Expression of the gap junction protein connexin-36 in the adult big brown bat cochlear nucleus may be involved in temporally precise biosonar processing

2012 ◽  
Vol 131 (4) ◽  
pp. 3361-3361
Author(s):  
Alyssa Wheeler ◽  
Carolina Veltri ◽  
Victoria Flores ◽  
Andrea Simmons ◽  
James Simmons
Keyword(s):  
Gap Junction ◽  
Cochlear Nucleus ◽  
Connexin 36 ◽  
Junction Protein ◽  
Big Brown Bat ◽  
Gap Junction Protein

Sharp Wave-Like Activity in the Hippocampus In Vitro in Mice Lacking the Gap Junction Protein Connexin 36

2003 ◽  
Vol 89 (4) ◽  
pp. 2046-2054 ◽  
Author(s):  
Isabel Pais ◽  
Sheriar G. Hormuzdi ◽  
Hannah Monyer ◽  
Roger D. Traub ◽  
Ian C. Wood ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Frequency Oscillation ◽  
Connexin 36 ◽  
Sharp Wave ◽  
Bath Application ◽  
Junction Protein ◽  
Gap Junction Protein ◽  
Electrical Signaling

Bath application of kainate (100–300 nM) induced a persistent gamma-frequency (30–80 Hz) oscillation that could be recorded in stratum radiatum of the CA3 region in vitro. We have previously described that in knockout mice lacking the gap junction protein connexin 36 (Cx36KO), γ-frequency oscillations are reduced but still present. We now demonstrate that in the Cx36KO mice, but not in wild-type (WT), large population field excitatory postsynaptic potentials, or sharp wave-burst discharges, also occurred during the on-going γ-frequency oscillation. These spontaneous burst discharges were not seen in WT mice. Burst discharges in the Cx36KO mice occurred with a mean frequency of 0.23 ± 0.11 Hz and were accompanied by a series of fast (approximately 60–115 Hz) population spikes or “ripple” oscillations in many recordings. Intracellular recordings from CA3 pyramidal cells showed that the burst discharges consisted of a depolarizing response and presumed coupling potentials (spikelets) could occasionally be seen either before or during the burst discharge. The burst discharges occurring in Cx36KO mice were sensitive to gap junctions blockers as they were fully abolished by carbenoxolone (200 μM). In control mice we made several attempts to replicate this pattern of sharp wave activity/ripples occurring with the on-going kainate-evoked γ-frequency oscillation by manipulating synaptic and electrical signaling. Partial disruption of inhibition, in control slices, by bath application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (1–4 μM) completely abolished all γ-frequency activity before any burst discharges occurred. Increasing the number of open gap junctions in control slices by using trimethylamine (TMA; 2–10 mM), in conjunction with kainate, failed to elicit any sharp wave bursts or fast ripples. However, bath application of the potassium channel blocker 4-aminopyridine (4-AP; 20–80 μM) produced a pattern of activity in control mice (13/16 slices), consisting of burst discharges occurring in conjunction with kainate-evoked γ-frequency oscillations, that was similar to that seen in Cx36KO mice. In a few cases ( n = 9) the burst discharges were accompanied by fast ripple oscillations. Carbenoxolone also fully blocked the 4-AP-evoked burst discharges ( n = 5). Our results show that disruption of electrical signaling in the interneuronal network can, in the presence of kainate, lead to the spontaneous generation of sharp wave/ripple activity similar to that observed in vivo. This suggests a complex role for electrically coupled interneurons in the generation of hippocampal network activity.

Expression and function of the neuronal gap junction protein connexin 36 in developing mammalian retina

2005 ◽  
Vol 493 (2) ◽  
pp. 309-320 ◽  
Author(s):  
Kristi A. Hansen ◽  
Christine L. Torborg ◽  
Justin Elstrott ◽  
Marla B. Feller
Keyword(s):  
Gap Junction ◽  
Connexin 36 ◽  
Junction Protein ◽  
Mammalian Retina ◽  
Gap Junction Protein ◽  
And Function

scholarly journals The Roles of Calmodulin and CaMKII in Cx36 Plasticity

2021 ◽  
Vol 22 (9) ◽  
pp. 4473
Author(s):  
Georg R. Zoidl ◽  
David C. Spray
Keyword(s):  
Synaptic Transmission ◽  
Gap Junctions ◽  
Gap Junction ◽  
Network Activity ◽  
Adaptive Plasticity ◽  
Electrical Synapses ◽  
Connexin 36 ◽  
Neuronal Network Activity ◽  
Junction Protein ◽  
Gap Junction Protein

Anatomical and electrophysiological evidence that gap junctions and electrical coupling occur between neurons was initially confined to invertebrates and nonmammals and was thought to be a primitive form of synaptic transmission. More recent studies revealed that electrical communication is common in the mammalian central nervous system (CNS), often coexisting with chemical synaptic transmission. The subsequent progress indicated that electrical synapses formed by the gap junction protein connexin-36 (Cx36) and its paralogs in nonmammals constitute vital elements in mammalian and fish synaptic circuitry. They govern the collective activity of ensembles of coupled neurons, and Cx36 gap junctions endow them with enormous adaptive plasticity, like that seen at chemical synapses. Moreover, they orchestrate the synchronized neuronal network activity and rhythmic oscillations that underlie the fundamental integrative processes, such as memory and learning. Here, we review the available mechanistic evidence and models that argue for the essential roles of calcium, calmodulin, and the Ca2+/calmodulin-dependent protein kinase II in integrating calcium signals to modulate the strength of electrical synapses through interactions with the gap junction protein Cx36.

The effect of connexin 36 deletion on chemotherapy-induced peripheral neuropathy (CIPN).

2016 ◽  
Vol 34 (26_suppl) ◽  
pp. 1-1
Author(s):  
Adam Sterman ◽  
Regina Hanstein ◽  
David C. Spray
Keyword(s):  
Gap Junction ◽  
Sensory Neurons ◽  
Chemotherapeutic Agents ◽  
Satellite Glial Cells ◽  
Connexin 36 ◽  
Junction Protein ◽  
Tactile Threshold ◽  
Gap Junction Protein ◽  
Novel Target ◽  
Von Frey Filaments

1 Background: CIPN is a debilitating side effect and dose limiting toxicity of many chemotherapeutic agents. CIPN induces pathological changes in dorsal root ganglia (DRG), leading to increased cross-talk among the glia that surround sensory neurons (Satellite Glial Cells, SGC’s) and between sensory neurons and their adjacent SGCs via gap junctions. Since Connexin 36 (Cx36) is the main neuronal gap junction protein, we investigated CIPN in mice with deletion of Cx36. Methods: To induce CIPN, mice were given two i.p. oxaliplatin (oxa) injections 2 days apart. Controls received saline (sal). We used transgenic mice, which were either heterozygous for Cx36 or complete Cx36 knockouts (Cx36 Het or Cx36 KO), and littermate controls (Cx36 wildtype), 6-14 per group. Tactile sensitivity of the hindpaws was assessed prior to and every week after injections for 4 weeks using von Frey filaments. The number of paw withdrawals to 10 stimulations with each filament and pain thresholds (corresponding to filament that elicits 8/10 responses) were recorded. Results: Oxa-injected wildtype mice had higher response rates to filaments compared to sal-injected controls (p < 0.05), and lower tactile thresholds (at 9 days: sal 6.0±0.0g vs. oxa 1.9±0.5g, p < 0.0001), indicating hypersensitivity. Compared with wildtype, mice lacking Cx36 (Cx36 KO) displayed significantly less tactile hypersensitivity after oxa (tactile threshold at 9 days: WT 1.9±0.5g vs. KO 4.0±0.4g, p < 0.01), whereas oxa induced tactile hypersensitivity occurred in a similar fashion in Cx36 Het mice (tactile threshold at 9 days: WT 1.9±0.5g vs. Het 1.5±0.1g). At 9 days, there were fewer responses to filaments in oxa-injected Cx36 KO mice compared to oxa-injected wildtype mice (p < 0.05), but not in oxa-injected Cx36 Het mice. Conclusions: We found that oxaliplatin induces transient CIPN, represented by tactile hypersensitivity, in wildtype mice. Deletion of the gap junction protein Cx36, as displayed in the Cx36 KO mice, resulted in significantly less CIPN. This is the first report that a neuronal gap junction protein may modulate pain sensitivity, and points to a new molecule (Cx36) as a potential novel target for CIPN therapy.

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