Post-trial injections of an anti-cholinesterase drug and maze learning in two strains of rats
โ Scribed by Lois O. Stratton; Lewis Petrinovich
- Publisher
- Springer
- Year
- 1963
- Tongue
- English
- Weight
- 469 KB
- Volume
- 5
- Category
- Article
- ISSN
- 0033-3158
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โฆ Synopsis
Recently, a great deal of evidence has been accumulated in support of the perseveration-consolidation theory of learning and memory. This theory assumes that the neural traces representing to-be-associated elements perseverate as a closed system for a period of time following the cessation of stimulation. If this perseveration continues long enough, the trace system becomes consolidated in the form of stable changes (presumably at the synapse) and memory is the result (H]~BB 1949). If the perseverating traces are interrupted soon enough following a learning trial, retrograde amnesia is produced. This interruption of perseveration, and consequent retrograde amnesia, has been successfully demonstrated with post-trial electroconvulsive shock, anoxia, hypothermia, and concussion (cf. GLICKMA~r 1961). McGAvGH and P~TRI~COVlC~ (1959) found that a pre-trial injection of strychnine sulphate increased the rate at which rats learned a Lashley III maze. Enhancement following pre-trial injections of strychnine has been found subsequently using a 14-unit T-maze (McGAUGH 1961a), a simultaneous discrimination problem (McGAvGH and THo~so~ 1962), a successive discrimination problem (P~Tm~OVICH 1963), and simple escape and avoidance responses (KELEM]~ and BOV]~T 1961). B~]s]~ and McGAuG~ (1961) reasoned that, if the perseverationconsolidation theory is correct, post-trial injections of a neural stimulant should also enhance the learning rate, since the critical events underlying acquisition presumably occur during the post-trial interval. They found that post-trial injections of pierotoxin, a central neural stimulant, enhanced the rate at which rats learned a 14-unit T-maze.
The cholinergie system is one of the biochemical mechanisms which determines the level of neural excitability. Acetylcholine (ACh) has been acknowledged to be the synpatic transmitter substance throughout much of the central nervous system and the cholinesterases (ChE) are present to inactivate ACh soon after its release (Bu~G]SN and MACINToSg 1955).
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