Critical role of V1a vasopressin receptor in murine parturition

2021 ◽  
Author(s):  
Hiroyoshi Tsuchiya ◽  
Shyota Fujimura ◽  
Yoko Fujiwara ◽  
Taka-aki Koshimizu
Keyword(s):  
Critical Role ◽  
Contractile Force ◽  
Reproductive Physiology ◽  
Receptor Subtype ◽  
Pituitary Hormone ◽  
Receptor Subtypes ◽  
Expression Of Genes ◽  
Uterine Contractile ◽  
Posterior Pituitary Hormone

Abstract The precise mechanisms of the reproductive physiological processes, such as labor initiation, are poorly understood. Oxytocin (OT) is one of the well-known uterotonics and is clinically adopted as a medication to facilitate childbirth. Vasopressin (VP), a posterior pituitary hormone similar to OT, has also been proposed to be involved in the reproductive physiology. In this study, we found that a total deficiency of V1a receptor subtype (V1aR) in mice resulted in a reduced number of pups, delayed labor initiation, and increased post-delivery hemorrhage compared with those in wild-type mice. Among the VP receptor subtypes, only V1aR was found to be expressed in the murine uterus and its distribution pattern was different from that of the oxytocin receptor (OTR); V1aR expression was mainly distributed in the circular myometrium, whereas OTR was strongly expressed in both the circular and longitudinal myometrium. The maximum contractile force of the circular myometrium, induced by VP or OT, was attenuated in the pregnant uterus of Avpr1a-deficient mice. Contrarily, while OT expression was decreased in the Avpr1a-deficient uterus, OTR expression was significantly increased. These results suggest that V1aR deficiency not only reduces the uterine contractile force but also perturbs the expression of genes responsible for the reproductive physiology. Therefore, V1aR is necessary to exert the maximum contraction of the circular myometrium to deliver pups. This study revealed an important role of V1aR in physiological contraction and term parturition in mice.

Critical role of V1a vasopressin receptor in murine parturition†

2019 ◽  
Vol 102 (4) ◽  
pp. 923-934
Author(s):  
Hiroyoshi Tsuchiya ◽  
Shyota Fujimura ◽  
Yoko Fujiwara ◽  
Taka-aki Koshimizu
Keyword(s):  
Critical Role ◽  
Contractile Force ◽  
Reproductive Physiology ◽  
Receptor Subtype ◽  
Pituitary Hormone ◽  
Receptor Subtypes ◽  
Expression Of Genes ◽  
Uterine Contractile ◽  
Posterior Pituitary Hormone

Abstract The precise mechanisms of the reproductive physiological processes, such as labor initiation, are poorly understood. Oxytocin (OT) is one of the well-known uterotonics and is clinically adopted as a medication to facilitate childbirth. Vasopressin (VP), a posterior pituitary hormone similar to OT, has also been proposed to be involved in the reproductive physiology. In this study, we found that a total deficiency of V1a receptor subtype (V1aR) in mice resulted in a reduced number of pups, delayed labor initiation, and increased post-delivery hemorrhage compared with those in wild-type mice. Among the VP receptor subtypes, only V1aR was found to be expressed in the murine uterus, and its distribution pattern was different from that of the oxytocin receptor (OTR); V1aR expression was mainly distributed in the circular myometrium, whereas OTR was strongly expressed in both the circular and longitudinal myometrium. The maximum contractile force of the circular myometrium, induced by VP or OT, was attenuated in the pregnant uterus of Avpr1a-deficient mice. Contrarily, while OT expression was decreased in the Avpr1a-deficient uterus, OTR expression was significantly increased. These results suggest that V1aR deficiency not only reduces the uterine contractile force but also perturbs the expression of genes responsible for the reproductive physiology. Therefore, V1aR is necessary to exert the maximum contraction of the circular myometrium to deliver pups. This study revealed an important role of V1aR in physiological contraction and term parturition in mice.

scholarly journals Sex Differences in Aggression: Differential Roles of 5-HT2, Neuropeptide F and Tachykinin

2018 ◽  
Author(s):  
Andrew N. Bubak ◽  
Michael J. Watt ◽  
Kenneth J. Renner ◽  
Abigail A. Luman ◽  
Jamie D. Costabile ◽  
...  
Keyword(s):  
Sex Differences ◽  
Aggressive Behavior ◽  
Critical Role ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Valuable Insight ◽  
Invertebrate Model ◽  
Neuropeptide F ◽  
Initiation Stage

AbstractDespite the conserved function of aggression across taxa in obtaining critical resources such as food and mates, serotonin’s (5-HT) modulatory role on aggressive behavior appears to be largely inhibitory for vertebrates but stimulatory for invertebrates. However, critical gaps exist in our knowledge of invertebrates that need to be addressed before definitively stating opposing roles for 5-HT and aggression. Specifically, the role of 5-HT receptor subtypes are largely unknown, as is the potential interactive role of 5-HT with other neurochemical systems known to play a critical role in aggression. Similarly, the influence of these systems in driving sex differences in aggressive behavior of invertebrates is not well understood. Here, we investigated these questions by employing complementary approaches in a novel invertebrate model of aggression, the stalk-eyed fly. A combination of altered social conditions, pharmacological manipulation and 5-HT2 receptor knockdown by siRNA revealed an inhibitory role of this receptor subtype on aggression. Additionally, we provide evidence for 5-HT2’s involvement in regulating neuropeptide F activity, a suspected inhibitor of aggression. However, this function appears to be stage-specific, altering only the initiation stage of aggressive conflicts. Alternatively, pharmacologically increasing systemic concentrations of 5-HT significantly elevated the expression of the neuropeptide tachykinin, which did not affect contest initiation but instead promoted escalation via production of high intensity aggressive behaviors. Notably, these effects were limited solely to males, with female aggression and neuropeptide expression remaining unaltered by any manipulation that affected 5-HT. Together, these results demonstrate a more nuanced role for 5-HT in modulating aggression in invertebrates, revealing an important interactive role with neuropeptides that is more reminiscent of vertebrates. The sex-differences described here also provide valuable insight into the evolutionary contexts of this complex behavior.Significance StatementSerotonin’s (5-HT) modulatory role in aggression is generally reported as inhibitory in vertebrates but stimulatory in invertebrates. Using a novel invertebrate model system, we provide evidence of common pathways of aggression at the 5-HT receptor subtype level as well as 5-HT’s interactive role with other neurochemical systems namely neuropeptide F and tachykinin. Additionally, we found that these effects were sex-dependent as well as stage-dependent affecting either the initiation or escalation stage of an aggressive contest. Our results reveal the impressive level of conservation with respect to neurochemical mechanisms among species as diverse as vertebrates and invertebrates, and highlights the need to consider multiple factors when determining potential taxonomic differences in how 5-HT mediates aggression.

scholarly journals Social Isolation: How Can the Effects on the Cholinergic System Be Isolated?

2021 ◽  
Vol 12 ◽  
Author(s):  
Jaromir Myslivecek
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Social Isolation ◽  
Cholinergic System ◽  
System Response ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Cholinergic Signaling ◽  
The Central Nervous System

Social species form organizations that support individuals because the consequent social behaviors help these organisms survive. The isolation of these individuals may be a stressor. We reviewed the potential mechanisms of the effects of social isolation on cholinergic signaling and vice versa how changes in cholinergic signaling affect changes due to social isolation.There are two important problems regarding this topic. First, isolation schemes differ in their duration (1–165 days) and initiation (immediately after birth to adulthood). Second, there is an important problem that is generally not considered when studying the role of the cholinergic system in neurobehavioral correlates: muscarinic and nicotinic receptor subtypes do not differ sufficiently in their affinity for orthosteric site agonists and antagonists. Some potential cholinesterase inhibitors also affect other targets, such as receptors or other neurotransmitter systems. Therefore, the role of the cholinergic system in social isolation should be carefully considered, and multiple receptor systems may be involved in the central nervous system response, although some subtypes are involved in specific functions. To determine the role of a specific receptor subtype, the presence of a specific subtype in the central nervous system should be determined using search in knockout studies with the careful application of specific agonists/antagonists.

Abstract 424: Activation of the S1P3 Receptors is Responsible for S1P-mediated RhoA Activation and Cardioprotection

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Bryan S Yung ◽  
Sunny Y Xiang ◽  
Nicole Purcell ◽  
Hugh Rosen ◽  
Jerold Chun ◽  
...  
Keyword(s):  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Cardiovascular Responses ◽  
Neonatal Rat ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
S1p Receptors ◽  
Rhoa Activation ◽  
Therapeutic Benefits

Sphingosine-1-phoshpate (S1P) is a bioactive lysophospholipid, generated and released at sites of tissue injury. S1P signals through a variety of G-protein coupled receptor subtypes and there are three major sub-types, S1P 1 , S1P 2 , and S1P 3 , to mediate cardiovascular responses. S1P 2 and S1P 3 receptors couple to Gα i , Gα 12 , Gα 13 and Gα q and we first examined the contribution of S1P 2 and S1P 3 to cardiac hypertrophy using S1P 2 and S1P 3 knockout (KO) mice and found that there is no difference in hypertrophy induced by pressure-overload. We previously showed that S1P provides cardioprotection against oxidative stress such as ischemia/reperfusion in which RhoA activation and its downstream effector PKD1 play an important role. It has not, however, been determined which S1P receptor subtype is responsible for S1P mediated cardioprotection. We knocked down the three major S1P receptors using siRNA in neonatal rat ventricular myocytes (NRVMs) and assessed RhoA and PKD1 activation induced by S1P. Knockdown of S1P 3 abolished RhoA activation and largely attenuated phosphorylation of PKD1 while knockdown of S1P 1 and S1P 2 did not. Using siRNA or pertussis toxin to inhibit different G-proteins, we further established that S1P regulates RhoA activation through Gα 13 , but not Gα 12 , Gα q , or Gα i . To investigate the role of S1P 3 receptors in the adult heart, hearts were isolated from wild-type or S1P 3 KO adult mice, perfused in the Langendorff mode and subjected to ex vivo ischemia/reperfusion. As previously reported, S1P perfusion significantly reduced infarct size induced by ischemia/reperfusion in WT hearts (by 50%), but this protection was abolished in the S1P 3 KO mouse heart. To further confirm the role of S1P 3 in cardioprotection we perfused WT mouse hearts with an S1P 3 -specific agonist CYM-51736. We observed that CYM-51736 attenuated the infarct size to a similar degree as that observed with S1P. Our findings reveal that activation of the S1P 3 receptor coupling to Gα 13 and subsequent RhoA activation is responsible for cardioprotection against ischemia/reperfusion. Accordingly specific drug targeting of S1P 3 receptors could provide therapeutic benefits in ischemic heart disease without the undesirable effects of global activation of other cardiac S1P receptors.

scholarly journals Critical role of 5-HT1A, 5-HT3, and 5-HT7 receptor subtypes in the initiation, generation, and propagation of the murine colonic migrating motor complex

2010 ◽  
Vol 299 (1) ◽  
pp. G144-G157 ◽  
Author(s):  
Eamonn J. Dickson ◽  
Dante J. Heredia ◽  
Terence K. Smith
Keyword(s):  
Critical Role ◽  
Circular Muscle ◽  
Migrating Motor Complex ◽  
Receptor Subtypes ◽  
Type Ii ◽  
Motor Complex ◽  
Intracellular Microelectrodes ◽  
Dogiel Type Ii ◽  
Colonic Migrating Motor Complex

The colonic migrating motor complex (CMMC) is necessary for fecal pellet propulsion in the murine colon. We have previously shown that 5-hydroxytryptamine (5-HT) released from enterochromaffin cells activates 5-HT3 receptors on the mucosal processes of myenteric Dogiel type II neurons to initiate the events underlying the CMMC. Our aims were to further investigate the roles of 5-HT1A, 5-HT3, and 5-HT7 receptor subtypes in generating and propagating the CMMC using intracellular microelectrodes or tension recordings from the circular muscle (CM) in preparations with and without the mucosa. Spontaneous CMMCs were recorded from the CM in isolated murine colons but not in preparations without the mucosa. In mucosaless preparations, ondansetron (3 μM; 5-HT3 antagonist) plus hexamethonium (100 μM) completely blocked spontaneous inhibitory junction potentials, depolarized the CM. Ondansetron blocked the preceding hyperpolarization associated with a CMMC. Spontaneous CMMCs and CMMCs evoked by spritzing 5-HT (10 and 100 μM) or nerve stimulation in preparations without the mucosa were blocked by SB 258719 or SB 269970 (1–5 μM; 5-HT7 antagonists). Both NAN-190 and (S)-WAY100135 (1–5 μM; 5-HT1A antagonists) blocked spontaneous CMMCs and neurally evoked CMMCs in preparations without the mucosa. Both NAN-190 and (S)-WAY100135 caused an atropine-sensitive depolarization of the CM. The precursor of 5-HT, 5-hydroxytryptophan (5-HTP) (10 μM), and 5-carboxamidotryptamine (5-CT) (5 μM; 5-HT1/5/7 agonist) increased the frequency of spontaneous CMMCs. 5-HTP and 5-CT also induced CMMCs in preparations with and without the mucosa, which were blocked by SB 258719. 5-HT1A, 5-HT3, and 5-HT7 receptors, most likely on Dogiel Type II/AH neurons, are important in initiating, generating, and propagating the CMMC. Tonic inhibition of the CM appears to be driven by ongoing activity in descending serotonergic interneurons; by activating 5-HT7 receptors on AH neurons these interneurons also contribute to the generation of the CMMC.

Role of metabotropic glutamate (ACPD) receptors at the parallel fiber-Purkinje cell synapse

1992 ◽  
Vol 68 (4) ◽  
pp. 1453-1462 ◽  
Author(s):  
S. R. Glaum ◽  
N. T. Slater ◽  
D. J. Rossi ◽  
R. J. Miller
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Parallel Fiber ◽  
Membrane Properties ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Fura 2 ◽  
Metabotropic Glutamate ◽  
Cell Synapse

1. The role of metabotropic glutamate receptors at the parallel fiber (PF)-Purkinje cell synapse in cerebellum was studied by examining the actions of the active stereoisomer (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [1S,3R-ACPD (25-50 microM)] on fura-2-loaded, patch-clamped rat Purkinje cells in thin slices. 2. The bath application of 1S,3R-ACPD evoked a direct post-synaptic depolarization that readily desensitized during prolonged (> 1 min) applications of the drug. This depolarizing response to 1S,3R-ACPD differed from the slow depolarization to 1S,3R-ACPD observed in cortical neurons mediated via closure of potassium channels in that it was not associated with an obvious change in membrane conductance and was not blocked by external barium. Similarly, slow inward rectifier currents were not affected during the 1S,3R-ACPD-induced depolarization. 3. The direct depolarization induced by 1S,3R-ACPD was not mediated by N-methyl-D-aspartate (NMDA) or (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid kainate (AMPA)-KA excitatory amino acid (EAA) receptor subtypes, because the response was not blocked in the presence of antagonists of these receptors. 4. The EAA antagonist L-2-amino-3-phosphonopropionic acid, which blocks 1S,3R-ACPD-induced inositide synthesis in other cell types, had no effect on the depolarizing response. 5. Fura-2 measurements of somatic [Ca2+]i revealed that [Ca2+]i was not elevated during the 1S,3R-ACPD-induced depolarization unless the cell fired calcium-dependent action potentials. 6. In addition to the direct depolarization induced by 1S,3R-ACPD, the amplitude of PF-evoked excitatory postsynaptic potentials (EPSPs) was profoundly and reversibly reduced. This effect was observed in all cells regardless of whether a direct depolarization was produced by 1S,3R-ACPD. This reduction of the PF EPSP generally preceded the onset of depolarizing responses, did not desensitize during prolonged applications of 1S,3R-ACPD, and was reversible. 7. The reversible reduction of the PF EPSP by 1S,3R-ACPD was not related to a postsynaptic blocking action of the drug, because responses of Purkinje cells to AMPA, an agonist of the EAA receptor subtype mediating the EPSP, were reversibly potentiated in the presence of 1S,3R-ACPD. 8. The nitric oxide synthesis promoter sodium nitroprusside (1-3 nM) had no effect on the amplitude of PF EPSP or the membrane properties of Purkinje cells.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals The role of angiotensin II in the early stages of bovine ovulation

Reproduction ◽  
2007 ◽  
Vol 134 (5) ◽  
pp. 713-719 ◽  
Author(s):  
Rogério Ferreira ◽  
João Francisco Oliveira ◽  
Rafael Fernandes ◽  
José Ferrugem Moraes ◽  
Paulo Bayard Gonçalves
Keyword(s):  
Receptor Antagonist ◽  
Gnrh Agonist ◽  
Saline Solution ◽  
Critical Role ◽  
Renin Angiotensin System ◽  
Ovulation Rate ◽  
Receptor Subtype ◽  
Ang Ii

There is evidence that the renin–angiotensin system plays an important role in ovulation in cattle. Using anin vivomodel, we investigated the role of angiotensin (Ang) II in bovine ovulation by injecting Ang II receptor antagonists into ovulatory follicles. Animals (n= 102) were pre-synchronized and, when the follicles reached 12 mm, they were given the respective treatment and the cows received GnRH agonist (i.m.) to induce ovulation. The ovulation rate was significantly lower when 100μM saralasin (Ang II receptor antagonist) was intrafollicularly injected (14.3%) in comparison with saline solution (83.3%). Based on these results, a second experiment was carried out to determine the timing of Ang II’s critical role in ovulation. Saralasin inhibited ovulation only when applied at 0 and 6 h (16.7 and 42.9% ovulation rate in the 0- and 6-h groups respectively), but not at 12 h (100%) following GnRH agonist treatment. To investigate the subtypes of Ang II receptors implicated in the LH-induced ovulation, losartan (LO; AT1-Ang II receptor antagonist), PD123 319 (AT2-Ang II receptor antagonist), LO+PD123 319, or saline were intrafollicularly injected when the cows were challenged with GnRH agonist. Ovulation was inhibited by PD123 319 and LO+PD123 319 (50.0 and 33.3% on ovulation rate respectively), but not by LO or saline solution (100% ovulation in both groups). From these results, we suggest that Ang II plays a pivotal role in the early mechanism of bovine ovulation via the AT2receptor subtype.

An Immunohistochemical Analysis on The Human Cerebellar Dopaminergic System

2020 ◽  
Author(s):  
Paolo Flace ◽  
Paolo Livrea ◽  
Diana Galletta ◽  
Antonella Bizzoca ◽  
Gianpaolo Basile ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Dopaminergic System ◽  
Critical Role ◽  
Neuronal Cell ◽  
Cerebellar Nuclei ◽  
Receptor Subtype ◽  
Critical Element ◽  
Receptor Subtypes ◽  
Neuronal System ◽  
Human Cerebellum

Abstract Background The cerebellum now it has not considered a dopaminergic region. Despite, is traditionally reported only the presence of dopaminergic afferents to the cerebellum. Currently, studies attribute to the cerebellum a critical role in motor and cognitive functions and suggest a cerebellar involvement in dopamine related neurologic and psychiatric disorders. In several studies has been demonstrated mainly in the cerebellum of rodents a widely distribution of all dopaminergic receptor subtypes (DRD1-DRD5), a poor number of dopaminergic Purkinje neurons, and the presence of several dopaminergic neurons in the deep cerebellar nuclei. Data on an intrinsic dopaminergic neuronal system in the human cerebellum are lacking. Methods The aim of the present study of chemical neuroanatomy was to investigate in human cerebellum on the presence of a dopaminergic neuronal system, through an immunohistochemical approach based on the use of specific antibodies against the dopamine membrane transporter (DAT) and the dopamine receptor subtype 2 (DRD2). Results The immunoreactions revealed the presence of DAT and DRD2 positive neuronal cell bodies and processes of all the layers of the cerebellar cortex and in the dentate nucleus. These results are in agreement with previous studies, and suggest which the intrinsic cerebellar neuronal dopaminergic system may be involved in intrinsic and extrinsic (projective) cerebellar circuits. Conclusions This study open a new scenario on the interpretation of the cerebellar role in dopaminergic related brain disorders. Finally, this study may be an innovative critical element for the development of pharmacologic and non-pharmacologic therapeutic strategies for neurologic and psychiatric disorders related to dopamine.

scholarly journals Selective Regulation of Somatostatin Receptor Subtype Signaling: Evidence for Constitutive Receptor Activation

2007 ◽  
Vol 21 (10) ◽  
pp. 2565-2578 ◽  
Author(s):  
Anat Ben-Shlomo ◽  
Oxana Pichurin ◽  
Nicole J. Barshop ◽  
Kolja A. Wawrowsky ◽  
John Taylor ◽  
...  
Keyword(s):  
Mapk Pathway ◽  
Somatostatin Receptor ◽  
Hormone Secretion ◽  
Receptor Activation ◽  
Receptor Subtype ◽  
Pituitary Hormone ◽  
Receptor Subtypes ◽  
Camp Accumulation ◽  
Acth Secretion ◽  
Somatostatin Receptor Subtypes

Abstract Anterior pituitary hormone secretion is under tonic suppression by hypothalamic somatostatin signaling through somatostatin receptor subtypes (SSTs). Because some hormonal axes are known to be abnormally regulated by ligand-independent constitutively active G protein-coupled receptors, we tested pituitary SSTs for selective constitutive signaling. We therefore differentially silenced endogenous SST2, SST3, and SST5 in somatostatin-sensitive ACTH-secreting mouse AtT-20 pituitary corticotroph cells using small inhibitory RNA (siRNA) and analyzed downstream SSTs-regulated pathways. Transfection with siRNA reduced specific receptor subtype mRNA expression up to 82%. Specificity of receptor silencing was validated against negative controls with different gene-selective siRNAs, concordance of mRNA and cAMP changes, reduced potency of receptor-selective agonists, and phenotype rescue by overexpression of the silenced receptor. Mouse SST3 > SST5 > SST2 knockdown increased basal cAMP accumulation (up to 200%) and ACTH secretion (up to 60%). SST2- and SST5-selective agonist potencies were reduced by SST3- and SST5-silencing, respectively. SST5 > SST2 = SST3 silencing also increased basal levels of ERK1/2 phosphorylation. SST3- and SST5-knockdown increased cAMP was only partially blocked by pertussis toxin. The results show that SST2, SST3, and SST5 exhibit constitutive activity in mouse pituitary corticotroph cells, restraining adenylate cyclase and MAPK activation and ACTH secretion. SST3 mainly inhibits cAMP accumulation and ACTH secretion, whereas SST5 predominantly suppresses MAPK pathway activation. Therefore, SST receptor subtypes control pituitary cell function not only through somatostatin binding to variably expressed cell membrane receptor subtypes, but also by differential ligand-independent receptor-selective constitutive action.

scholarly journals Noradrenergic Regulation of GABAergic Inhibition of Main Olfactory Bulb Mitral Cells Varies as a Function of Concentration and Receptor Subtype

2009 ◽  
Vol 101 (5) ◽  
pp. 2472-2484 ◽  
Author(s):  
Qiang Nai ◽  
Hong-Wei Dong ◽  
Abdallah Hayar ◽  
Christiane Linster ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Gabaergic Inhibition ◽  
Mitral Cells ◽  
Main Olfactory Bulb ◽  
Pontine Nucleus ◽  
Patch Clamp Electrophysiology ◽  
Α1 Receptors

The main olfactory bulb (MOB) receives a rich noradrenergic innervation from the pontine nucleus locus coeruleus (LC). Previous studies indicate that norepinephrine (NE) modulates the strength of GABAergic inhibition in MOB. However, the nature of this modulation and the NE receptors involved remain controversial. The goal of this study was to investigate the role of NE receptor subtypes in modulating the GABAergic inhibition of mitral cells using patch-clamp electrophysiology in rat MOB slices. NE concentration dependently and bi-directionally modulated GABAA receptor–mediated spontaneous and miniature inhibitory postsynaptic currents (sIPSCs/mIPSCs) recorded in mitral cells. Low doses of NE suppressed sIPSCs and mIPSCs because of activation of α2 receptors. Intermediate concentrations of NE increased sIPSCs and mIPSCs primarily because of activation of α1 receptors. In contrast, activation of β receptors increased sIPSCs but not mIPSCs. These results indicate that NE release regulates the strength of GABAergic inhibition of mitral cells depending on the NE receptor subtype activated. Functionally, the differing affinity of noradrenergic receptor subtypes seems to allow for dynamic modulation of GABAergic inhibition in MOB as function of the extracellular NE concentration, which in turn, is regulated by behavioral state.

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