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Novice Karate Group (ages 8 & up)

Публічна·29 учасників

Escape - Andrea Izquierdo.epub

Long-term forms of synaptic plasticity, such as LTP, are considered the physiological basis of human memory, since they are induced rapidly after synaptic stimulation, they are stable over time and can associate different stimuli in a functional network facilitating the encoding and recalling of information [42]. To prove these features of LTP many studies tried to demonstrate with electrophysiological techniques that it plays an important functional role in learning and memory. In 1983, Collingridge and colleagues showed that the selective blockage of N-methyl-D-aspartate (NMDA) glutamate receptors with the drug amino-phosphonovaleric acid (AP5) at excitatory hippocampal synapses, was able to block the induction of LTP [43]. The role of NMDA glutamate receptor in synaptic plasticity was later supported by the studies of Morris and colleagues, who studied the behavioral effects of chronic, in vivo, intraventricular infusion of D,L-AP5 in rats [44]. During their experiments, rats were located into a large pool of water with a hidden platform located at a corner, and they measured the mean time needed to find the hidden platform and escape from water, a test known as Morris water maze [44]. The authors showed that the infusion of a selective NMDA antagonist, capable to block LTP induction in vitro, caused a significant impairment in learning and spatial navigation, suggesting a key role for hippocampal LTP in memory and spatial learning [44]. Whitlock and colleagues studied hippocampal synaptic alterations induced by inhibitory avoidance test (IAT), a test capable to induce a rapidly acquired and stable spatial memory, with associated changes in gene expression in the CA1 area of hippocampus [42]. They showed that the molecular changes occurring at hippocampal synapses during the in vitro induction of LTP, like the phosphorylation of α-amino-3hydroxy-5methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor GluR1 subunit, where similar to those occurred after a cycle of active avoidance training, meaning that synapses responsible of controlling that form of learning probably expressed LTP [42]. These results support the hypothesis that spatial learning induces LTP in the CA1 area of the hippocampus.

Escape - Andrea Izquierdo.epub

Spatial learning ability was examined in the Barnes maze using methods described previously [36]. The Barnes maze apparatus is an opaque disc 100 cm in diameter elevated 1 m above the floor by a tripod. Twenty holes, 8 cm in diameter, are located 9.5 cm from the perimeter, and a black escape box is placed under one of the holes. Distinct spatial cues are located all around the maze and are kept constant throughout the study. A fluorescent lamp (21 W) was placed above the center of the arena. A naive set of previously untested animals was positioned under an acrylic dome in the middle of the maze for one minute. Once the dome was lifted, the animal was able to orient to spatial cues and find the hole with the hidden burrow. The session ended when the rat entered the escape burrow or after five minutes had elapsed. If the rat did not enter the burrow by itself, it was gently guided and allowed to remain there for one minute before being returned to its home cage. This test consisted of one day of habituation session and five consecutive days of testing sessions with two trials per day. The location of the burrow was the same for each individual rat, but position was changed among rats in a group. The maze was cleaned with 5% ethyl alcohol to remove any odor trails. Rats are expected to reduce their latency to find the burrow, as a measure of spatial memory. Because the Barnes maze lacks strong reinforcement stimuli, rats may lack motivation and occasionally explore the maze after finding the target hole without entering. To rectify this confounding factor, we used the primary latency, which is the time elapsed to the first encounter of the escape burrow. 041b061a72

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