scholarly journals Integration of energy homeostasis and stress by parvocellular neurons in rat hypothalamic paraventricular nucleus

2020 ◽  
Vol 598 (5) ◽  
pp. 1073-1092
Author(s):  
Igor Melnick ◽  
Oleg A. Krishtal ◽  
William F. Colmers
Keyword(s):  
Paraventricular Nucleus ◽  
Energy Homeostasis ◽  
Hypothalamic Paraventricular Nucleus ◽  
Parvocellular Neurons

scholarly journals Neuropeptide FF and neuropeptide VF inhibit GABAergic neurotransmission in parvocellular neurons of the rat hypothalamic paraventricular nucleus

2007 ◽  
Vol 292 (5) ◽  
pp. R1872-R1880 ◽  
Author(s):  
Jack H. Jhamandas ◽  
Frédéric Simonin ◽  
Jean-Jacques Bourguignon ◽  
Kim H. Harris
Keyword(s):  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Inhibitory Input ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Gabaergic Neurotransmission ◽  
Whole Cell Patch Clamp ◽  
Neuropeptide Ff ◽  
Parvocellular Neurons ◽  
The Brain

Neuropeptide FF (NPFF) and neuropeptide VF (NPVF) are octapeptides belonging to the RFamide family of peptides that have been implicated in a wide variety of physiological functions in the brain, including central autonomic and neuroendocrine regulation. The effects of these peptides are mediated via NPFF1 and NPFF2 receptors that are abundantly expressed in the rat brain, including the hypothalamic paraventricular nucleus (PVN), an autonomic nucleus critical for the secretion of neurohormones and the regulation of sympathetic outflow. In this study, we examined, using whole cell patch-clamp recordings in the brain slice, the effects of NPFF and NPVF on inhibitory GABAergic synaptic input to parvocellular PVN neurons. Under voltage-clamp conditions, NPFF and NPVF reversibly and in a concentration-dependent manner reduced the evoked bicuculline-sensitive inhibitory postsynaptic currents (IPSCs) in parvocellular PVN neurons by 25 and 31%, respectively. RF9, a potent and selective NPFF receptor antagonist, blocked NPFF-induced reduction of IPSCs. Recordings of miniature IPSCs in these neurons following NPFF and NPVF applications showed a reduction in frequency but not amplitude, indicating a presynaptic locus of action for these peptides. Under current-clamp conditions, NPVF and NPFF caused depolarization (6–9 mV) of neurons that persisted in the presence of TTX but was abolished in the presence of bicuculline. Collectively, these data provide evidence for a disinhibitory role of NPFF and NPVF in the hypothalamic PVN via an attenuation of GABAergic inhibitory input to parvocellular neurons of this nucleus and explain the central autonomic effects of NPFF.

Noradrenaline Excites and Inhibits GABAergic Transmission in Parvocellular Neurons of Rat Hypothalamic Paraventricular Nucleus

2002 ◽  
Vol 87 (5) ◽  
pp. 2287-2296 ◽  
Author(s):  
Seong Kyu Han ◽  
Wonee Chong ◽  
Long Hua Li ◽  
In Se Lee ◽  
Kazuyuki Murase ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Synaptic Activity ◽  
Hypothalamic Paraventricular Nucleus ◽  
Anatomical Location ◽  
Type Ii ◽  
Inhibitory Effects ◽  
Patch Clamp Technique ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Parvocellular Neurons

Noradrenaline (NA) is a major neurotransmitter that regulates many neuroendocrine and sympathetic autonomic functions of the hypothalamic paraventricular nucleus (PVN). Previously NA has been shown to increase the frequency of excitatory synaptic activity of parvocellular neurons within the PVN, but little is known about its effects on inhibitory synaptic activity. In this work, we studied the effects of NA (1–100 μM) on the spontaneous inhibitory synaptic currents (sIPSC) of type II PVN neurons in brain slices of the rat using the whole cell patch-clamp technique. Spontaneous IPSCs were observed from most type II neurons ( n = 121) identified by their anatomical location within the PVN and their electrophysiological properties. Bath application of NA (100 μM) increased sIPSC frequency by 256% in 59% of the neurons. This effect was blocked by prazosin (2–20 μM), the α1-adrenoceptor antagonist and mimicked by phenylephrine (10–100 μM), the α1-adrenoceptor agonist. However, in 33% of the neurons, NA decreased sIPSC frequency by 54%, and this effect was blocked by yohimbine (2–20 μM), the α2-adrenoceptor antagonist and mimicked by clonidine (50 μM), the α2-adrenoceptor agonist. The Na+ channel blocker, tetrodotoxin (0.1 μM) blocked the α1-adrenoceptor–mediated effect, but not the α2-adreonoceptor–mediated one. Both of the stimulatory and inhibitory effects of NA on sIPSC frequency were observed in individual neurons when tested with NA alone, or both phenylephrine and clonidine. Furthermore, in most neurons that showed the stimulatory effects, the inhibitory effects of NA were unmasked after blocking the stimulatory effects by prazosin or tetrodotoxin. These data indicate that tonic GABAergic inputs to the majority of type II PVN neurons are under a dual noradrenergic modulation, the increase in sIPSC frequency via somatic or dendritic α1-adrenoceptors and the decrease in sIPSC frequency via axonal terminal α2-adrenoceptors on the presynaptic GABAergic neurons.

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