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At least 1,297 records · Page 72Linked to original sources
PubMed1992

A critical period for experience-dependent synaptic plasticity in rat barrel cortex.

Recordings were made from neurons in layers II, III, and IV of rat barrel cortex. The animals were raised either from the day of birth (P0) or from P2, P4, or P7 with just the D1 vibrissa protruding on one side of the face and the contralateral side intact. Follicles were not ablated, but vibrissae were carefully removed by applying steady tension to the base of each vibrissa. Deprivation was continued until the day of recording (P30-P90), though in most cases vibrissae were allowed to regrow for 4-7 d prior to recording. The area of cortex driven by stimulating the spared D1 vibrissa was found to be enlarged in uni-vibrissae animals, but the characteristic anatomical map of the barrel field, defined by cytochrome oxidase staining, retained its normal form. In animals deprived from P0, layer IV cells outside the D1 barrel responded with short latencies (5-10 msec) to D1 stimulation, a condition never observed in normally reared animals. Short-latency responses to stimulation of regrown, deprived vibrissae were still present in layer IV despite the deprivation. Plasticity decreased rapidly in layer IV between P0 and P4 as judged by two measures: first, the percentage of cells in neighboring barrels that showed short-latency responses to D1 fell from 30% in P0 deprived animals to 18% in P2 and 13% in P4 deprived animals. Second, the percentage of cells in barrels surrounding D1 with larger responses to D1 stimulation than to stimulation of their anatomically related vibrissa also fell from 37% in P0 to 23% in P2 and 12% in P4 deprived animals. The percentage of "shifted cells" showed no further reduction in P7 deprived animals (14%). Plasticity in layers II and III showed little sign of decreasing between P2 and P7 after an initial drop between P0 and P2. Therefore, deprivation started at P4 and P7 had a far greater effect on layers II and III than on layer IV. In animals deprived from P4 onward, not only were responses to D1 stimulation greater in barrels neighboring D1 (in layers II/III), but responses were smaller to principal vibrissa stimulation. This suggests increased lateral transmission from the "experienced" barrel and a failure of vertical transmission within the "deprived" barrels. These results show that changes in the balance of experience acquired through vibrissae can affect development of connectivity in the barrel cortex. The main locus of plasticity is cortical when deprivations are started at P4 and beyond.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMedDate not supplied

[A mathematical model of the role of Ca2+/calmodulin-dependent protein kinase in the long term increase in effectiveness of synaptic plasticity].

A mathematical model describing initiation and restoring of the long-term potentiation (LTP) is proposed. This model is based on an assumption that Ca2+/Calmodulin-dependent protein kinase from some of second messengers exists in a number of states. The protein kinase ability for securing LTP restoring is connected with autophosphorylation.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1990

Memory, synaptic plasticity and neurotoxins.

Most neurotoxins induce serious impairments in cognitive or intellectual functioning; therefore, the ability of the individual to learn and remember forms a critical component of neurotoxin assessment. In depth investigations of neurotoxin-induced cognitive deficits have assisted in pinpointing the neural site of toxin activity. However, specific impairments in learning and memory can depend on the developmental stage at which the individual is exposed to the toxin, and certain neurotoxins show cognitive lifespan selectivity. There appears to be a basic sequence of events underlying neural development and information storage, and neurotoxins may disrupt this neuronal sequel critical for the storage or expression of "ancestral" or "environmental" memories. Certain primary rules govern the orderly development of the nervous system; these rules or mechanisms allow the expression of "ancestral memories" concerning neuronal differentiation and primitive behaviors. Following birth, these same mechanisms have been retained in a less robust form to allow learning and information storage, or the retention of "environmental memories." Neurotoxins which disrupt learning and memory capacities appear to interfere in this basic sequence of events, with the specific outcome depending on when during lifespan development the neurotoxin intervenes.

Animals↗
PubMed1990

Synaptic plasticity in fear conditioning circuits: induction of LTP in the lateral nucleus of the amygdala by stimulation of the medial geniculate body.

Electrical stimulation of the medial geniculate body in the anesthetized rat produces an evoked potential in the lateral nucleus of the amygdala. The potential varies in amplitude with stimulus intensity and reaches peak amplitude in 8.5 msec on the average. High-frequency stimulation of the pathway produces long-lasting increases in the amplitude and slope of the potential. These robust and enduring experience-dependent modifications in neural transmission occur in a pathway known to be involved in the formation of emotional memories and may offer a means for examining the cellular mechanisms of emotional learning, as well as a new approach to questions concerning the relevance of long-term potentiation to normal mnemonic processes.

Amygdala↗
PubMedDate not supplied

[Information characteristics of neuronal and synaptic plasticity].

Informational losses in neuronal nets(NN) with plastic elements were estimated. These losses are related with 1) transition from "complicated" decoding when from the modification state of such elements information of the whole set of recorded elements is extracted to "simple" decoding natural of NN functioning when information is extracted independently for individual events; 2) uncertainty concerning NN structure, if at decoding in one of the modification states the neuron reactivity totally or the weight of plastic synapse equals zero. After the transition from complicated to simple decoding these losses for gradual plasticity are so great that NN with such plasticity has no advantages in informational capacity as compared to the binary one. These losses are absent for plasticity of Olbus type. They are relatively high for neuronal plasticity of Hebb type. For Hebb synapses their value essentially depends on the net parameters.

Humans↗
PubMed1988

Synaptic plasticity and functional stabilization in the hippocampal formation: possible role in Alzheimer's disease.

In this chapter we have explored the hypothesis that reactive synaptogenesis is an adaptive mechanism that can compensate for loss of a fraction of a defined neuronal population. Partial cell loss occurs during the course of aging, neurodegenerative diseases, and minor traumatic brain injuries. As cells are lost or as their function severely declines, new connections made by healthy neurons from within the population can assume parallel functions (homotypic sprouting), or fibers from converging pathways (heterotypic sprouting) can act to boost weakened signals and maintain functional stability. When cell death (or disease) progresses to the point where the pathway is broken, sprouting can no longer maintain information flow along the circuit and thus is unable to preserve function, unless new circuits can also be compensatory as, for example, after unilateral injury. We have analyzed the consequences of cell loss on the nature of circuit regrowth within the primary hippocampal circuits--i.e., the entorhinal-dentate gyrus-CA3-CA1 pathways. Reactive synaptogenesis can occur throughout the system after loss of each major cell population. Homotypic sprouting predominates in several pathways (e.g., dentate gyrus after CA4 loss, CA1 field after CA3 loss), and heterotypic sprouting appears prominent in the dentate gyrus after entorhinal cell loss. Each reactive network as a result of the regrowth can, in principle, still function, if cell loss is partial. The observation that sprouting also occurs in Alzheimer's disease illustrates that a slow and fractional loss of a neuronal assembly can trigger reactive growth in humans even along with a severe neurodegenerative disease. Axon sprouting was predicted in the dentate gyrus after entorhinal cell loss from rodent studies and has now been demonstrated in the brain of Alzheimer's victims. Cholinergic septal inputs, if present, can sprout, thereby enhancing cholinergic function and transmission by entorhinal perforant path fibers. CA4 fibers also sprout, thereby increasing positive feedback on granule neurons. At present, however, the functional significance of these mechanisms has yet to be established in clinical studies. Alzheimer's disease has a prolonged course with progressive symptoms. We would propose that axon sprouting or reactive synapse formation provides additional stability beyond the decline predicted from cell loss alone (Fig. 8). Thus, the clinical threshold where functions disappear is postponed for longer periods of time. Some reports in the literature are consistent with rapid behavioral decline followed by intervening periods of stability.(ABSTRACT TRUNCATED AT 400 WORDS)

Alzheimer Disease↗