Early postnatal development of substantia nigra neurons in rat midbrain slices: hyperpolarization-activated inward current and dopamine-activated current

Washio, Hiroshi; Takigachi-Hayashi, Keiko; Konishi, Shiro

doi:10.1016/s0168-0102(99)00039-5

Cited by 33 publications

(33 citation statements)

References 29 publications

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“…4) as previously reported in other cell types (Bayliss et al 1994;Richter et al 1997;Washio et al 1999). Interestingly, the half-maximal activation was significantly shifted to more depolarized values during postnatal development (Fig.…”

Section: Discussionsupporting

confidence: 85%

“…Interestingly, the half-maximal activation was significantly shifted to more depolarized values during postnatal development (Fig. 5) in contrast to some previous studies (Bayliss et al 1994;Cerbai et al 1999;Washio et al 1999). The shift in V 1/2 suggests that during development, Mes V neurons become more efficient in stabilizing membrane potential in response to phasic inhibitory inputs, as well as more effective in controlling membrane excitability during spike discharge (discussed in the following text).…”

Section: Discussioncontrasting

confidence: 59%

“…As shown in Fig. 6A, in most instances, the time course of activation and deactivation were well fitted with double exponential function of the form (Hogg et al 2001;Washio et al 1999). …”

Section: Slow Inward Rectifying Current (I H )mentioning

confidence: 66%

“…1A). The time course of relaxation from the initial peak amplitude to a steadystate value was faster in older compared with younger animals, indicating developmental regulation of I h (Guido et al 1998;Washio et al 1999). In voltage-clamp recording in normal ACSF (Fig.…”

Section: Characterization Of Inward Rectification In Mes V Neuronsmentioning

confidence: 95%

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Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Tanaka

Wu²,

Hsaio³

et al. 2003

Journal of Neurophysiology

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. Development of inward rectification and control of membrane excitability in mesencephalic V neurons. J Neurophysiol 89: 1288 -1298, 2003. First published November 20, 2002 10.1152/jn.00850.2002. The present study was performed to assess the postnatal development and functional roles of inward rectifying currents in rat mesencephalic trigeminal (Mes V) neurons, which are involved in the genesis and control of oral-motor activities. Whole cell voltage-clamp recordings obtained from Mes V neurons in brain stem slices identified fast (I KIR ) and slow (I h ) inward rectifying currents, which were specifically blocked by BaCl 2 (300 -500 M) or 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride (ZD 7288, 10 M), respectively. The whole cell current density for these channels increased between postnatal days 2 to 12 (P2-P12), and the time courses for I h activation and deactivation were each well described by two time constants. Application of ZD 7288 produced membrane hyperpolarization in the majority of cells and prolonged afterhyperpolarization repolarization. Additionally, in the presence of ZD 7288, spike frequency was decreased and adaptation was more pronounced. Interestingly, these neurons exhibited a voltage-dependent membrane resonance (Ͻ10 Hz) that was prominent around resting potential and more negative to rest and was blocked by ZD 7288. These results suggest that I h contributes to stabilizing resting membrane potential and controlling cell excitability. The presence of I h imparts the neuron with the unique property of lowfrequency membrane resonance; the ability to discriminate between synaptic inputs based on frequency content.

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Section: Discussionsupporting

confidence: 85%

Section: Discussioncontrasting

confidence: 59%

“…As shown in Fig. 6A, in most instances, the time course of activation and deactivation were well fitted with double exponential function of the form (Hogg et al 2001;Washio et al 1999). …”

Section: Slow Inward Rectifying Current (I H )mentioning

confidence: 66%

Section: Characterization Of Inward Rectification In Mes V Neuronsmentioning

confidence: 95%

See 2 more Smart Citations

Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Tanaka

Wu²,

Hsaio³

et al. 2003

Journal of Neurophysiology

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“…Whole cell recordings are performed with an Axon Multipatch or Axopatch 1D amplifier (Axon Instruments). Dopaminergic neurons were identified by anatomy, morphology, and a hyperpolarization-activated cation current (Ih), which is characteristic for these cells in midbrain slices (33). All cells that displayed Ih currents of at least 200 pA at Ϫ130 mV were classified as dopaminergic.…”

Section: Methodsmentioning

confidence: 99%

Knockin mice with Leu9′Ser α4-nicotinic receptors: substantia nigra dopaminergic neurons are hypersensitive to agonist and lost postnatally

Orb

Wieacker

Labarca

et al. 2004

Physiological Genomics

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mice with Leu9ЈSer ␣4 nicotinic receptors: substantia nigra dopaminergic neurons are hypersensitive to agonist and lost postnatally. Physiol Genomics 18: 299-307, 2004. First published June 15, 2004 10.1152/ physiolgenomics.00012.2004.-This study analyzes the electrophysiological cause and behavioral consequence of dopaminergic cell loss in a knockin mouse strain bearing hypersensitive nicotinic ␣4-receptor subunits ("L9ЈS mice"). Adult brains of L9ЈS mice show moderate loss of substantia nigra dopaminergic neurons and of striatal dopaminergic innervation. Amphetamine-stimulated locomotion is impaired, reflecting a reduction of dopamine stored in presynaptic vesicles. Recordings from dopaminergic neurons in L9ЈS mice show that 10 M nicotine depolarizes cells and increases spiking rates in L9ЈS cells but hyperpolarizes and decreases spiking rates in wild-type (WT) cells. Thus dopaminergic neurons of L9ЈS mice have an excitatory response to nicotine which is qualitatively different from that of WT neurons. The cause of dopaminergic cell death is therefore probably an increased sensitivity to acetylcholine or choline of ␣4-containing nicotinic receptors. Hypersensitive excitatory stimulation during activation of ␣4-containing receptors provides the first evidence for cholinergic excitotoxicity as a cause of dopaminergic neuron death. This novel concept may be relevant to the pathophysiology of Parkinson disease. cholinergic excitotoxicity; mouse NEURONAL NICOTINIC RECEPTORS (nAChRs) containing ␣4-subunits are highly expressed on cell bodies of dopaminergic neurons in the midbrain (2). nAChRs on dopaminergic neurons regulate dopamine release in striatum and frontal cortex (20,26) and play a role in nicotine addiction and motor control. Chronic treatment with nicotine facilitates dopamine release and locomotor responses, which is consistent with an upregulation of nAChRs in dopaminergic neurons (24). Chronic continuous treatment with nicotine does not alter locomotor behavior (30) but induces upregulation of dopamine D 2 receptors, which was interpreted as a consequence of downregulation of dopamine turnover (8). Thus chronic continuous administration of nicotine seems to suppress net dopamine release, perhaps via desensitization of nAChRs on dopaminergic neurons.This study analyzes the only known instance of dopaminergic cell death caused by chronic activation of nicotinic receptors (17). The pathology occurs in knockin mice carrying a leucine-to-serine mutation at the 9Ј position of the pore-lining second transmembrane domain (M2) in the ␣4-subunit. To retain viability, we work with 1) a strain that displays reduced expression of the hypersensitive allele, because of a deliberate insertion of the neomycin selection cassette in an intron adjoining the mutated exon; and 2) with heterozygotes of this strain. These viable and fertile heterozygous mice are termed "L9ЈS." L9ЈS mice do not show a significant reduction of dopaminergic neurons during embryonic development but have a reduction of amphetamine-induced locomot...

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Immunohistochemical localization of I_h channel subunits, HCN1–4, in the rat brain

Notomi

Shigemoto

2004

J of Comparative Neurology

517

555

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Hyperpolarization‐activated cation currents (Ih) contribute to various physiological properties and functions in the brain, including neuronal pacemaker activity, setting of resting membrane potential, and dendritic integration of synaptic input. Four subunits of the Hyperpolarization‐activated and Cyclic‐Nucleotide‐gated nonselective cation channels (HCN1–4), which generate Ih, have been cloned recently. To better understand the functional diversity of Ih in the brain, we examined precise immunohistochemical localization of four HCNs in the rat brain. Immunoreactivity for HCN1 showed predominantly cortical distribution, being intense in the neocortex, hippocampus, superior colliculus, and cerebellum, whereas those for HCN3 and HCN4 exhibited subcortical distribution mainly concentrated in the hypothalamus and thalamus, respectively. Immunoreactivity for HCN2 had a widespread distribution throughout the brain. Double immunofluorescence revealed colocalization of immunoreactivity for HCN1 and HCN2 in distal dendrites of pyramidal cells in the hippocampus and neocortex. At the electron microscopic level, immunogold particles for HCN1 and HCN2 had similar distribution patterns along plasma membrane of dendritic shafts in layer I of the neocortex and stratum lacunosum moleculare of the hippocampal CA1 area, suggesting that these subunits could form heteromeric channels. Our results further indicate that HCNs are localized not only in somato‐dendritic compartments but also in axonal compartments of neurons. Immunoreactivity for HCNs often occurred in preterminal rather than terminal portions of axons and in specific populations of myelinated axons. We also found HCN2‐immunopositive oligodendrocytes including perineuronal oligodendrocytes throughout the brain. These results support previous electrophysiological findings and further suggest unexpected roles of Ih channels in the brain. J. Comp. Neurol. 471:241–276, 2004. © 2004 Wiley‐Liss, Inc.

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Early postnatal development of substantia nigra neurons in rat midbrain slices: hyperpolarization-activated inward current and dopamine-activated current

Cited by 33 publications

References 29 publications

Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Knockin mice with Leu9′Ser α4-nicotinic receptors: substantia nigra dopaminergic neurons are hypersensitive to agonist and lost postnatally

Immunohistochemical localization of I_h channel subunits, HCN1–4, in the rat brain

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Early postnatal development of substantia nigra neurons in rat midbrain slices: hyperpolarization-activated inward current and dopamine-activated current

Cited by 33 publications

References 29 publications

Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Development of Inward Rectification and Control of Membrane Excitability in Mesencephalic V Neurons

Knockin mice with Leu9′Ser α4-nicotinic receptors: substantia nigra dopaminergic neurons are hypersensitive to agonist and lost postnatally

Immunohistochemical localization of Ih channel subunits, HCN1–4, in the rat brain

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Immunohistochemical localization of I_h channel subunits, HCN1–4, in the rat brain