scholarly journals Rebound Bursts in GABAergic Neurons of the Thalamic Reticular Nucleus in Postnatal Mice

2010 ◽  
pp. 273-280
Author(s):  
X Wang ◽  
G Yu ◽  
X Hou ◽  
J Zhou ◽  
B Yang ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Receptor Antagonist ◽  
Channel Blocker ◽  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
K Channel ◽  
Whole Cell Patch Clamp ◽  
Gabaa Receptor Antagonist ◽  
Inactive Analog

Whole cell patch-clamp recordings from GABAergic cells of thalamic reticular nucleus (RTN) in thalamocortical slices made from postnatal day 6 (P6) to 10 (P10) were used to investigate the pattern of rebound bursts (RBs) triggered by an injection of hyperpolarizing current into RTN cells. The number of RBs in the RTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely on the amplitude of the after-hyperpolarizations (AHPs). RB patterns in response to hyperpolarizing current injection into relay cells were markedly different from RB patterns in RTN cells with an after-depolarization. GABAA receptor antagonist bicuculline methiodide (BMI) changed burst firing patterns, increasing the duration of RB and decreasing the amplitude of AHP in RTN cells. Furthermore, local puffs of NMDA in the presence of BMI induced RBs. K+ channel blocker 4-aminopyridine partially mimicked the effect of BMI on AHPs. The shapes of RBs were altered by a selective CaMKII inhibitor KN-62, but not by an inactive analog KN-04.

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1993-2003 ◽  
Author(s):  
R. A. Warren ◽  
A. Agmon ◽  
E. G. Jones
Keyword(s):  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Initial Response ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Synaptic Interactions ◽  
Gabaa Receptor Antagonist

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

Nucleus-Specific Differences in GABAA-Receptor-Mediated Inhibition Are Enhanced During Thalamic Development

2000 ◽  
Vol 83 (1) ◽  
pp. 350-358 ◽  
Author(s):  
Molly M. Huntsman ◽  
John R. Huguenard
Keyword(s):  
Patch Clamp ◽  
Decay Time ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Aged Rats ◽  
Decay Kinetics ◽  
Physiological Conditions ◽  
Postsynaptic Currents ◽  
Ventrobasal Complex ◽  
Whole Cell Patch Clamp

Inhibitory postsynaptic currents (IPSCs) mediated by GABAA receptors are much slower in neurons of the thalamic reticular nucleus (RTN) versus those in the ventrobasal complex (VB) of young rats. Here we confirm and extend those findings regarding GABAA response heterogeneity especially in relation to development. Whole cell patch-clamp recordings were used to investigate GABAAspontaneous and electrically evoked IPSCs (sIPSCs/eIPSCs) in RTN and VB cells of different aged rats. Consistent with earlier findings, sIPSC duration at P8–12 was considerably longer in RTN (weighted decay time constant: τD,W = 56.2 ± 4.9 ms; mean ± SE) than in VB (τD,W = 15.8 ± 1.0 ms) neurons. Decay kinetics in RTN neurons did not differ at P21–30 (45.5 ± 4.7 ms) or P42–60 (51.6 ± 10.6 ms). In contrast, VB sIPSCs were significantly faster at both P21–30 (τD,W = 10.8 ± 0.9 ms) and P42–60 (τD,W = 9.2 ± 0.4 ms) compared with P8–12 animals. IPSCs displayed differential outward rectification and temperature dependence, providing further support for nucleus-specific responses. τD,W increased with membrane depolarization but with a net larger effect in VB. By contrast, τD,W was always smaller at higher temperatures but with relatively greater difference observed in RTN. Thus nuclear differences in GABAA IPSCs are not only maintained, but enhanced in the mature rodent under physiological conditions. These findings support our hypothesis that unique GABAA receptors mediate slowly decaying RTN IPSCs that are a critical and enduring feature of the thalamic circuit. This promotes powerful intranuclear inhibition and likely prevents epileptiform thalamocortical hypersynchrony.

scholarly journals Significance of the Thalamic Reticular Nucleus GABAergic Neurons in Normal and Pathological Activity of the Brain

2012 ◽  
Vol 02 (04) ◽  
pp. 436-444 ◽  
Author(s):  
Zakaria I. Nanobashvili ◽  
Arkadi G. Surmava ◽  
Irine G. Bilanishvili ◽  
Maia G. Barbaqadze ◽  
Magda D. Mariamidze ◽  
...  
Keyword(s):  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
The Brain

scholarly journals Different Topography of the Reticulothalmic Inputs to First- and Higher-Order Somatosensory Thalamic Relays Revealed Using Photostimulation

2007 ◽  
Vol 98 (5) ◽  
pp. 2903-2909 ◽  
Author(s):  
Ying-Wan Lam ◽  
S. Murray Sherman
Keyword(s):  
Laser Scanning ◽  
Higher Order ◽  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Local Inhibition ◽  
Strategic Position ◽  
Almost All ◽  
Laser Scanning Photostimulation ◽  
Lateral Nucleus

The thalamic reticular nucleus is a layer of GABAergic neurons that occupy a strategic position between the thalamus and cortex. Here we used laser scanning photostimulation to compare in young mice (9–12 days old) the organization of the reticular inputs to first- and higher-order somatosensory relays, namely, the ventral posterior lateral nucleus and posterior nucleus, respectively. The reticulothalamic input footprints to the ventral posterior lateral nucleus neurons consisted of small, single, topographically organized elliptical regions in a tier away from the reticulothalamic border. In contrast, those to the posterior nucleus were complicated and varied considerably among neurons: although almost all contained a single elliptical region near the reticulothalamic border, in most cases, they consisted of additional discontinuous regions or relatively diffuse regions throughout the thickness of the thalamic reticular nucleus. Our results suggest two sources of reticular inputs to the posterior nucleus neurons: one that is relatively topographic from regions near the reticulothalamic border and one that is relatively diffuse and convergent from most or all of the thickness of the thalamic reticular nucleus. We propose that the more topographic reticular input is the basis of local inhibition seen in posterior nucleus neurons and that the more diffuse and convergent input may represent circuitry through which the ventral posterior lateral and posterior nuclei interact.

GABA-Mimetic Actions of Withania somnifera on Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis in Mice

2013 ◽  
Vol 41 (05) ◽  
pp. 1043-1051 ◽  
Author(s):  
Hua Yin ◽  
Dong Hyu Cho ◽  
Soo Joung Park ◽  
Seong Kyu Han
Keyword(s):  
Patch Clamp ◽  
Receptor Antagonist ◽  
Withania Somnifera ◽  
Substantia Gelatinosa ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Whole Cell ◽  
Cell Patch Clamp ◽  
Whole Cell Patch Clamp ◽  
Inward Currents

The plant Withania somnifera (WS), also known as Ashwagandha, has been used widely in traditional medicine systems in India and Nepal (Ayurveda), and has been accepted to cure various ailments. In this study, the whole-cell patch clamp technique was performed to examine the mechanism of action of WS on the SG neurons of the Vc from mouse brainstem slices. In whole-cell patch clamp mode, methanol extract of Withania somnifera (mWS) induced short-lived and repeatable inward currents in all SG neurons tested (31.3±8.51 pA, n = 7) using a high chloride pipette solution. The mWS-induced inward currents were concentration dependent and maintained in the presence of tetrodotoxin (TTX), a voltage gated Na + channel blocker, CNQX, a non-NMDA glutamate receptor antagonist, AP5, an NMDA receptor antagonist and strychnine, a glycine receptor antagonist. The mWS induced currents were blocked by picrotoxin, a GABAA receptor antagonist. These results show that mWS has an inhibitory effects on SG neurons of the Vc through GABAA receptor-mediated activation of chloride ion channels, indicating that mWS contains compounds with sedative effects on the central nervous system. These results also suggest that mWS may be a potential target for modulating orofacial pain processing.

scholarly journals Thapsigargin-induced Ca2+ mobilization in acutely isolated mouse lacrimal acinar cells is dependent on a basal level of Ins(1,4,5)P3 and is inhibited by heparin

1994 ◽  
Vol 299 (1) ◽  
pp. 37-40 ◽  
Author(s):  
P M Smith ◽  
D V Gallacher
Keyword(s):  
Patch Clamp ◽  
Atpase Activity ◽  
Receptor Antagonist ◽  
Acinar Cells ◽  
Cell Types ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Whole Cell Patch Clamp ◽  
Subsequent Exposure ◽  
Lacrimal Acinar Cells

The tumour-promoting agent thapsigargin has been shown to inhibit the microsomal Ca(2+)-ATPase and cause Ca2+ mobilization in a variety of cell types including exocrine acinar cells [Bird, Obie and Putney (1992) J. Biol. Chem. 267, 18382-18386]. When applied to acutely isolated lacrimal acinar cells, thapsigargin caused a slow biphasic activation of both the Ca(2+)-dependent K+ and Cl- currents measured using the whole-cell patch-clamp technique. If the only action of thapsigargin is to inhibit sequestration into Ca2+ pools, then Ca2+ mobilization following exposure to thapsigargin indicates that there is a significant ‘leak’ of Ca2+ into the cytoplasm, which is normally countered by Ca(2+)-ATPase activity. In the present study, we introduced the Ins(1,4,5)P3 receptor antagonist heparin (200 micrograms/ml) into lacrimal acinar cells via the patch-clamp pipette. Following a 5 min preincubation in the presence of heparin, neither acetylcholine (1 microM) nor thapsigargin (1 microM) caused any significant increase in either Ca(2+)-dependent current. Caffeine has been shown to suppress basal Ins(1,4,5)P3 levels in exocrine acinar cells [Toescu, O'Neill, Petersen and Eisner (1992) J. Biol. Chem. 267, 23467-23470]. Preincubation with caffeine (10 mM) also inhibited the response to subsequent exposure to thapsigargin. These data suggest that, in acutely isolated lacrimal cells, the source of the Ca2+ leak which gives rise to Ca2+ mobilization following inhibition of Ca2+ re-uptake by thapsigargin is Ca2+ release, from Ins(1,4,5)P3-dependent Ca2+ pools, caused by resting Ins(1,4,5)P3 levels.

scholarly journals Selectively driving cholinergic fibers optically in the thalamic reticular nucleus promotes sleep

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Kun-Ming Ni ◽  
Xiao-Jun Hou ◽  
Ci-Hang Yang ◽  
Ping Dong ◽  
Yue Li ◽  
...  
Keyword(s):  
Eye Movement ◽  
Nicotinic Acetylcholine Receptors ◽  
Rem Sleep ◽  
Sleep Onset ◽  
Cholinergic Neurons ◽  
Nrem Sleep ◽  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Rapid Eye Movement

Cholinergic projections from the basal forebrain and brainstem are thought to play important roles in rapid eye movement (REM) sleep and arousal. Using transgenic mice in which channelrhdopsin-2 is selectively expressed in cholinergic neurons, we show that optical stimulation of cholinergic inputs to the thalamic reticular nucleus (TRN) activates local GABAergic neurons to promote sleep and protect non-rapid eye movement (NREM) sleep. It does not affect REM sleep. Instead, direct activation of cholinergic input to the TRN shortens the time to sleep onset and generates spindle oscillations that correlate with NREM sleep. It does so by evoking excitatory postsynaptic currents via α7-containing nicotinic acetylcholine receptors and inducing bursts of action potentials in local GABAergic neurons. These findings stand in sharp contrast to previous reports of cholinergic activity driving arousal. Our results provide new insight into the mechanisms controlling sleep.

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