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M E Gibbs

Publications and source records attributed to M E Gibbs.

At least 55 records · Page 3Linked to original sources
PubMed1986

Effect of testosterone on intermediate memory in day-old chicks.

Day-old chicks trained on a single trial passive avoidance discrimination task show three well-defined behavioural stages in memory formation: short-term, intermediate and long-term memory. Testosterone (2 mg), given subcutaneously, yielded results which may be tentatively interpreted as an extension of the time of availability of recall from the intermediate stage by between 20 and 50 min, provided the hormone is administered no earlier than 90 min before learning. A higher dose (12.5 mg) of testosterone administered 30 min before learning had a similar effect. The findings with testosterone are comparable to those reported for pituitary-adrenal hormones.

Animals↗
PubMed1986

Effect of stress-related hormones on short term memory.

Adrenocorticotropic hormone (ACTH)1-24, ACTH4-10, corticosterone (CS) or arginine vasopressin (AVP) was administered subcutaneously to one day-old chicks immediately after learning a single trial passive avoidance task. Chicks were pretreated with 2 mM KC1 or 4 mM monosodium glutamate 5 min before learning. With KC1 or monosodium glutamate alone, no evidence of memory was observed on retention tests carried out as early as 5 min and as late as 24 h postlearning. However, the addition of ACTH1-24, ACTH4-10 or AVP to KC1-pretreated animals yielded normal retention levels up till 10 min, 10 min and 20 min after learning, respectively. Similar results were obtained with ACTH1-24 and AVP given to glutamate-pretreated birds. CS had no effect on KC1- or glutamate-induced amnesia. The calcium channel blocker, lanthanum chloride, also inhibited the formation of short-term memory, with amnesia still present as late as 24 h following learning. ACTH1-24, but not CS or AVP, yielded normal retention levels until 10 min postlearning in the presence of lanthanum chloride. Thus ACTH1-24 and AVP can overcome KC1 or glutamate inhibition of STM formation but will not prevent subsequent amnesia. The mechanisms underlying this action of ACTH1-24 and AVP are different. The possibility that the effect of ACTH1-24 is related to the role of calcium in STM formation is explored.

Animals↗
PubMed1984

Diphenylhydantoin extension of short-term and intermediate stages of memory.

Diphenylhydantoin was shown to extend the duration of maximum availability of both short-term and intermediate memory in day-old chicks following a single trial passive avoidance learning task. Diphenylhydantoin also extended the time of susceptibility of long-term memory to inhibition by cyloheximide, suggesting that the extention of the life of intermediate memory was accompanied by a delay in long-term memory formation. Furthermore, while diphenylhydantoin counteracted amnesia induced by cycloheximide given 5 min before or immediately after learning, it had no effect on amnesia induced by cycloheximide administered 5 min or later after learning. For the latter, a second injection of diphenylhydantoin was necessary. This is consistent with the argument that the first injection of diphenylhydantoin extended the life of intermediate memory and delayed the formation of long-term memory.

Animals↗
PubMed1984

Hormonal influence on the duration of short-term and intermediate stages of memory.

In day-old chicks trained on a single trial passive avoidance learning task, ACTH1-24 and corticosterone delayed the formation of long-term memory and the decay of the immediately preceding intermediate memory. This action of ACTH1-24 was attributed to its glucocorticoid activity since ACTH4-10 did not yield the same effect. ACTH1-24 and ACTH4-10, but not corticosterone, enhanced short-term memory retention levels. The effects of arginine vasopressin and arginine vasotocin were similar to those observed with ACTH1-24, but they also delayed the decay of short term memory and hence the formation of intermediate memory. These findings were discussed in the context of hormonal modulation of memory formation and counteraction of antibiotic-induced amnesia.

Adrenocorticotropic Hormone↗
PubMed1984

Effects of hypoxia on memory consolidation: implications for a multistage model of memory.

Anoxia treatment given 2.5 or 5 min after a single trial passive avoidance task in day-old chicks yielded a temporary retention loss between 20 and 50 min after learning. No effect was obtained when the treatment was administered immediately or 10 min after learning. The temporary retention deficit was not due to a generalized retrieval loss since anoxia given at various times after 10 min following learning with retention tested 30 or 60 min after anoxia treatment, did not yield a retention deficit. Similar findings were obtained with hypoxia. The implications of the results for a multistage model of memory were examined. In particular, it was suggested that the temporary retention deficit may be due to the breakdown of retrieval mechanisms associated with the second stage in a 3-stage model of memory processing.

Animals↗
PubMed1984

Dual action of cycloheximide on memory formation in day-old chicks.

Amnesia for a single trial discriminated passive avoidance learning task in day-old chicks, resulting from the antibiotic cycloheximide, is shown to begin after 30 min following learning when cycloheximide is given immediately after or before learning. However, amnesia does not begin until after 50 min following learning when cycloheximide is given 5 min or later after learning. The results are interpreted in the context of a 3 stage model of memory formation. It is suggested that the second or intermediate stage involves two phases: phase A which lasts up to 30 min following learning, is energy dependent, and is susceptible to inhibition by 2,4-dinitrophenol; phase B which occurs after phase A, lasts up to 50 min following learning, is energy independent, and is not susceptible to inhibition by 2,4-dinitrophenol. It is concluded that cycloheximide given immediately after or before learning inhibits expression of phase B of intermediate memory as well as formation of long-term memory, while cycloheximide given 5 min or later after learning only inhibits formation of long-term memory. Another antibiotic, anisomycin, is shown to have no effect on intermediate memory, independent of time of administration.

2,4-Dinitrophenol↗
PubMed1983

Inhibition of long-term memory formation in the chicken by anti chick Thy-1 antibody.

Anti-chick Thy-1 antibodies administered close to a single trial passive avoidance learning task in day-old chicks resulted in inhibition of long-term memory formation. The retention time course was comparable to that obtained with the protein synthesis inhibitor anisomycin. The amnestic effect of the anti-chick Thy-1 antibody appears to be mediated solely by immunoglobulin G, and is species specific since anti-rat Thy-1 antibodies did not produce amnesia. The results are consistent with a three stage model of memory formation, suggest a role for glycoproteins in long term memory formation, and emphasise the potential of neuroimmunological tools for investigating the neurological bases of memory formation.

Animals↗
PubMed1982

Limited period of actin of testosterone on memory formation in the chick.

Domestic chicks will normally peck readily at small colored beads. However, a peck at a bead with an unpleasant taste usually results in a long-lasting aversion to beads of that type. If prior experience ("pretraining") of a bead of the type that is to be used in a later aversive training trial is given to testosterone-treated chicks, it interferes with the retention of avoidance. Interference by pretraining is effective only within sharply defined periods of time: when the pretraining-training interval is either less than 2 min (short term) or greater than about 25 min (long term). When pretraining and training are separated by 90 min or more, the steroid can be effective when injected up to 30 min after pretraining. It appears to change the character of the consolidating memory trace of pretraining in such a way as to make the consolidating memory trace of pretraining in such a way as to make the consolidation of later, contradictory information from training loss likely. The initial storage of this information is apparently unaffected, since retention does not begin to decay until 30-60 min after training. Sort-term interference leads to loss of avoidance within 5 min of training and can be used to demonstrate that the latency of action of the hormone in this task is less than 20 min following a subcutaneous injection.

Animals↗
PubMed1981

Enhancement of effectiveness of learning by testosterone in domestic chicks.

In young male domestic chicks, the presentation of a nonaversive colored bead to be pecked (pretraining) interfered with subsequent avoidance training, in which the bead presented tasted unpleasant, when two conditions were fulfilled: (a) Beads used at pretraining and training were of similar appearance, and (b) testosterone was injected either before or a little after pretraining. This effect of the hormone was not a consequence of changes in behavior at training or at test. It appeared to reflect changes during the consolidation of the pretraining memory trace which made it more effective in subsequent competition with training. Beads that are blue in color were unusual in evoking high levels of avoidance in naive chicks and, when used in pretraining in the presence of testosterone, in failing to oppose subsequent training on the blue bead. Such pretraining became effective when paired with avoidance training with a bead of different color, apparently by changing the information stored about pretraining.

Animals↗
PubMed1979

Biochemical aspects of protein synthesis inhibition by cycloheximide in one or both hemispheres of the chick brain.

Instracrnial administration of cycloheximide into one hemisphere of the chick brain resulted in inhibition of 14C-leucine incorporation into protein only in that hemisphere when the labelled amino acid was administered intracranially. With pericardial injections of labelled amino acid, inhibition of 14C-leucine incorporation was obtained in both the CXM-treated and the untreated hemisphere, when compared with bilateral saline-treated controls. The levels of inhibition were comparable to those obtained with bilateral administration of CXM. There was, however, a slight but significantly higher level of inhibition in the CXM-treated hemisphere. The results were interpreted as supporting the conclusion that monocular learning in chicks resulted in the formation of an engram only in the trained hemisphere.

Animals↗
PubMed1979

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.

Animals↗
PubMed1979

Interhemispheric engram transfer in chick.

Monocular training on a one-trial passive avoidance task in the young chick has been shown to establish an engram in the forebrain hemisphere contralateral to the trained eye, and hence interocular transfer of this task must involve the naive hemisphere making access to the engram in the opposite hemisphere. We have studied the consequences for the untrained hemisphere of accessing a unilateral engram during two short term stages of its consolidation, by conducting interocular transfer tests at 7.5 min and 30 min after learning, prior to onset of amnesia induced by intracranial injection of ouabain or cycloheximide. Testing the naive hemisphere 24 h later indicated that engram transfer had occurred in chicks receiving one access trial at 7.5 min, during the first stage of consolidation of the unilateral engram. At 30 min, during second consolidation stage, five access trials were required to achieve engram transfer. These experiments confirm the findings from the rat that engram transfer can follow from making access to the unilateral engram. However, it has not previously been recognised that interhemispheric memory transfer depends on the recency of formation of the unilateral engram.

Animals↗