Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 10 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.

Thesis (M.S.)--Ohio University, August, 2006. / Title from PDF t.p. Includes bibliographical references.

Thesis (Ph.D.)--Murdoch University, 2008. / Thesis submitted to the Faculty of Health Sciences. Includes bibliographical references (leaves 210-247)

Thesis (Ph. D.)--University of Hong Kong, 1994. / Includes bibliographical references (leaves 128-140).

Thesis (Ph. D.)--University of Virginia, 1999. / Spine title: K-ATP channels & memory. Includes bibliographical references (p. 101-119). Also available online through Digital Dissertations.

Thesis (Honors)--College of William and Mary, 2009. / Includes bibliographical references (leaves 75-79). Also available via the World Wide Web.

Neurons transmit information through spikes in neural network through synaptic couplings. Given the prevalence of correlation among neural spike trains experimentally observed in different brain areas, it is of interest to study how neurons compute correlated input. Yet how it depends on the synaptic properties and conductance kinetics in neuronal interaction is very little known. Through simulation of leaky integrate-and-fire (LIF) neurons, we have studied the effects of excitatory and inhibitory synaptic decay times, level of background activities and higher-order conductance effects on the output correlation of different time scales for neurons receiving correlated excitatory input, and provided important understanding on the mechanism of how these factors influence neural computation of such correlated input. We showed that when the conductance effects are totally ignored, increasing excitatory synaptic decay time jitters output spike time and shapes the output correlation of short to medium time scale, while the output correlation of very long time scale is determined by the membrane time constant. When conductance effects are considered, this is no longer the case as the effective membrane time constant becomes comparable to the excitatory decay time. We found that the ratio of long-term correlation to short-term correlation (synchrony) increases with excitatory synaptic decay time and decreases with the level of input activities due to the combined effects of jittered spike time, which can be predicted from the time window and magnitude of the effects of a single input spike on membrane potential, and burst firing. In particular, it is possible for neurons with small excitatory synaptic decay time in high conductance state to respond to correlated input by solely giving extra precisely timed synchronous spikes without exhibiting correlation of longer time scale. In addition, we found that inhibitory synaptic decay time shapes correlation by controlling the relative contribution of excitatory and inhibitory input to output firing. As a result, both output correlation and synchrony increase with it. These results are qualitatively true for a wide range of input correlation and synaptic efficacies. Finally, we showed that fluctuations of conductance and membrane potential reduce output correlation, which can be explained by the reduced prevalence of burst firing. These results suggest that spike initiation dynamics of neurons can be well characterized by their synaptic decay times and the level of input activities. These properties are therefore expected to influence neurons’ ability to code temporal information. These results also hint that correlation, in particular that of long time scale, would be lower if more realistic biophysical features like neural adaptations and network circuitry with feed-forward or recurrent inhibition are considered. It suggests that studies using single LIF neurons tend to overestimate output correlation and underestimate the ability of neurons in producing precisely timed output.

Introduction Norepinephrine-containing neurons clustered within the locus coeruleus (LC) provide most of the norepinephrine present within the central nervous system. These cells have tonic pacemaker activity and this activity is regulated by a variety of neurotransmitter inputs. The focus of this review is primarily on classical, non-neuropeptide, neurotransmitter input to the LC and the reciprocal projections of noradrenergic neurons to those classical neurotransmitter systems. Input to the LC from serotonin-, dopamine-, γ-aminobutyric acid (GABA)-, glutamate-, and acetylcholine-containing neurons are described. In addition, input from the neuropeptide, substance P, receives attention because of the interest in this neuropeptide in psychiatric disease. Special attention is given to reciprocal projections from the LC to the monoamine neurotransmitters dopamine and serotonin. See Chapter 1 for a detailed description of the anatomy of the LC. Noradrenergic circuitry: input to the LC Early tract-tracing studies suggested that the LC received widespread input from many sites in the brain. A combination of techniques, however, including discrete injections of a more sensitive tract-tracing compound, anterograde labeling studies, and single-pulse stimulation studies forced a reconsideration of brain areas with direct input to the LC. The major afferents to the LC are rostral medullary in origin, with cell bodies located in the nucleus paragigantocellularis (PGi, using excitatory amino acid neurotransmitters) and nucleus prepositus hypoglossi (PrH, using GABA). However, dense projections from many brain regions terminate in the pericoerulear area, an area heavily invested with dendrites from LC neurons, and in the PGi and PrH.

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