Date of Completion

6-13-2011

Embargo Period

6-13-2011

Advisors

Heather Read; Joseph LoTurco

Field of Study

Psychology

Degree

Master of Arts

Open Access

Campus Access

Abstract

Associative Hebbian-type synaptic plasticity underlies the mechanisms of learning and memory, but it leads to runaway dynamics of synaptic weights and lacks mechanisms for synaptic competition. Heterosynaptic plasticity may solve these problems by complementing plasticity at synapses that were active during the induction, with opposite-sign changes at non-activated synapses. In visual cortex a potential candidate mechanism for normalization is plasticity induced by purely postsynaptic protocol, intracellular tetanization. Here we asked if intracellular tetanization can induce long-term plasticity in auditory cortex. We recorded evoked excitatory postsynaptic potentials (EPSPs) in layer 2/3 pyramidal cells in slices from rat auditory cortex. Two types of inputs were observed. Regular inputs (observed at 68 of 90 inputs, 76%) were characterized by a high-variance, gap-free distribution of response amplitudes, while all-or-none inputs (22 inputs, 24%) were characterized by a low-variance, high-amplitude distribution of successful responses, and a low-variance, low-amplitude distribution of failures. After intracellular tetanization at regular inputs, 27 of 68 synapses (40%) showed long-term depression, 20 synapses (29%) showed potentiation and 21 synapses (31%) did not change. The direction of plasticity was correlated with the initial release probability: inputs with initially low release probability tended to be potentiated, while inputs with initially high release probability tended to be depressed. Thus, intracellular tetanization had a normalizing effect on synaptic transmission. The long-term changes induced by intracellular tetanization involved presynaptic mechanisms. Changes of EPSP amplitudes were correlated with changes of two indicators of probability of release: paired pulse ratio (PPR) and the reversed coefficient of variation (CV-2). Similar trends were observed at at all-or-none inputs. These results indicate that the ability of purely postsynaptic challenges to induce plasticity is a general property of neurons, not restricted to a specific cortical region. The role of this type of plasticity may be involved in controlling runaway plasticity.

Major Advisor

Maxim Volgushev

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