Biomedical subjects

Xinhuai Liu

Publications and source records attributed to Xinhuai Liu.

4 recordsLinked to original sources

PubMed2005

NMDA receptors regulate developmental gap junction uncoupling via CREB signaling.

Signaling through gap junctions (electrical synapses) is important in the development of the mammalian central nervous system. Abundant between neurons during postnatal development, gap junction coupling subsequently decreases and remains low in the adult, confined to specific subsets of neurons. Here we report that developmental uncoupling of gap junctions in the rat hypothalamus in vivo and in vitro is associated with a decrease in connexin 36 (Cx36) protein expression. Both developmental gap junction uncoupling and Cx36 downregulation are prevented by the blockade of NMDA glutamate receptors, action potentials and the calcium-cyclic AMP response element binding protein (CREB), and are accelerated by CREB overexpression. Developmental gap junction uncoupling and Cx36 downregulation are not affected by blockade of non-NMDA glutamate receptors, and do not occur in hypothalamic neurons from NMDA receptor subunit 1 (NMDAR1) knockout mice. These results demonstrate that NMDA receptor activity contributes to the developmental uncoupling of gap junctions via CREB-dependent downregulation of Cx36.

Action Potentials↗

PubMed2005

Suppression of potassium channels elicits calcium-dependent plateau potentials in suprachiasmatic neurons of the rat.

By using whole-cell recordings in acute and organotypic hypothalamic slices, we found that following K+ channel blockade, sustained plateau potentials can be elicited by current injection in suprachiasmatic neurons. In an attempt to determine the ionic basis of these potentials, ion-substitution experiments were carried out. It appeared that to generate plateau potentials, calcium influx was required. Plateau potentials were also present when extracellular calcium was replaced by barium, but were independent upon an increase in the intracellular free calcium concentration. Substitution of extracellular sodium by the impermeant cation N-methyl-D-glucamine indicated that sodium influx could also contribute to plateau potentials. To gain some information on the pharmacological profile of the Ca++ channels responsible for plateau potentials, selective blocker of various types of Ca++ channel were tested. Plateau potentials were unaffected by isradipine, an L-type Ca++ channel blocker. However, they were slightly reduced by omega-conotoxin GVIA and omega-agatoxin TK, blockers of N-type and P/Q-type Ca++ channels, respectively. These data suggest that R-type Ca++ channels probably play a major role in the genesis of plateau potentials. We speculate that neurotransmitters/neuromodulators capable of reducing or suppressing potassium conductance(s) may elicit a Ca++-dependent plateau potential in suprachiasmatic neurons, thus promoting sustained firing activity and neuropeptide release.

Animals↗

PubMed2004

Sodium-activated potassium conductance participates in the depolarizing afterpotential following a single action potential in rat hippocampal CA1 pyramidal cells.

The depolarizing afterpotential (DAP) following an action potential increases the excitability of a neuron. Mechanisms related to the DAP following an antidromic or current-induced spike were studied in CA1 pyramidal cells by whole-cell recordings in hippocampal slices in vitro. In DAP-holding voltage curves, the DAP at 10 ms after the spike peak (DAP10) was extrapolated to reverse at about -50 mV. Increase of extracellular K(+) concentration increased DAP and neuronal bursting. DAP10 reversal potential shifted positively with an increase in [K(+)](o) and with the blockade of K(+) conductance using pipettes filled with Cs(+). Similarly, extracellular tetraethylammonium (TEA; 10 mM), 4-aminopyridine (3-10 mM) increased DAP and shifted the DAP10 reversal potential to a depolarizing direction. Decrease of [Ca(2+)](o) did not alter DAP significantly, suggesting a nonessential role of Ca(2+) in the DAP. Perfusion of tetrodotoxin (TTX; 0.1-1 microM) and replacement of extracellular Na(+) by choline(+) suppressed both spike height and DAP simultaneously. Replacement of extracellular Na(+) by Li(+) increased DAP and spike bursts, and caused a positive shift of the DAP10 reversal potential. It is suggested that Li(+) increased DAP by blocking an Na(+)-activated K(+) current. In summary, multiple K(+) conductances are normally active during the DAP following a single action potential.

4-Aminopyridine↗

PubMed2003

Partial hippocampal kindling increases GABAB receptor-mediated postsynaptic currents in CA1 pyramidal cells.

In previous studies, we showed that partial hippocampal kindling decreased the efficacy of the presynaptic GABAB receptors on both GABAergic and glutamatergic terminals of CA1 neurons in hippocampal slices in vitro. In this study, GABAB receptor-mediated inhibitory postsynaptic currents (GABAB-IPSCs) were assessed by whole-cell recordings in CA1 pyramidal neurons in hippocampal slices of male Long-Evans rats. The peak GABAB-IPSC evoked by a brief train of supramaximal stratum radiatum stimuli (20 pulses of 300 Hz) in the presence of picrotoxin (0.1 mM) and kynurenic acid (1 mM) was larger in neurons of kindled (65.9 +/- 5.2 pA, N=42 cells) than control (45.8 +/- 4.8 pA, N=32 cells) rats (P<0.01). Adding GABA uptake blocker nipecotic acid (1 mM) or GABAB receptor agonist baclofen (0.01 mM) in the perfusate induced outward currents that were blocked by GABAB receptor antagonist CGP 55845A (1 microM). The peak outward current induced by nipecotic acid was larger in neurons of the kindled (55.4 +/- 5.7 pA, N=30) than the control group (39.8 +/- 4.5 pA, N=28) (P<0.05). However, the magnitude of the baclofen-induced current was not different between kindled (90.8 +/- 6.9 pA, N=29) and control (87.2 +/- 5.9 pA, N=21) groups (P>0.05). We concluded that partial hippocampal kindling increased GABAB-IPSCs in hippocampal CA1 pyramidal cells via multiple presynaptic mechanisms.

Animals↗