Norepinephrine Facilitates Inhibitory Transmission in Substantia Gelatinosa of Adult Rat Spinal Cord (Part 1)

Baba, Hiroshi; Shimoji, Koki; Yoshimura, Michihiro

doi:10.1097/00000542-200002000-00030

Cited by 149 publications

(101 citation statements)

References 36 publications

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“…Moreover, the actions of NA that we observed in the AOB are reminiscent of NA action in other brain regions and spinal cord. Most prominently, NA facilitates GABAergic transmission in stellate cells of the cerebellum (Llano and Gerschenfeld, 1993;Kondo and Marty, 1998), amygdala (Braga et al, 2004), sensorimotor cortex (Bennett et al, 1998), ventral bed nucleus of the stria terminalis (Dumont and Williams, 2004), and hypothalamus in the brain and in the substantia gelatinosa of the spinal cord (Baba et al, 2000). In our studies, the increase in mIPSC frequency was mediated by activation of ␣1 adrenergic receptors.…”

Section: Discussionsupporting

confidence: 53%

Adrenergic Enhancement of Inhibitory Transmission in the Accessory Olfactory Bulb

Araneda¹,

Firestein²

2006

J. Neurosci.

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Noradrenergic modulation of dendrodendritic synapses between the mitral and granule cells in the accessory olfactory bulb (AOB) is postulated to play a key role in the formation of memory in olfactory-mediated behaviors. Current models propose that noradrenaline (NA) increases excitation of mitral/tufted cells (M/TCs) by decreasing the release of GABA from granule cells. However, surprisingly little is known about the actions of NA at the cellular level in the AOB. Here, in recordings from AOB slices, we show that NA decreases the firing frequency of M/TCs in response to stimulation. This effect is attributable to an increase in the GABA inhibitory input to M/TCs. Application of NA (10 M) produced an ϳ20-fold increase in the frequency of GABA-induced miniature IPSCs (mIPSCs) without changing their amplitude. A pharmacological analysis indicated that the increase in mIPSCs frequency results from activation of ␣1 adrenergic receptors. In addition to increasing the mIPSC frequency, NA also potentiated GABA inhibitory currents induced by direct stimulation of granule cells. Together, our results suggest that NA increases the release of GABA from granule cells by acting on presynaptic receptors. Thus, the role of the noradrenergic activity in the AOB may be opposite than suggested previously: we find that the overall effect of NA in the AOB is inhibition of M/TCs.

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Section: Discussionsupporting

confidence: 53%

Adrenergic Enhancement of Inhibitory Transmission in the Accessory Olfactory Bulb

Araneda¹,

Firestein²

2006

J. Neurosci.

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“…In addition, we found that NA increased sEPSC through α1 receptors in some populations of regular type neurons. Several studies have addressed the relevance of NAergic modulation of synaptic events in the spinal cord (1,2,5,20,29). In this study, α2 receptor-mediated synaptic inhibition of sEPSC was observed in both types of neurons, consistent with previous reports.…”

Section: Synaptic Current Modulation Of Nasupporting

confidence: 91%

<b>Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp r</b><b>ecordings </b>

et al. 2017

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Noradrenergic modulation has been frequently discussed in the context of neural activities that are related to pelvic organs. The sacral preganglionic nucleus (SPN) is a spinal nucleus containing parasympathetic preganglionic neurons that send fibers to pelvic nerves. In spite of the abundant presence of noradrenergic fibers around the SPN, the effects of noradrenaline (NA) remain obscure. To explore this issue, NA (50 μM) was applied to parasympathetic preganglionic neurons in the SPN during whole-cell patch clamp recording. The SPN was labeled with the retrograde tracer, DiI. These neurons demonstrated two classes of firing patterns (delayed and regular) in terms of initiation of firing. Independent of these firing patterns, NA induced inward (56%) or outward (32%) currents in labeled SPN neurons. Phenylephrine, an α1 receptor agonist, induced an inward current, and clonidine, an α2 receptor agonist, induced an outward current, indicating the existence of both α1 and α2 adrenoreceptors in DiI-labeled SPN neurons. NA also modulated synaptic currents according to the firing patterns. In delayed firing neurons, NA inhibited both spontaneous excitatory post-synaptic currents (sEPSCs) and spontaneous inhibitory post-synaptic currents (sIPSCs). Hence, NA facilitated sEPSCs and sIPSCs in about a half of regular firing neurons. Bath application of phenylephrine facilitated sEPSCs and sIPSCs, and clonidine inhibited them. These results support the hypothesis of multiple effects of NA in the SPN, and may suggest functional differences among SPN neurons.The sacral parasympathetic nerve controls the functions of pelvic organs such as the urinary bladder, distal end of the colon, and penis. Preganglionic neurons in the sacral parasympathetic nucleus (SPN), which constitutes the pelvic nerve, are located in the lateral edge and/or medial part of laminae V-VII of L6-S1 in the spinal cord of the rat. These neurons receive input from several brainstem nuclei and spinal interneurons. Retrograde tracers such as fast blue and fast DiI are frequently used to distinguish parasympathetic preganglionic neurons (PGNs) within the SPN, because the SPN also contains interneurons, which show similar membrane properties to the PGNs (6). Induced firing of retrogradely labeled SPN neurons in the rat shows several distinct properties (4,19). One type of neurons show delayed firing in response to injected current pulse, and the other type of neurons show regular firing as a response. Various neurotransmitters and chemicals modulate SPN neuronal activities. However, differences in neurochemical modulation of these two types of neurons have not been fully studied. Noradrenaline (NA) is a well-known neurotransmitter in the central nervous system (CNS) and is present in descending pathways from brainstem nuclei A5 and A6 (locus coeruleus) to the spinal cord (27). NAergic modulation of spinal regions has been extensively studied. NA directly depolarizes motor

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“…Presynaptic actions of NA: To address whether spinally administered NA acts presynaptically to alter the excitatory and inhibitory transmitter release and, if so, to identify which receptor subtype is involved, a blind patch-clamp technique to study the action of NA on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs, respectively) in SG neurons from adult rat spinal cord slices was made (45,63,64). In the majority of SG neurons, NA dosedependently increased the frequency of GABAergic and glycinergic mIPSCs, while mEPSCs are not significantly altered in the presence of tetrodotoxin (TTX).…”

Section: Electrophysiological Study 1) In Vitro Studymentioning

confidence: 99%

“…These results indicate that NA enhances inhibitory transmitter release on the SG through the activation of presynaptic α 1 receptors, thus providing a mechanism underlying the clinical use of α 1 agonists with local anesthetics in spinal anesthesia. Baba et al (64) further addressed the action of NA on the somatodendritic sites or the terminals of inhibitory interneurons, in particular GABAergic ones. NA causes an increase in not only the frequency but also the amplitude of GABAergic IPSCs.…”

Section: Electrophysiological Study 1) In Vitro Studymentioning

confidence: 99%

“…Nevertheless, the possibility that excitatory interneurons activated by NA terminate on neurons located at some site other than SG still cannot be ruled out. Since both frequency and amplitude of IPSPs are enhanced by NA, not only the presynaptic terminals but also the soma-dendritic membrane is endowed with the α 1 adrenoceptors, producing neuron firing (63,64). NA exerts its antinociceptive actions not only by direct membrane hyperpolarization and enhancement of inhibitory transmitter release, but also reduce the excitatory transmitter release.…”

Section: Electrophysiological Study 1) In Vitro Studymentioning

confidence: 99%

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Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

2006

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Abstract. The sensation of pain plays a critical role as an alert and as a protection system against tissue damage from mechanical, chemical, and thermal stimuli. Despite the protective role of pain, the severity of pain sensation is markedly attenuated by the endogenous pain inhibitory systems that predominantly originate at the brain stem. Both behavioral and in vivo extracellular recording studies have sought the loci producing analgesia and clarification of the anti-nociceptive actions. Among those loci, the main descending systems to the spinal dorsal horn are noradrenergic and serotonergic. Although, in vivo studies have provided basic knowledge of these systems, the precise synaptic mechanisms underlying the analgesic actions have not yet been elucidated until recently. The newly developed in vitro slice and in vivo patchclamp recordings have disclosed the synaptic mechanisms of the noradrenergic and serotonergic effects at the level of spinal dorsal horn. This paper reviews the anti-nociceptive action of these systems, while particularly focusing on the electrophysiological aspects of the systems at the single neuron level in the spinal dorsal horn as well as their origins and responsible receptor subtypes.

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Norepinephrine Facilitates Inhibitory Transmission in Substantia Gelatinosa of Adult Rat Spinal Cord (Part 1)

Abstract: These results suggest that norepinephrine enhances inhibitory synaptic transmission in the substantia gelatinosa through activation of presynaptic alpha1 receptors, thus providing a mechanism underlying the clinical use of alpha1 agonists with local anesthetics in spinal anesthesia.

Cited by 149 publications

References 36 publications

Adrenergic Enhancement of Inhibitory Transmission in the Accessory Olfactory Bulb

Adrenergic Enhancement of Inhibitory Transmission in the Accessory Olfactory Bulb

<b>Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp r</b><b>ecordings </b>

Mechanisms for the Anti-nociceptive Actions of the Descending Noradrenergic and Serotonergic Systems in the Spinal Cord

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