Muscarinic Receptor Modulation of Slow Afterhyperpolarization and Phasic Firing in Rat Supraoptic Nucleus Neurons

Ghamari‐Langroudi, Masoud; Bourque, Charles W.

doi:10.1523/jneurosci.1240-04.2004

Cited by 57 publications

(72 citation statements)

References 57 publications

(95 reference statements)

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“…Blocking M-type K + channels with 10 mM XE-991 does not affect the sAHP in IL neurons (Santini and Porter, 2010), therefore muscarine also blocks the calcium-dependent potassium channels underlying the sAHP. Consistent with this, modulation of the sAHP by muscarinic receptors has been previously shown in other brain regions (Cox et al, 1994;Zhang et al, 1996;Bond et al, 1999;Egorov et al, 1999;Scroggs et al, 2001;Krause et al, 2002;Sah and Faber, 2002;Ghamari-Langroudi and Bourque, 2004).…”

Section: Muscarinic Receptors Inhibit M-currents and The Sahp In Il Psupporting

confidence: 86%

Muscarinic Receptors Modulate the Intrinsic Excitability of Infralimbic Neurons and Consolidation of Fear Extinction

Santini

Sepulveda-Orengo

Porter

2012

Neuropsychopharmacol

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There is considerable interest in identifying pharmacological compounds that could be used to facilitate fear extinction. Recently, we showed that the modulation of M-type K + channels regulates the intrinsic excitability of infralimbic (IL) neurons and fear expression. As muscarinic acetylcholine receptors inhibit M-type K + channels, cholinergic inputs to IL may have an important role in controlling IL excitability and, thereby, fear expression and extinction. To test this model, we combined whole-cell patch-clamp electrophysiology and auditory fear conditioning. In prefrontal brain slices, muscarine enhanced the intrinsic excitability of IL neurons by reducing the M-current and the slow afterhyperpolarization, resulting in an increased number of spikes with shorter inter-spike intervals. Next, we examined the role of endogenous activation of muscarinic receptors in fear extinction. Systemic injected scopolamine (Scop) (muscarinic receptor antagonist) before or immediately after extinction training impaired recall of extinction 24-h later, suggesting that muscarinic receptors are critically involved in consolidation of extinction memory. Similarly, infusion of Scop into IL before extinction training also impaired recall of extinction 24-h later. Finally, we demonstrated that systemic injections of the muscarinic agonist, cevimeline (Cev), given before or immediately after extinction training facilitated recall of extinction the following day. Taken together, these findings suggest that cholinergic inputs to IL have a critical role in modulating consolidation of fear extinction and that muscarinic agonists such as Cev might be useful for facilitating extinction memory in patients suffering from anxiety disorders.

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Section: Muscarinic Receptors Inhibit M-currents and The Sahp In Il Psupporting

confidence: 86%

Muscarinic Receptors Modulate the Intrinsic Excitability of Infralimbic Neurons and Consolidation of Fear Extinction

Santini

Sepulveda-Orengo

Porter

2012

Neuropsychopharmacol

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“…We show here that a critical feature for burst firing by GnRH neurons is their ability to exhibit prolonged Ca 2ϩ transients that act, in turn, to control very slow I AHP s that regulate intraburst and interburst properties. It is interesting to note that magnocellular oxytocin and vasopressin neurons can exhibit somewhat similar bursting behaviors to GnRH neurons but do not exhibit prolonged calcium transients or use calcium-dependent potassium channels in the same manner (Li and Hatton, 1997;Ghamari-Langroudi and Bourque, 2004;Teruyama and Armstrong, 2005). The dynamics of Ca 2ϩ transients in GnRH neurons are unique in the mature nervous system as is the existence of a very slow AHP generated by two sI AHP s in these cells.…”

Section: Discussionmentioning

confidence: 99%

Two Slow Calcium-Activated Afterhyperpolarization Currents Control Burst Firing Dynamics in Gonadotropin-Releasing Hormone Neurons

Lee¹,

Duan²,

Sneyd³

et al. 2010

J. Neurosci.

157

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Gonadotropin-releasing hormone (GnRH) neurons release GnRH in a pulsatile manner to control fertility in all mammals. The mechanisms underlying burst firing in GnRH neurons, thought to contribute to pulsatile GnRH release, are not yet understood. Using minimally invasive, dual electrical-calcium recordings in acute brain slices from GnRH-Pericam transgenic mice, we find that the soma/proximal dendrites of GnRH neurons exhibit long-duration (ϳ10 s) calcium transients that are perfectly synchronized with their burst firing. These transients were found to be generated by calcium entry through voltage-dependent L-type calcium channels that was amplified by inositol-1,4,5-trisphosphate receptor-dependent store mechanisms. Perforated-patch current-and voltage-clamp electrophysiology coupled with mathematical modeling approaches revealed that these broad calcium transients act to control two slow afterhyperpolarization currents (sI AHP ) in GnRH neurons: a quick-activating apamin-sensitive sI AHP that regulates both intraburst and interburst dynamics, and a slow-onset UCL2077-sensitive sI AHP that regulates only interburst dynamics. These observations highlight a unique interplay between electrical activity, calcium dynamics, and multiple calcium-regulated sI AHP s critical for shaping GnRH neuron burst firing.

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“…The findings of Greffrath et al (1998) suggest that the induction, maintenance and termination of the plateau potential underlying bursting in MNCs are regulated by the balance between the DAP and the slow AHP. Experimental evidence of a contribution of the slow AHP to burst termination was presented by Ghamari-Langroudi and Bourque (2004). However, the best characterized mechanism for burst termination is an activity-dependent inhibition of the DAP (Brown and Bourque 2004;Brown et al 2006), which was incorporated in the model of Roper et al (2004).…”

Section: Depolarizing After Potential-magnocellularmentioning

confidence: 99%

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

2007

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Magnocellular neuroendocrine cells (MNCs) of the hypothalamus synthesize the neurohormones vasopressin and oxytocin, which are released into the blood and exert a wide spectrum of actions, including the regulation of cardiovascular and reproductive functions. Vasopressin-and oxytocinsecreting neurons have similar morphological structure and electrophysiological characteristics. A realistic multicompartmental model of a MNC with a bipolar branching structure was developed and calibrated based on morphological and in vitro electrophysiological data in order to explore the roles of ion currents and intracellular calcium dynamics in the intrinsic electrical MNC properties. The model was used to determine the likely distributions of ion conductances in morphologically distinct parts of the MNCs: soma, primary dendrites and secondary dendrites. While reproducing the general electrophysiological features of MNCs, the model demonstrates that the differential spatial distributions of ion channels influence the functional expression of MNC properties, and reveals the potential importance of dendritic conductances in these properties.

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Muscarinic Receptor Modulation of Slow Afterhyperpolarization and Phasic Firing in Rat Supraoptic Nucleus Neurons

Cited by 57 publications

References 57 publications

Muscarinic Receptors Modulate the Intrinsic Excitability of Infralimbic Neurons and Consolidation of Fear Extinction

Muscarinic Receptors Modulate the Intrinsic Excitability of Infralimbic Neurons and Consolidation of Fear Extinction

Two Slow Calcium-Activated Afterhyperpolarization Currents Control Burst Firing Dynamics in Gonadotropin-Releasing Hormone Neurons

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

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