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At least 19 recordsLinked to original sources

PubMed1978

Studies on memory: spontaneous return of memory in 6-hydroxydopamine-treated mice and its relation to cycloheximide-induced transient amnesia.

We suggested previously that cycloheximide-induced transient amnesia was due in part to side-effects of the antibiotic on the central adrenergic system at the time of testing and that spontaneous return of memory depended upon recovery of the adrenergic system. To test these possibilities, mice chronically depleted of brain catecholamines (CAs) by 6=hydroxydopamine (6-OHDA) were trained in an avoidance-discrimination task and tested for spontaneous return of memory. Contrary to our hypothesis, amnesia at 24 hr after training was followed by recovery of memory by 72 hr, which indicates that recovery of memory can occur independently of adrenergic recovery. Injection of alpha-methyl-para-tyrosine immediately after training prevented return of memory at 72 hr, suggesting that the residual CAs remaining after 6-OHDA are necessary for memory to spontaneously return at this time.

Amnesia↗

PubMed1979

Studies on B-cell memory. I. Generation and exhaustion of B-cell memory by thymus-dependent antigen in T-cell depleted mice.

Mice depleted of T cells by adult thymectomy, X-irradiation and reconstitution with syngeneic bone marrow cells, either untreated or treated with anti-Thy-1 serum and complement, were immunized intensively with alum-precipitated bovine serum albumin (AP-BSA) along with or without bacterial lipopolysaccharide (LPS), but no significant anti-BSA antibody response was detected. Priming of the T-cell depleted mice, however, either by a single injection of AP-BSA plus LPS or by multiple injections of AP-BSA without LPS, resulted in the generation of immunological memory. A single injection of AP-BSA without LPS was ineffective. The memory required the aid of syngeneic T cells to be recalled by the challenge with AP-BSA plus LPS. On the other hand, multiple injections of AP-BSA plus LPS did not cause the generation of memory and the response of these mice to the challenge was lower than that of unprimed control mice. These results suggest that (1) the anti-BSA response is highly dependent on the helper function of T cells, (2) the degree of T-cell requirement for the memory generation is very low, and (3) priming with too much strong stimulation in the absence of functional T cells leads to the suppression or abortion of previously generated immunological memory.

Animals↗

PubMed1977

B memory cells in the thymus: part of the pool of potentially circulating memory cells.

Immunization of mice with sheep red blood cells (SRBC) or Escherichia coli lipopolysaccharide (LPS) induces the appearance of B memory cells in the thymus. In this paper the origin of these B memory cells was investigated. Therefore, mice primed with either SRBC or LPS 6 months previously and nonprimed mice were joined for parabiosis. Four weeks later the parabiotic mice were separated from each other. Another 3 weeks later thymus cells from the primed and nonprimed mice were transferred separately into lethally irradiated mice in order to determine the adoptive PFC response. It was found that the 4-week period of parabiosis could account for the appearance of a distinct population of B memory cells in the thymus of the nonprimed mice. This result suggest that the B memory cells which appear in the thymus belong to the pool of potentially circulating memory cells.

Animals↗

PubMed1979

Studies on B-cell memory. II. T-cell independent antigen can induce B-cell memory.

Both athymic nude mice and normal mice primed with a T-cell independent antigen, i.e. dinitrophenylated dextran (DNP-DE), at a sub-immunogenic dose, produced very poor anti-DNP responses to a later challenge with the same antigen. B-cell memory was expressed, however, as an enhanced IgM response after the challenge of the DNP-DE-primed mice with the T-cell dependent antigen (dinitrophenylated haemocyanin, DNP-KLH) in the presence of functional T-cells. Moreover, DNP-DE-primed spleen cells also revealed an enhanced IgM response after adoptive transfer into irradiated recipients and challenge with DNP-DE. The injections of DNP-DE-primed nude mouse serum into unprimed mice resulted in the reduction of anti-DNP response to the immunization with DNP-DE. These results indicate that (a) T-cell independent DNP-DE causes the differentiation of B cells not only into antibody-forming cells but also into memory cells, (b) these memory cells can be triggered in situ by the T-cell dependent DNP-KLH in the presence of helper T cells but not by T-cell independent antigen, and (c) some humoral factor(s) induced by DNP-DE-priming seems to interfere with the expression of B-cell memory only when challenged with T-cell independent DNP-DE.

Animals↗

PubMed1976

Transition in the character of immunological memory in mice after immunization. I. Memory for IgM and IgG antibody responses.

The immunological memory in antibody response of mice to bovine serum albumin was investigated at the level of IgM and IgG antibody-forming cells, The antigen at a dose much lower than required for eliciting a detectable level of the primary antibody response could latently activate the immune machinery to an extent adquate for specific recall, whereas higher doses of antigen were effective in evoking strong anamnestic response. The potentiality to develop the anamnestic response was found even in the latent phase of the primary antibody response and was maintained for more than 2 months. The immunological memory acquired in an early phase after the primary immunization mainly involved IgM antibody response and late memory concerned IgG response.

Animals↗

PubMed1977

The generation of memory cells. I. The role of C3 in the generation of B memory cells.

Adult thymectomized, repopulated mice were chronically depleted of circulating C3 by treatment with cobra venom factor after primary immunization with dinitrophenylated haemocyanin (DNP-KLH). This treatment totally abrogated the development of B-cell memory in such mice, as assayed by a co-operative lymphocyte transfer. The failure of memory development appeared to involve impaired precursor proliferation following priming. It was further shown that the localization of DNP-KLH in splenic lymphoid follicles is both antibody and C3-dependent; thymus-deprived mice make sufficient antibody to DNP-KLH to effect follicular localization of the antigen. On the basis of these and earlier observations we suggest that the development of B-memory cells involves the formation of antigen-antibody-C3 complexes on dendritic cells in lymphoid follicles. C3 may serve to stabilize the antigen bridge between dendritic cells and virgin precursors. In complete contrast, C3 depletion had little effect on the functional expression of primed B cells, thus suggesting that only the early stages of B-cell triggering are C3 dependent.

Animals↗

PubMed1978

The generation of memory cells. II. Generation of B memory cells with preformed antigen-antibody complexes.

Mice were immunized with preformed complexes of dinitrophenylated haemocyanin (DNP-KLH) and anti-DNP or anti-KLH antibodies, and subsequently assayed for the generation of B memory (BM) cells. Complexes formed at equivalence or in slight antigen excess were far more effective than antigen alone in generating memory: as little as 100 ng DNP-KLH-anti-DNP produced substantial B cell priming. Anti-carrier and anti-hapten antibodies were equally effective. Complexes generated memory more rapidly than antigen alone, and the adjuvant effect was not simply due to aggregation of the antigen. Optimal priming by complexes required the integrity of the Fc portion of the antibody: F(ab')2 antibody fragments were less effective. The capacity of complexes to prime BM cells was abrogated by depriving mice of C3. C3 was also required for localization of complexes within splenic lymphoid follicles; complexes made with F(ab')2 localized in follicles, but less efficiently than those made with intact antibody. These results extend earlier findings (Klaus & Humphrey, 1977) and strongly suggest that the generation of BM cells involves the C3-dependent localization of antigen-antibody complexes within lymphoid follicles and strengthen the concept that germinal centres are the birthplace of BM cells.

Animals↗

PubMed1979

Generation of memory cells. III. Antibody class requirements for the generation of B-memory cells by antigen--antibody complexes.

Immunizing mice with preformed antigen--antibody complexes is a highly effective means of generating B-memory cells. In the present study we have compared the capacity of mouse anti-dinitrophenyl (DNP) IgM, IgG1, IgG2 and IgA antibodies to generate DNP-specific memory, when given in complex with antigen (DNP-KLH: keyhole limpet haemocyanin). Two monoclonal IgM antibodies exerted no adjuvant effect, whereas a monoclonal IgA antibody was effective, IgG2 antibodies were a more powerful adjuvant than IgG1, regardless of whether anti-DNP or anti-KLH antibodies were used. Furthermore, the capacity of DNP-KLH--antibody complexes to localize in splenic lymphoid follicles could be ranked IgG2 greater than IgG1 greater than IgA; IgM complexes did not localize in follicles. These results correlate well with data (presented elsewhere) on the capacity of these different antibodies to activate mouse complement, and confirm that C activation is an essential requirement for both follicular localization of immune complexes, and for the generation of B-memory cells. Although activation of the alternative complement pathway is sufficient to effect both processes, the results with IgG2 antibodies raise the possibility that classical pathway activation may be more effective.

Animals↗

PubMedDate not supplied

[Bencyclane in memory disorders. Treatment of memory disorders caused by electroshock in a group of depressed patients].

Subjects treated with electroshock and subjected simultaneously to bencyclan at a dose of 00 mg (2 ampoules) i.v. and 100 mg (1 pill) per os pro die did not present dysmnesia either during the intervals between one electroshock treatment and another, nor at the conclusion of treatment (on average 12 sessions in about 40 days), while a control group treated at the same rhythm and with the same number of sessions, but without bencyclan, presented considerable memory lapses which disappeared only after a lengthy period of this latter treatment. Memory disturbances have been evaluated with a memorization test to which all patients were subjected. This test belongs to the group of intellectual efficiency reactive tests used in the psychology laboratory of the Catholic University of Milan; it consists of a group of 12 figures of common objects which, once observed, have to be recalled exactly immediately and some time later by the patient, who has to indicate the name and position of the objects represented in the chart.

Adult↗

PubMed1978

Cholinergic mechanisms in the learning and memory facilitating effect of the central stimulants. II. Influence of anticholinergic agents on the learning and memory facilitating effect of strychnine.

In experiments involving training of albino rats in a maze it has been found that strychnine (1 mg/kg) introduced 5 min before or immediately after training, improves learning and retention. Upon blocking of the central muscarine-sensitive cholinergic structures (scopolamine 2 mg/kg) and of the nicotine-sensitive structures (spasmolytin 20 mg/kg), the learning and memory facilitating effect of strychnine is not manifested. The realization of the learning and memory facilitating effect of strychnine requires optimum functional level of the activity of the central cholinergic system.

Animals↗

PubMed1978

Cholinergic mechanisms in the learning and memory facilitating effect of the central stimulants. III. Influence of the anticholinergic agents on the learning and memory facilitating effect of amphetamine.

In experiments involving training of albino rats in a maze it has been established that amphetamine in a dose of 0.5 mg/kg introduced 15 min before learning has almost no effect, in a dose of 2 mg/kg it slightly deteriorates learning and retention, while in a dose of 1 mg/kg both learning and retention are markedly improved. However, introduced immediately after training, all three doses tested improve retention upon testing 24 hours and 14 days after training. Upon blocking of the central muscarine-sensitive cholinergic structures (scopolamine 2 mg/kg) and of the nicotine-sensitive structures (spasmolytin 20 mg/kg), the learning and memory facilitating effect of amphetamine is not manifested in the two experimental setups (introduction before and after training). The results resemble the case of independent administration of cholinolytics only, i.e. complete blocking of learning and memory induced by scopolamine and considerable deterioration induced by spasmolytin. The results obtained show that the realization of the learning and retention facilitating effect of amphetamine requires optimum functional level of the activity of the central cholinergic system.

Amphetamine↗

PubMed1977

Memory for lists of sounds by the bottle-nosed dolphin: convergence of memory processes with humans?

After listening to a list of as many as six discriminably different 2-second sounds, a bottle-nosed dolphin classified a subsequent probe sound as either "old" (from the list) or "new." The probability of recognizing an old probe was close to 1.0 if it matched the most recent sound in the list and decreased sigmoidally for successively earlier list sounds. Memory span was estimated to be at least four sounds. Overall probabilities of correctly classifying old and new probes corresponded closely, as if recognition decisions were made according to an optimum maximum likelihood criterion. The data bore many similarities to data obtained from humans tested on probe recognition tasks.

Animals↗

PubMed1975

Nature of "memory" in T-cell mediated antibacterial immunity: cellular parameters that distinguish between the active immune response and a state of "memory".

Immunizing infection in mice with Listeria monocytogenes resulted in the generation of two distinct states of immunological reactivity. There was generated (i) a short-lived state of active immunity that functioned to urgently eliminate the infection organism from the tissues and (ii) a long-lives state of increased immunological potential that enabled the host to respond to seconday infection in an accelerated manner. Short-lived active immunity was mediated by replicating T cells and expressed by activated macrophages, and it ended when these cell types disappeared from the tissue soon after complete elimination of the parasite. Long-lived immunological protential was associated with a persistent level of delayed sensitivity and with the presence of a small number of nonreplicating protective T cells. It is suggested that the state of delayed sensitivity represents a state of immunological T-cell memory of the cell-mediated type.

Animals↗

PubMed1979

Discrimination learning without short-term memory: dissociation of memory processes in pigeons.

Pigeons were trained to perform delayed matching to samples of food and no food when each sample concurrently served as the outcome of a discrimination learning trial which immediately preceded each matching trial. Ambient light presented during the delays after the samples of food or no food severely disrupted matching but had no effect on the rate of discrimination learning.

Animals↗

PubMed1979