On the dynamic organization of memory

The interaction of memory structures and retrieval dynamics is discussed. A mathematical model for associative free recall is presented to support the view that the organization of simple processing units plays an important role in the retrieval of memory traces. Computer simulations show that "flexibility" and "fidelity" of the dynamics strongly depend on the network structure, the amplification and decay parameters, and the noise term.     

It is Rous sarcoma virus protein P12 and not P19 that binds tightly to Rous sarcoma virus RNA

The interactions between Rous Sarcoma virus (RSV) RNA and the viral proteins in the virus have been analysed by Sen & Todaro (1977) using ultraviolet light irradiation; they showed that the major protein ultraviolet light cross-linked to the viral RNA was P19 as identified by polyacrylamide gel electrophoresis. We report here that it is not viral protein P19 but P12 that binds tightly to RSV RNA upon ultraviolet light irradiation of the virus. Therefore, the binding sites of the viral protein along RSV RNA that we have characterized previously should be correctly attributed now to P12 and not P19.     

Histocompatibility Gene Organization and Mixed Lymphocyte Reaction

TRANSFORMATION of allogenic lymphocytes in mixed cultures depends chiefly on an incompatibility between the lymphocyte donors at the major histocompatibility locus in man (HL-A), mouse (H-2) and rat (H-l)¹. Although the mouse H-2 locus can be divided into several regions each of which controls one or more antigenic specificities² and two or more subloci control HL-A antigens in man³, it is not known whether all parts of the major histocompatibility locus are equally important in eliciting transformation in mixed lymphocyte cultures. We now show that capacity to elicit lymphocyte transformation is different for different parts of the mouse H-2 locus.     

Interactions between Marek's Disease Herpesvirus and Avian Leucosis Virus in Tissue Culture

A GROUP B herpesvirus is important in the aetiology of Marek's disease, a highly contagious lymphoproliferative disease of chickens^1,2. Chicks inoculated with enveloped Marek's disease herpesvirus (MDHV), extracted from feather follicle epithelium of chickens with the disease, developed tumour-like aggregates of lymphoid cells in the viscera and frequently in the peripheral nerves^3,4. Cultures of chicken embryo fibroblast (CEF) cells infected with MDHV develop discrete foci of altered cells⁵. Our data show that MDHV infection of cultures of CEF cells, previously infected with an avian leucosis virus (RAV-2), results in both a reduction in the number of MDHV foci and an increase in the complement fixing avian leucosis antigen (COFAL)⁶ titre.     

Convergence of signals of various sensory modalities on the neurons of the sensorimotor zone of the rabbit cerebral cortex

The responses of the neurons to electrocutaneous stimulation, light flashes, and clicks in the cortical region of the motor representation of the rabbit forelimb were investigated by means of intra- and quasiintracellular recordings. In unanesthetized animals, in only eight out of 65 neurons did postsynaptic potentials (PSP) with a short (10–30 msec) latent period arise in response to light and sound. In 15 neurons, long latency (50–150 msec) responses to one or both of these stimuli were recorded. In most of the cells, short latency stable responses to stimulation of the contralateral forelimb and unstable long latency responses to light and/or sound, frequently of the nature of an increase in the background "synaptic noise," were observed. Under deep chloralose narcosis, the type of convergence was sharply changed: in most of the neurons, short latency responses to all the stimuli used appeared. However, the picture of convergence differed from that described earlier [5,6] for the motor cortex of the cat under chloralose narcosis. The responses to various stimuli were less similar to one another; the somesthetic modality substantially "predominated" (judging by the stability and nature of the interaction of the response).Brain Institute, Academy of Medical Sciences of the USSR. Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 3, No. 5, pp. 474–483, September–October, 1971.     

Postinhibitory unit response of crustacean stretch receptors after direct and recurrent inhibition

The postinhibitory response of a slowly adapting neuron was investigated in experiments on an isolated preparation of crustacean stretch receptor and abdominal nerve chain. The structural features of this preparation are such that this response can be regarded as the response of the postsynaptic membrane to synaptic inhibition and not the action of synaptic excitation. IPSPs arise in the slowly adapting neuron in response to stimulation of the abdominal nerve chain (direct inhibition) or to excitation of the neuron itself (recurrent inhibition). The postinhibitory response consists of the development of action potentials or an increase in their amplitude and frequency. The magnitude of the response is determined by the duration of the inhibition and the state of the neuron membrane. The postinhibitory response was strongest when IPSPs were superposed on cathodal depression. IPSPs and an intracellular hyperpolarizing current evoke similar postinhibitory responses. Repetitive excitation of an inhibitory neuron may result in the appearance of a regular spike discharge from a previously inactive neuron through the mechanism of the postinhibitory response. Activation of a chain of recurrent inhibition increases the duration of the postinhibitory response evoked by direct inhibition or by a hyperpolarizing current. The existence of a chain of recurrent inhibition prevents the cessation of firing by a neuron during increasing cathodal depression. A mechanism of postinhibitory rebound lies at the basis of this phenomenon.     

Analysis of theta-rhythms recorded in an isolated strip of rabbit sensomotor cortex

To test the possibility that the theta-rhythm may spread passively from the hippocampus into the neocortex in rabbits and to analyze the properties of these rhythms recorded from the surface of the neocortex, an investigation was made of activity recorded simultaneously from the hippocampus and various points of the neocortex, including from a strip of the sensomotor cortex isolated completely with respect to its nervous connections. The use of special correlation methods showed that an appreciable contribution to the potentials recorded from the isolated strip can be made by the passive conduction of hippocampal activity (provided that it generates a regular high-amplitude theta-rhythm). At the same time, potentials in a theta-rhythm may be generated in the isolated strip itself. The theta-rhythm recorded in the intact rabbit cortex may thus be of combined genesis: generated in the neocortex itself and spreading passively from the hippocampus through the brain tissues as through a volume conductor.     

Singlet oxygen production in thylakoid membranes during photoinhibition as detected by EPR spectroscopy

Exposure of isolated spinach thylakoids to high intensity illumination (photoinhibition) results in the well-characterized impairment of Photosystem II electron transport, followed by degradation of the D1 reaction centre protein. In the present study we demonstrate that this process is accompanied by singlet oxygen production. Singlet oxygen was detected by EPR spectroscopy, following the formation of stable nitroxide radicals from the trapping of singlet oxygen with a sterically hindered amine TEMP (2,2,6,6-tetramethylpiperidine). There was no detectable singlet oxygen production during anaerob photoinhibition or in the presence of sodium-azide. Comparing the kinetics of the loss of PS II function and D1 protein with that of singlet oxygen trapping suggests that singlet oxygen itself or its radical product initiates the degradation of D1.Abbreviations HEPES 4-(2-hydroxyethyl)-1-piperazine ethanesulphonle acid - PS Photosystem - TEMP 2,2,6,6-tetramethylpiperidine - TEMPO 2,2,6,6-tetramethylpiperidine-1-oxyl