazol groups when tested for retention 48-96 h posttreatment. On the other hand, the non-amnesic control, pentobarbitone, and ether groups showed signs of forgetting at these longer intervals. Consolidation failure and/or retrieval block was surmised to be the cause of amnesia; recovery was the possible result of removing the block.

Amnesie effects of cooling and heating in mice

Albino CF1 female mice were heated with a diathermy unit immediately following training on a single-trial passive-avoidance task. Retention, tested 24 h later, was significantly impaired only in those animals that had heat-induced convulsions. Even elevations of temperature more than 5 deg C above normal, whenever they did not produce convulsions, failed to produce amnesia. These results indicate that even the strong stimulation provided by hyperthermia is not sufficient in itself to produce amnesia.