Thesis (Ph. D.)--University of Wisconsin--Madison, 1981. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

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Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Acetylcholine (Ach) has been shown to have excitatory effects on the mammalian heart, and it is possible that these actions may be related to certain arrhythmias. To test this hypothesis experiments were designed to study in vivo and in vitro these effects of Ach on atrial refractoriness, excitability, and rate and tension [TRUNCATED] / 2031-01-01

The ability of the brain to store information and adapt to changes in the sensory environment stems from the capability of neurons to change their communication with other neurons (“synaptic plasticity”). However, the ability of synapses to change (e.g., strengthen) is profoundly influenced by various chemical signals released in the nervous system (neuromodulators). Such modulatory effects may be preferential for different types of synapses. For example, cortical acetylcholine (ACh) has been shown to result in a relative enhancement of thalamocortical over intracortical synapses. Here, I tested the hypothesis that field postsynaptic potentials (fPSPs) in the rat primary visual cortex (V1) evoked by single pulse stimulation of the lateral geniculate nucleus (LGN) can be potentiated when LGN stimulation is paired with short bursts of stimuli applied to the basal forebrain (BF), the major source of ACh released in the cortex. Stimulation of the ipsi- and contralateral LGN elicited fPSPs in V1, with fPSPs triggered from the contralateral LGN exhibiting longer latencies and smaller amplitudes relative to fPSPs in ipsilateral projections. Stimulation bursts applied to the BF, paired with single, delayed LGN pulses, resulted in an enhancement of fPSP amplitude (~25%) for contralateral inputs at short (130 ms), but not longer (200-1000 ms) pairing intervals, while ipsilateral fPSPs failed to show significant potentiation over these intervals. The enhancement of the contralateral LGN-V1 fiber system induced by BF pairings was abolished by systemic or V1 application of the muscarinic receptor antagonist scopolamine, while systemic nicotinic receptor blockade was ineffective. These data suggest that there is a differential capacity for plasticity induction between strong, ipsilateral and weaker, contralateral fiber inputs to V1, with weaker inputs exhibiting greater synaptic enhancement following pairing with BF stimulation to elicit cortical ACh release. This preferential readiness for synaptic potentiation in normally weaker, non-dominant fiber inputs to V1 may facilitate the detection and integration of separate sensory signals originating in thalamic sensory nuclei. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2009-03-31 08:49:23.896

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (Ph. D.)--University of Chicago, 1941. / Reproduced from type-written copy. "List of references": p. 16-18.

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