However, recent data obtained in terrestrial snails demonstrated a peculiar phenomenon of irreversibility of amnesia produced by protein-synthesis inhibition during memory consolidation or reconsolidation ( Solntseva et al.
Until recently, a natural assumption from these experiments has been that amnesia returns the brain to a sort of a tabula rasa state with respect to the impaired experience, making the animal ready for the subsequent reacquisition of the lost memory. Though it is still disputable whether the interference-induced deficit reflects memory loss or a retrieval failure, it is presently well established that such treatments impair performance on subsequent retention tests, thus producing amnesia ( Hardt et al. The neurobiology of memory has gained considerably from methods of experimental interference with memory consolidation or reconsolidation ( Schafe et al. We suggest that such pharmacologically induced experience-specific anterograde amnesia might reflect general properties of normal memory allocation, and we discuss its possible neural bases. This memory reacquisition deficit was specific and was not transferred to a new conditioned stimulus, which was readily learned. Retraining of the amnestic chicks with the bead that was presented during the initial training failed to produce new avoidance memory for this stimulus at all the between-training and training-to-test intervals. The interval between the first and second training was 2 or 24 h, and the retention test was given from 30 min to 48 h after the second training. A second training was given to the amnestic animals either using a bead of the same color (retraining) or a new color (novel training). Both drugs produced permanent amnesia, and no spontaneous recovery of memory was observed.
Training was preceded by administration of the protein synthesis inhibitor anisomycin or the NMDA receptor antagonist MK-801. We trained day-old chicks in a one-trial passive avoidance task by presenting them a bead of a specific color covered with a repellent substance, methyl anthranilate. Here we examined whether such specific memory reacquisition deficit can also be observed in vertebrate learning. However, recent studies in terrestrial snail classical conditioning revealed an odd phenomenon: animals were unable to relearn conditioned avoidance of specific food after this memory had been impaired by protein-synthesis inhibitors or N-methyl-D-aspartate (NMDA) receptor antagonists. The article recommends that FZ be declared illegal.A common assumption from experiments that interfere with memory consolidation is that the resultant amnesia returns the brain of an animal to a tabula rasa state with respect to disturbed experience. Psychiatrically or psychologically vulnerable males are at particularly high risk of violent and bizarre behavior when under the influence of FZ.
The article claims that FZ-facilitated violent behavior leading to impulsive decision-making has become increasingly common in males. The article discusses, among other topics: the medical use of FZ its neuropsychopharmacologic properties the concept of vulnerable personality and disposition for abuse psychological aberration or confusion while intoxicated with FZ amnesic effect of FZ and legal issues and biological vulnerability. Their crimes were extremely violent, and the subjects lacked both the ability to think clearly and to have empathy with their victims. At the times of their crimes all were intoxicated with FZ. This study observed five forensic psychiatric patients, all of whom had reported earlier reactions to FZ, including hostility and anterograde amnesia. Many male juvenile delinquents commit violent crimes while intoxicated with flunitrazepam (FZ), often in combination with alcohol or other drugs.