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Cited by 17Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionEpilepsy research and treatment

The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.

Regionally Selective Blockade of GABAergic Inhibition by Zinc in the Thalamocortical System: Functional Significance

Gibbs III, John W., Zhang, Yun-Fu, Shumate, Melissa D., Coulter, Douglas A.·2000·Journal of Neurophysiology
DOI 10.1152/jn.2000.83.3.1510
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Abstract

The thalamocortical (TC) system is a tightly coupled synaptic circuit in which GABAergic inhibition originating from the nucleus reticularis thalami (NRT) serves to synchronize oscillatory TC rhythmic behavior. Zinc is colocalized within nerve terminals throughout the TC system with dense staining for zinc observed in NRT, neocortex, and thalamus. Whole cell voltage-clamp recordings of GABA-evoked responses were conducted in neurons isolated from ventrobasal thalamus, NRT, and somatosensory cortex to investigate modulation of the GABA-mediated chloride conductance by zinc. Zinc blocked GABA responses in a regionally specific, noncompetitive manner within the TC system. The regional levels of GABA blockade efficacy by zinc were: thalamus > NRT > cortex. The relationship between clonazepam and zinc sensitivity of GABA A-mediated responses was examined to investigate possible presence or absence of specific GABA A receptor (GABAR) subunits. These properties of GABARs have been hypothesized previously to be dependent on presence or absence of the γ2 subunit and seem to display an inverse relationship. In cross-correlation plots, thalamic and NRT neurons did not show a statistically significant relationship between clonazepam and zinc sensitivity; however, a statistically significant correlation was observed in cortical neurons. Spontaneous epileptic TC oscillations can be induced in vitro by perfusion of TC slices with an extracellular medium containing no added Mg 2+. Multiple varieties of oscillations are generated, including simple TC burst complexes (sTBCs), which resemble spike-wave discharge activity. A second variant was termed a complex TC burst complex (cTBC), which resembled generalized tonic clonic seizure activity. sTBCs were exacerbated by zinc, whereas cTBCs were blocked completely by zinc. This supported the concept that zinc release may modulate TC rhythms in vivo. Zinc interacts with a variety of ionic conductances, including GABAR currents, N-methyl-d-aspartate (NMDA) receptor currents, and transient potassium (A) currents.d−2-amino-5-phosphonovaleric acid and 4-aminopyridine blocked both s- and cTBCs in TC slices. Therefore NMDA and A current-blocking effects of zinc are insufficient to explain differential zinc sensitivity of these rhythms. This supports a significant role of zinc-induced GABAR modulation in differential TC rhythm effects. Zinc is localized in high levels within the TC system and appears to be released during TC activity. Furthermore application of exogenous zinc modulates TC rhythms and differentially blocks GABARs within the TC system. These data are consistent with the hypothesis that endogenously released zinc may have important neuromodulatory actions impacting generation of TC rhythms, mediated at least in part by effects on GABARs.

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Crossref · 10.1152/jn.2000.83.3.1510

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  • Thalamocortical oscillations provide modulatory inputs to the thalamus via GABAergic neurons that synapse in the reticular nucleus of the thalamus.

    “Thalamocortical oscillations also provide modulatory inputs to the thalamus via GABAergic neurons that synapse in the reticular nucleus of the thalamus [38].”

    From Cerebral hierarchies: predictive processing, precision and the pulvinar (2015) · cites this paper as [38]

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Research works printed but not linked: 5

  1. Brooks-Kayal A., 1998, Nature, 4, 1166
  2. Celentano J. J., 1991, Mol. Pharmacol., 40, 766
  3. De Lean A., 1987, Am. J. Physiol., 235, E97
  4. Gibbs J. W., 1996, Soc. Neurosci. Abstr., 22, 104
  5. Olsen R. W., 1990, J. Chem. Neuroanat., 3, 59

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Metadata

Authors
Gibbs III, J. W., Zhang, Y.-F., Shumate, M. D., & Coulter, D. A.
Affiliations
  • Department of Anatomy, Medical College of Virginia of Virginia Commonwealth University, Richmond, Virginia 23298-0599; and
  • Department of Neurology,
  • Department of Physiology, and
  • Children's Hospital of Philadelphia (US)
ORCID
Coulter, Douglas A.
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
2000-03-01
Volume
83
Issue
3
Pages
1510-1521
ISSN
  • 0022-3077 (ISSN-L)
  • 1522-1598
DOI
10.1152/jn.2000.83.3.1510
OpenAlex
W2295455646
Cited by
17
References
62
Citations by year
2026: 1 · 2022: 1 · 2015: 1 · 2012: 1
FWCI
0.77
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurophysiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS-31000)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
Keywords
zinc, thalamocortical system, GABAergic inhibition, GABAA receptor, nucleus reticularis thalami, ventrobasal thalamus, somatosensory cortex, regional specificity, non-competitive inhibition, gamma2 subunit, thalamocortical oscillations, spike-wave discharges, NMDA receptor, transient potassium current
MeSH terms
Animals, Coloring Agents, Extracellular Space, gamma-Aminobutyric Acid, Neurons, Somatosensory Cortex, Thalamic Nuclei, Zinc, 4-Aminopyridine, 2-Amino-5-phosphonovalerate, Patch-Clamp Techniques, Excitatory Amino Acid Antagonists, Subthalamic Nucleus, Ventral Thalamic Nuclei, Rats, GABA-A Receptor Antagonists

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