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Neuromodulation of inhibitory activi...

University of Illinois at Urbana-Champaign.

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Neuromodulation of inhibitory activity in thalamocortical circuits.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Neuromodulation of inhibitory activity in thalamocortical circuits./
Author:	Yang, Sunggu.
Description:	140 p.
Notes:	Adviser: Charles L. Cox.
Contained By:	Dissertation Abstracts International69-11B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3337971
ISBN:	9780549911524

Neuromodulation of inhibitory activity in thalamocortical circuits.
Yang, Sunggu.

Neuromodulation of inhibitory activity in thalamocortical circuits. - 140 p.

Adviser: Charles L. Cox.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008.

In my first study, I examined the effect of the neuromodulator, nitric oxide (NO) on thalamic neuron excitability and subsequent circuit activities. Nitric oxide synthase (NOS), an essential enzyme for NO production, is localized in thalamic inhibitory neurons as well as cholinergic brainstem neurons that innervate the thalamus. I investigated NO-mediated effects on inhibitory activity in the dorsal lateral geniculate nucleus (dLGN) using an in vitro slice preparation. NO donors selectively potentiated the frequency, but not amplitude of spontaneous inhibitory postsynaptic currents (sIPSCs) in thalamocortical relay neurons. This increase persisted in tetrodotoxin (TTX), consistent with an increase in presynaptic GABA release. These NO-mediated actions were attenuated by guanylyl cyclase inhibitors indicating the involvement of cGMP pathway.

ISBN: 9780549911524Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Neuromodulation of inhibitory activity in thalamocortical circuits.
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020 $a 9780549911524
035 $a (UMI)AAI3337971
035 $a AAI3337971
040 $a UMI $c UMI
100 1 $a Yang, Sunggu. $3 1025304
245 1 0 $a Neuromodulation of inhibitory activity in thalamocortical circuits.
300 $a 140 p.
500 $a Adviser: Charles L. Cox.
500 $a Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6623.
502 $a Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008.
520 $a In my first study, I examined the effect of the neuromodulator, nitric oxide (NO) on thalamic neuron excitability and subsequent circuit activities. Nitric oxide synthase (NOS), an essential enzyme for NO production, is localized in thalamic inhibitory neurons as well as cholinergic brainstem neurons that innervate the thalamus. I investigated NO-mediated effects on inhibitory activity in the dorsal lateral geniculate nucleus (dLGN) using an in vitro slice preparation. NO donors selectively potentiated the frequency, but not amplitude of spontaneous inhibitory postsynaptic currents (sIPSCs) in thalamocortical relay neurons. This increase persisted in tetrodotoxin (TTX), consistent with an increase in presynaptic GABA release. These NO-mediated actions were attenuated by guanylyl cyclase inhibitors indicating the involvement of cGMP pathway.
520 $a Secondly, I found that in addition to a presynaptic action, NO activation also led to a robust, long-lasting depolarization of GABAergic thalamic reticular nucleus (TRN) neurons. NO agonists depolarized both TRN and thalamic relay neurons; however, the magnitude produced in TRN neurons was significantly greater than that in relay neurons. In contrast, dLGN interneurons were unaffected by NO donors. Overall, my results indicate that NO upregulates thalamic inhibitory activity that could in turn enhance surround antagonistic actions, and functionally may sharpen receptive fields. In addition, these excitatory actions of NO on GABAergic TRN may alter the firing mode and thereby reduce intrathalamic rhythmic activities.
520 $a In my second series of experiments, I investigated the role of glia-mediated glutamate-glutamine cycle on intrathalamic rhythmic activities. Glia play an important role in glutamine synthesis via glutamate metabolism and subsequent transport to presynaptic terminals of neurons where glutamine can be converted to either glutamate or GABA (glutamate-glutamine shuttle). I found that disrupting this shuttle by inhibiting the neuronal glutamine transporter (system A transporter) or using a selective gliotoxic agent dramatically decreased intrathalamic rhythmic activities. The disruption of the rhythmic activities was associated with a significant attenuation of the synaptically evoked inhibitory postsynaptic current (eIPSC) in thalamic relay neurons. These data suggest that glutamate-glutamine cycle is a key contributor to sustaining inhibitory synaptic transmission, and thereby influence intrathalamic rhythmic activities associated with absence epilepsy.
520 $a In last chapter, I demonstrate that the inhibitory currents arising from interneurons and TRN neurons can be distinguished by their kinetics. The local interneurons are of interest because these neurons have two distinct outputs: axonal and dendritic. These cells have classical axonal outputs, termed F1 terminals, as well as presynaptic dendrites that also release GABA and have been termed F2 terminals. In contrast, TRN neurons give rise to only axonal, F1 outputs. My data indicate that the rise time, slope and half-width of miniature ISPCs (mIPSCs) recorded in dLGN relay neurons have greater variance than those recorded in ventrobasal nucleus (VB) neurons. It is important to note that in rodents, the dLGN has local interneurons (F1 & F2 inputs) whereas VB does not contain interneurons and thus lack F2 innervation. Paired recordings from synaptically-coupled interneurons and dLGN relay cells were used to characterize the IPSCs of this connection. The rise time and half-width of these unitary IPSCs were similar to mIPSCs in dLGN relay neurons and were significantly larger than mIPSCs in VB relay neurons. In order to differentiate F1 outputs from F2 output, we next subdivided relay neurons based upon their response to mGluR activation. In ACPD-positive neurons (F2 + F1 activity) mIPSCs have larger rise times and half-widths compared to those in ACPD-negative neurons (F1 only) as well as VB neurons. These results suggest that dendritic output might provide functionally distinct inhibitory current that differ from axon-originated inhibition, and thereby may play distinct role in modulating the visual information processing. (Abstract shortened by UMI.)
590 $a School code: 0090.
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Physiology. $3 1017816
690 $a 0317
690 $a 0719
710 2 $a University of Illinois at Urbana-Champaign. $3 626646
773 0 $t Dissertation Abstracts International $g 69-11B.
790 $a 0090
790 1 0 $a Cox, Charles L., $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3337971