Vasopressin Increases GABAergic Inhibition of Rat Hypothalamic Paraventricular Nucleus Neurons In Vitro

2000 ◽  
Vol 83 (2) ◽  
pp. 705-711 ◽  
Author(s):  
M.L.H.J. Hermes ◽  
J. M. Ruijter ◽  
A. Klop ◽  
R. M. Buijs ◽  
L. P. Renaud
Keyword(s):  
Paraventricular Nucleus ◽  
Receptor Agonist ◽  
Hypothalamic Paraventricular Nucleus ◽  
Membrane Properties ◽  
Magnocellular Neurons ◽  
Membrane Hyperpolarization ◽  
Perforated Patch ◽  
Intrinsic Membrane Properties ◽  
Brain Slice Preparation

This investigation used an in vitro hypothalamic brain slice preparation and whole cell and perforated-patch recording to examine the response of magnocellular neurons in hypothalamic paraventricular nucleus (PVN) to bath applications of vasopressin (VP; 100–500 nM). In 22/38 cells, responses were characterized by an increase in the frequency of bicuculline-sensitive inhibitory postsynaptic potentials or currents with no detectable influence on excitatory postsynaptic events. Perforated-patch recordings confirmed that VP did not have an effect on intrinsic membrane properties of magnocellular PVN neurons ( n = 17). Analysis of intrinsic membrane properties obtained with perforated-patch recording ( n = 23) demonstrated that all of nine VP-sensitive neurons showed a rebound depolarization after transient membrane hyperpolarization from rest. By contrast, 12/14 nonresponding neurons displayed a delayed return to resting membrane potentials. Recordings of reversed inhibitory postsynaptic currents with chloride-loaded electrodes showed that responses to VP persisted in media containing glutamate receptor antagonists but were abolished in the presence of tetrodotoxin. In addition, responses were mimicked by vasotocin [Phe2, Orn8], a selective V1a receptor agonist, and blocked by [β-Mercapto-β,β-cyclopentamethylenepropionyl1,O-Me-Tyr2, Arg8]-VP (Manning compound), a V1a/OT receptor antagonist. Neither [deamino-Cys1,Val4,d-Arg8]-VP, a selective V2 receptor agonist, nor oxytocin were effective. Collectively, the results imply that VP acts at V1a receptors to excite GABAergic neurons that are presynaptic to a population of magnocellular PVN neurons the identity of which features a unique rebound depolarization. Endogenous sources of VP may be VP-synthesizing neurons in suprachiasmatic nucleus, known to project toward the perinuclear regions of PVN, and/or the magnocellular neurons within PVN.

Effect of hypertonic saline on rat hypothalamic paraventricular nucleus magnocellular neurons in vitro

2004 ◽  
Vol 355 (1-2) ◽  
pp. 117-120 ◽  
Author(s):  
De-Lai Qiu ◽  
Tetsuro Shirasaka ◽  
Chun-Ping Chu ◽  
Shoichi Watanabe ◽  
Nan-Shou Yu ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Magnocellular Neurons

Morphological and Membrane Properties of Rat Magnocellular Basal Forebrain Neurons Maintained in Culture

1998 ◽  
Vol 80 (4) ◽  
pp. 1653-1669 ◽  
Author(s):  
J. A. Sim ◽  
T.G.J. Allen
Keyword(s):  
Basal Forebrain ◽  
Cell Types ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
Delayed Rectifier ◽  
Magnocellular Neurons ◽  
Membrane Hyperpolarization ◽  
Cell Excitability ◽  
Forebrain Neurons

Sim, J. A. and T.G.J. Allen. Morphological and membrane properties of rat magnocellular basal forebrain neurons maintained in culture. J. Neurophysiol. 80: 1653–1669, 1998. Morphological and electrophysiological characteristics of magnocellular neurons from basal forebrain nuclei of postnatal rats (11–14 days old) were examined in dissociated cell culture. Neurons were maintained in culture for periods of 5–27 days, and 95% of magnocellular (>23 μm diam) neurons stained positive with acetylcholinesterase histochemistry. With the use of phase contrast microscopy, four morphological subtypes of magnocellular neurons could be distinguished according to the shape of their soma and pattern of dendritic branching. Corresponding passive and active membrane properties were investigated with the use of whole cell configuration of the patch-clamp technique. Neurons of all cell types displayed a prominent (6–39 mV; 6.7–50 ms duration) spike afterdepolarization (ADP), which in some cells reached firing threshold. The ADP was voltage dependent, increasing in amplitude and decreasing in duration with membrane hyperpolarization with an apparent reversal potential of −59 ± 2.3 (SE) mV. Elevating [Ca2+]o (2.5–5.0 mM) or prolonging spike repolarization with 10 mM tetraethylammonium (TEA) or 1 mM 4-aminopyridine (4-AP), potentiated the ADP while it was inhibited by reducing [Ca2+]o (2.5–1 mM) or superfusion with Cd2+ (100 μM). The ADP was selectively inhibited by amiloride (0.1–0.3 mM or Ni2+ 10 μM) but unaffected by nifedipine (3 μM), ω-conotoxin GVIA (100 nM) or ω-agatoxin IVA (200 nM), indicating that Ca2+ entry was through T-type Ca2+ channels. After inhibition of the ADP with amiloride (300 μM), depolarization to less than −65 mV revealed a spike afterhyperpolarization (AHP) with both fast and slow components that could be inhibited by 4-AP (1 mM) and Cd2+ (100 μM), respectively. In all cell types, current-voltage relationships exhibited inward rectification at hyperpolarized potentials ≥ E K (approximately −90 mV). Application of Cs+ (0.1–1 mM) or Ba2+ (1–10 μM) selectively inhibited inward rectification but had no effect on resting potential or cell excitability. At higher concentrations, Ba2+ (>10 μM) also inhibited an outward current tonically active at resting potential ( V H −70 mV), which under current-clamp conditions resulted in small membrane depolarization (3–10 mV) and an increase in cell excitability. Depolarizing voltage commands from prepulse potential of −90 mV ( V H −70 mV) in the presence of tetrodotoxin (0.5 μM) and Cd2+ (100 μM) to potentials between −40 and +40 mV cause voltage activation of both transient A-type and sustained delayed rectifier-type outward currents, which could be selectively inhibited by 4-AP (0.3–3 mM) and TEA (1–3 mM), respectively. These results show that, although acetylcholinesterase-positive magnocellular basal forebrain neurons exhibit considerable morphological heterogeneity, they have very similar and characteristic electrophysiological properties.

Dendritic arbor of locus coeruleus neurons contributes to opioid inhibition

1996 ◽  
Vol 75 (5) ◽  
pp. 2029-2035 ◽  
Author(s):  
R. A. Travagli ◽  
M. Wessendorf ◽  
J. T. Williams
Keyword(s):  
Locus Coeruleus ◽  
Horizontal Plane ◽  
Reversal Potential ◽  
Outward Current ◽  
Membrane Properties ◽  
Equilibrium Potential ◽  
Intrinsic Membrane Properties ◽  
In Cells

1. The nucleus locus coeruleus (LC) is made up of noradrenergic cells all of which are hyperpolarized by opioids. Recent work has shown that the reversal potential of the opioid-induced current is more negative than the potassium equilibrium potential. The aim of the present study was to determine whether the extent of the dendritic field could contribute to the very negative opioid reversal potential. 2. Individual LC cells were labeled in the brain slice preparation. The number of dendrites found on cells in slices sectioned in the horizontal plane was greater than cells in coronal slices. However, the dimensions of the cell body slices from each plane were not significantly different. 3. The resting conductance of neurons from slices cut in the horizontal plane was significantly larger than in cells from coronal plane. 4. The amplitude of the outward current induced by [Met5]-enkephalin (ME) was larger in cells from horizontal slices and the reversal potential was more negative than that of cells in coronal slices. 5. The results show that the plane of section influences the membrane properties and opioid actions of LC neurons in vitro and suggest that these differences correlate with the numbers of dendrites. The results suggest that in vivo, in addition to intrinsic membrane properties and synaptic inputs, the structural makeup of the nucleus is an important factor in determining the activity.

Membrane properties of rat substantia gelatinosa neurons in vitro

1989 ◽  
Vol 62 (1) ◽  
pp. 109-118 ◽  
Author(s):  
M. Yoshimura ◽  
T. M. Jessell
Keyword(s):  
Time Dependent ◽  
Substantia Gelatinosa ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Membrane Hyperpolarization ◽  
Anomalous Rectification ◽  
Outward Rectification

1. The membrane properties of substantia gelatinosa (SG) neurons in an in vitro adult rat transverse spinal cord slice preparation with attached dorsal root have been examined. Intracellular recordings were obtained from identified SG neurons. 2. Seventy-six percent of SG neurons exhibited a time-dependent anomalous rectification (AR) when the membrane was hyperpolarized from the resting potential. The time-dependent AR was blocked by cesium (Cs+, 2 mM) but not by barium (Ba2+, 2 mM). Application of Cs+ itself caused membrane hyperpolarization in those SG neurons that expressed the time-dependent AR. The activation of the time-dependent AR was maximal at potentials 5-10 mV below the resting membrane potential. 3. In a few SG neurons, the current-voltage relationship revealed a marked inward rectification, even though there was no detectable time-dependent anomalous rectification during hyperpolarization. Analysis of the Ba2+- and Cs+-sensitivity of these neurons confirmed that SG neurons expressed two distinct ARs, one of which is fast and Ba2+-sensitive and the other of which is time-dependent and Ba2+-insensitive. 4. Fifty-one percent of SG neurons exhibited a transient outward rectification when hyperpolarizing current pulses were applied from potentials more positive than -60 mV or when depolarizing pulses were applied from potentials more negative than -65 mV. The transient outward rectification persisted for 0.3-2 s when hyperpolarizing pulses were applied at -55 mV. 5. The transient outward rectification was associated with a decrease in membrane resistance and was enhanced in low K+ solutions. 4-aminopyridine (4-AP, 2 mM) reversibly blocked the transient outward rectification. 6. The time-dependent anomalous and transient outward rectifying currents exerted opposite effects on the firing properties of SG neurons. Activation of the time-dependent AR increased neuronal excitability. In neurons that exhibited the time-dependent AR, membrane depolarization caused the appearance of a rebound depolarization that resulted in the generation of spikes with only a short delay after application of the depolarizing pulse. In contrast, the transient outward rectifying current markedly delayed spike firing in response to depolarizing pulses. This delay was blocked by application of 4-AP. 7. The diversity in response properties of subpopulations of SG neurons may result in part from this heterogeneity in membrane properties.

scholarly journals Cold Exposure Increases the Biosynthesis and Proteolytic Processing of Prothyrotropin-Releasing Hormone in the Hypothalamic Paraventricular Nucleus via β-Adrenoreceptors

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4952-4964 ◽  
Author(s):  
Mario Perello ◽  
Ronald C. Stuart ◽  
Charles A. Vaslet ◽  
Eduardo A. Nillni
Keyword(s):  
Paraventricular Nucleus ◽  
Molecular Mechanisms ◽  
Protein Biosynthesis ◽  
Camp Response Element Binding ◽  
Proteolytic Processing ◽  
Hypothalamic Paraventricular Nucleus ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Different physiological conditions affect the biosynthesis and processing of hypophysiotropic proTRH in the hypothalamic paraventricular nucleus, and consequently the output of TRH. Early studies suggest that norepinephrine (NE) mediates the cold-induced activation of the hypothalamic-pituitary-thyroid axis at a central level. However, the specific role of NE on the biosynthesis and processing of proTRH has not been fully investigated. In this study, we found that NE affects gene transcription, protein biosynthesis, and secretion in TRH neurons in vitro; these changes were coupled with an up-regulation of prohormone convertase enzymes (PC) 1/3 and PC2. In vivo, NE is the main mediator of the cold-induced activation of the hypothalamic-pituitary-thyroid axis at the hypothalamic level, in which it potently stimulates the biosynthesis and proteolytic processing of proTRH through a coordinated up-regulation of the PCs. This activation occurs via β-adrenoreceptors and phosphorylated cAMP response element binding signaling. In contrast, α-adrenoreceptors regulate TRH secretion but not proTRH biosynthesis and processing. Therefore, this study provides novel information on the molecular mechanisms of control of hypophysiotropic TRH biosynthesis.

Forced swimming stimulates the expression of vasopressin and oxytocin in magnocellular neurons of the rat hypothalamic paraventricular nucleus

2001 ◽  
Vol 13 (12) ◽  
pp. 2273-2281 ◽  
Author(s):  
Carsten T. Wotjak ◽  
Tetsuro Naruo ◽  
Shinichiro Muraoka ◽  
Renate Simchen ◽  
Rainer Landgraf ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Forced Swimming ◽  
Hypothalamic Paraventricular Nucleus ◽  
Magnocellular Neurons

scholarly journals Regulation of Action Potential Size and Excitability in Substantia Nigra Compacta Neurons: Sensitivity to 4-Aminopyridine

1999 ◽  
Vol 82 (6) ◽  
pp. 2903-2913 ◽  
Author(s):  
S. Nedergaard
Keyword(s):  
Substantia Nigra ◽  
Time Window ◽  
Slow Component ◽  
Brain Slices ◽  
Membrane Properties ◽  
Initial Time ◽  
Direct Excitation ◽  
Spontaneous Action ◽  
Intrinsic Membrane Properties

Slow, pacemaker-like firing is due to intrinsic membrane properties in substantia nigra compacta (SNc) neurons in vitro. How these properties interact with afferent synaptic inputs is not fully understood. In this study, intracellular recordings from SNc neurons in brain slices showed that spontaneous action potentials (APs) were attenuated when generated from lower than normal threshold. Such APs were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and could be related to non– N-methyl-d-aspartate (NMDA) receptor–mediated spontaneous excitatory postsynaptic potentials (EPSPs). The AP attenuation was reproduced by stimulus-evoked EPSPs and by current injections to the soma. APs evoked from holding potentials between −40 and −60 mV were reduced in width by Cd2+ (0.2 mM). Tetraethylammonium chloride (TEA, 10 mM) or 4-aminopyridine (4-AP, 5 mM) increased the AP width. However, at more negative holding potentials, Cd2+ and TEA were inefficacious, whereas 4-AP enlarged the AP, partly via induction of a Cd2+-sensitive component. A monophasic afterhyperpolarization (AHP), following attenuated APs, was little affected by either Cd2+ or TEA, but inhibited by 4-AP, which induced an additional, slow component, sensitive to Cd2+ or apamin (100 nM). The AP delay showed a discontinuous relation to the amplitude or slope of the injected current (delay shift), which was sensitive to low doses of 4-AP (0.05 mM). The initial time window before the delay shift was longer than the rise time of EPSPs. It is suggested that a 4-AP–sensitive current prevents or postpones discharge during slow depolarization's, but allows direct excitation by fast EPSPs. Fast excitation leads to AP attenuation, primarily due to strong activation of 4-AP–sensitive current. This seems to cause inhibition of the Ca2+ current during the AP and reduction of Ca2+-dependent K+ currents. Together, these properties are likely to influence the excitability and the local, somatodendritic effects of the AP, in a manner that discriminates between firing induced by the intrinsic pacemaker mechanism and fast synaptic potentials.

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