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G Sedman

Publications and source records attributed to G Sedman.

At least 19 recordsLinked to original sources

Phosphorylation changes following weakly reinforced learning and ACTH-induced memory consolidation for a weak learning experience.

The formation of a protein synthesis-dependent long-term memory stage in day-old chicks trained on a passive discriminated avoidance task has been shown to occur only with an adequate level of reinforcement, and is preceded by a significant change in the phosphorylation state of the forebrain synaptosomal membrane protein GAP43 protein. In the present study, it is shown that weakly reinforced training did not lead to formation of a long-term memory stage or to any change in phosphate incorporation into forebrain P2M protein bands. However, administration of ACTH immediately posttraining led to both the formation of the long-term memory stage and a preceding significant increase in the phosphorylation of GAP43. These findings are consistent with the view that a reinforcement-dependent neurohormone-mediated change to the phosphorylation of this synaptosomal membrane protein may be implicated in the triggering of long-term memory consolidation.

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Na+,K(+)-ATPase activity in young chicks after taste stimulation.

The activity of specific ouabain-sensitive Na+,K(+)-ATPase was studied in crude membrane fraction of the brain of 1- to 3-day-old chicks after the administration of a chemical aversant methylanthranilate (MeA), shown in previous behavioral studies to induce avoidance of pecking of an otherwise attractive stimulus. Enzyme activity was dramatically decreased (by 40-50%) in the time interval between 10 min-2 h after MeA administration onto the tongue of awake chicks. It was possible to localize these changes in Na+,K(+)-ATPase activity into forebrain structures contained within the dorsal ventricular ridge comprising the hyperstriatum accessorium (HA), hyperstriatum ventrale (HV), hyperstriatum dorsale (HD), and parts of neostriatum (N). In contrast, Na+,K(+)-ATPase activity in the ectostriatum (E), the medial neostriatum (NM), and the paleostriatal complex were unaffected. Results from experiments involving preincubation of membrane fractions and with partial purification using detergents, suggest that some substances with inhibitory effects were produced under the effect of MeA and bound to membrane fractions in their respective areas. A similar decrease of Na+,K(+)-ATPase activity as after MeA administration in vivo was observed when inhibitory mediators (GABA, glycine) were added to membrane fractions in vitro. These findings may have implications for memory processing in chicks following aversive learning using MeA as the aversant.

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Purified antichick Thy-1 IgG abolishes intermediate and long-term memory.

One- to 2-day-old chicks administered purified antichick Thy-1 IgG showed substantial amnesia for a single-trial passive discriminated avoidance task. Amnesia was clearly evident at 30 min after learning, during the intermediate stage of a three-stage model of memory processing, and persisted for at least 3 h. A similar effect was also observed with Fab and F(ab')2 fragments. Fc fragments, the non-IgG fraction of ascites, and saline yielded normal retention levels at all times. These results contrast with our earlier reports that both polyclonal and monoclonal antibodies to chick Thy-1 inhibited long-term memory formation only. The present findings are interpreted as possibly representing a dual effect of the purified IgG.

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Brain metabolic activity associated with long-term memory consolidation.

The use of day-old chickens trained on a single-trial passive avoidance task provides a useful paradigm for investigations into cellular mechanisms underlying memory formation. Pharmacological intervention studies indicate that there are three temporally identifiable stages of memory processing leading to the consolidation of information for this task. These stages, designated as short-term (STM; up to 15 min), intermediate-term (ITM; 15-55 min), and long-term (LTM; more than 55 min) memory, have been found to be sequentially dependent (Ng and Gibbs, 1989). In addition, ITM appears to consist of two physiologically distinguishable phases, A and B. Evidence in this laboratory suggests that the crossover between these ITM phases (at 30 min after training) represents a critical time-point for the triggering of LTM.

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Activity-related rise in extracellular potassium concentration in the brain of 1-3-day-old chicks.

The concentration of K+ [( K+]) was measured in the cerebrospinal fluid (CSF) and in the extracellular fluid [( K+]e) in the medial forebrain of two-day-old chicks by means of K(+)-sensitive microelectrodes (K-ISM). The K-ISM potential in the CSF was compared with that in artificial CSF with 3, 4 or 6 mmol/l of [K+]. The [K+] found in CSF was 3.79 +/- 0.57 (n = 8), in the hyperstriatum accessorium (HA) 3.70 +/- 0.32 (n = 13) and in the neostriatum (N) 3.51 +/- 0.32 (n = 13; mmol/l; mean +/- SEM). Trains of local electrical stimuli (10-100 Hz, 30 sec) applied to the surface of the forebrain increased [K+]e in both HA and N by 11-13 mmol/l. Increases in [K+]e in the ectostriatum (E) of 5-6 mmol/l was found in response to electrical stimulation (30-100 Hz, 5-10 sec) of the contralateral optic nerve, and of about 2 mmol/l by applying pressure to the bulb. In chicks adapted to the dark, stimulation of the contralateral eye or both eyes with bright light flashes (1-2 Hz) or with continuous light resulted in an increase in [K+]e of 0.5-1.0 mmol/l. Smaller increases in [K+]e of 0.15-1.25 mmol/l were found in HV and N after the application of a small quantity (0.1 ml) of the chemical taste aversant methylanthranilate (MeA) or the electrical stimulation of the beak by two needle electrodes inserted into the palatum or into the tongue. After application of MeA the increase in [K+]e began 3-4 min after application and persisted for 20 min.(ABSTRACT TRUNCATED AT 250 WORDS)

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