Ultrastructural relationships between choline acetyltransferase- and neuropeptide Y-containing neurons in the rat striatum

Vuillet, J.; Dimova, R; Nieoullon, A.; Goff, Lydia Kerkerian‐Le

doi:10.1016/0306-4522(92)90057-9

Cited by 56 publications

(38 citation statements)

References 27 publications

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“…In addition, hydroxylamine-induced membrane depolarization was prevented by intracellular injection of either sGC or PKG inhibitors, indicating that NO likely acts as an anterograde transmitter on striatal cholinergic interneurons, leading to cGMP-dependent stimulation of PKG. These electrophysiological data are in good agreement with ultrastructural and immunocytochemical studies, demonstrating that NOS-positive terminals do synapse on cholinergic cells in the striatum (Vuillet et al, 1992) and that intracellular cGMP synthesis occurs in cholinergic cells but not in dopaminergic or glutamatergic presynaptic fibers of the rat striatum in response to NO (De Vente et al, 2000). It should be noted, however, that the compounds used in this study to block sGC or PKG are all membrane-permeable and, therefore, it is also possible that the enzymes mediating the response of cholinergic cells to NO are located in other cellular subtypes of our slice preparation.…”

Section: Discussionsupporting

confidence: 78%

Stimulation of Nitric Oxide–cGMP Pathway Excites Striatal Cholinergic Interneurons via Protein Kinase G Activation

et al. 2001

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Conflicting data have been collected so far on the action of nitric oxide (NO) on cholinergic interneurons of the striatum. In the present in vitro electrophysiological study, we reported that intracellularly recorded striatal cholinergic interneurons are excited by both hydroxylamine and S-nitroso-N-acetylpenicillamine, two NO donors. This excitation persisted unchanged in the presence of glutamate, dopamine, and substance P receptor antagonists as well as after blockade of tetrodotoxin (TTX)-and calcium channel-sensitive transmitter release, suggesting that NO produces its effects by modulating directly resting ion conductances in the somatodendritic region of striatal cholinergic cells. The depolarizing effect of hydroxylamine was greatly reduced by lowering external concentrations of sodium ions (from 126 to 38 mM) and did not reverse polarity in the voltage range from Ϫ120 to Ϫ40 mV. The sodium transporter blockers bepridil and 3Ј,4Ј-dichlorobenzamil were conversely ineffective in preventing NO-induced membrane depolarization. Intracellular cGMP elevation is required for the action of hydroxylamine on striatal cholinergic cells, as demonstrated by the findings that the membrane depolarization produced by this pharmacological agent was prevented by bath and intracellular application of two inhibitors of soluble guanylyl cyclase and was mimicked and occluded by zaprinast, a cGMP phosphodiesterase inhibitor. Finally, intracellular Rp-8-Br-cGMPS, a protein kinase G (PKG) inhibitor, blocked the hydroxylamine-induced membrane depolarization of cholinergic interneurons, whereas both okadaic acid and calyculin A, two protein phosphatase inhibitors, enhanced it, indicating that intracellular PKG and phosphatases oppositely regulate the sensitivity of striatal cholinergic interneurons to NO. The characterization of the cellular mechanisms involved in the regulation of striatal interneuron activity is a key step for the understanding of the role of these cells in striatal microcircuitry.

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Section: Discussionsupporting

confidence: 78%

Stimulation of Nitric Oxide–cGMP Pathway Excites Striatal Cholinergic Interneurons via Protein Kinase G Activation

et al. 2001

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“…In the guinea pig, the density of SOM-IR and NPY-IR fibers is higher in ventromedial regions of the dorsal striatum. A similar pattern of fiber distribution was described by Kowall et al in humans [21] and by Vuillet et al in rats [39]. In the guinea pig, a high density of fibers containing SOM and NPY was also seen in the part corresponding to the tail of the caudate nucleus.…”

Section: Discussionsupporting

confidence: 85%

“…In the striatum, SOM is produced by intrinsic interneurons, the axons and dendrites of which are selectively concentrated in the major striatal compartment, the matrix [5]. The axons of SOM-positive cells in the striatum may extend up to 1 mm from the cell body, which allows these cells to influence other neurotransmissions and the flow of blood in a larger space than the other striatal interneurons do [3,5,39,45]. It is possible that some of the SOM neurons may have axons projecting to the globus pallidus [31].…”

Section: Discussionmentioning

confidence: 99%

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Distribution and chemical coding pattern of somatostatin immunoreactivity in the dorsal striatum of the guinea pig

Wasilewska¹,

Robak²,

Równiak³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The present study provides a detailed description of somatostatin (SOM) distribution and the colocalization pattern of SOM, neuropeptide Y (NPY) and nitric oxide synthase (NOS) in the dorsal striatum (caudate-putamen complex) of the guinea pig. Within the dorsal striatum, SOM is found in a population of medium-sized aspiny interneurons. We found that 97% of all SOM-IR neurons expressed NPY simultaneously, while 98% of all NPY-ergic perikarya was simultaneously SOM-IR. On the other hand, while 98% of all SOM-IR cells were simultaneously NOS-IR, only 91% of all NOS-containing neurons exhibited SOM-immunoreactivity. Irrespective of their chemical coding, both types of SOM-IR neurons were scattered throughout the dorsal striatum, sometimes in the form of small, loosely arranged clusters of 2-4 cells. While SOM-IR and NPY-IR nerve fibers were present in all of the studied regions, they were more numerous in the ventro-medial part of the studied structure, with the exception of its caudal portion, where SOM-IR and NPY-IR fibers additionally formed a dense network in the part corresponding to the caudate nucleus. A low expression of staining for NOS-IR fibers was seen throughout the entire dorsal striatum. In some fibers, SOM and NPY were co-expressed. Fibers expressing both SOM and NOS were not found.

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“…Since the activation of D 1/5 receptors stimulates cholinergic interneurons (Aosaki et al, 1998) that have reciprocal connections with NOS interneurons (Vuillet et al, 1992), the potential role of this and other indirect circuits in the D 1/5 -mediated facilitation of NOS activity needs to be assessed in future studies. Moreover, high-frequency electrical stimulation of the SN can activate fibers of passage in the midbrain, and potentially, antidromically activate corticospinal neurons which also send axon collaterals to the striatum (Wilson, 2004).…”

Section: Technical Considerationsmentioning

confidence: 99%

Phasic Dopaminergic Transmission Increases NO Efflux in the Rat Dorsal Striatum via a Neuronal NOS and a Dopamine D1/5 Receptor-Dependent Mechanism

Sammut

Dec

Mitchell

et al. 2005

Neuropsychopharmacol

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Dysfunctional neurotransmission within striatal networks is believed to underlie the pathophysiology of several neurological and psychiatric disorders. Nitric oxide (NO)-producing interneurons have been shown to play a critical role in modulating striatal synaptic transmission. These interneurons receive synaptic contacts from midbrain dopamine (DA) neurons and may be regulated by DA receptor activation. In the current study, striatal NO efflux was measured in anesthetized male rats using an NO-selective electrochemical microsensor and the role of DA in modulating NO synthase (NOS) activity was assessed during electrical or chemical (bicuculline) stimulation of the substantia nigra (SN). Electrical stimuli were patterned to approximate the natural single spike or burst firing activity of midbrain DA neurons. Electrical stimulation of the SN at low frequencies induced modest increases in striatal NO efflux. In contrast, train stimulation of the SN robustly increased NO efflux in a stimulus intensity-dependent manner. NO efflux evoked by SN stimulation was similar in chloral hydrate-and urethane-anesthetized rats. The facilitatory effect of train stimulation on striatal NO efflux was transient and attenuated by systemic administration of the neuronal NOS inhibitor 7-nitroindazole and the nonselective NOS inhibitor methylene blue. Moreover, the increase in NO efflux observed during chemical and train stimulation of the SN was attenuated following systemic administration of the DA D 1/5 receptor antagonist SCH 23390. SCH 23390 also blocked NO efflux induced by systemic administration of the D 1/5 agonist SKF 81297. These results indicate that neuronal NOS is activated in vivo by nigrostriatal DA cell burst firing via a DA D 1/5 -like receptor-dependent mechanism.

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Ultrastructural relationships between choline acetyltransferase- and neuropeptide Y-containing neurons in the rat striatum

Cited by 56 publications

References 27 publications

Stimulation of Nitric Oxide–cGMP Pathway Excites Striatal Cholinergic Interneurons via Protein Kinase G Activation

Stimulation of Nitric Oxide–cGMP Pathway Excites Striatal Cholinergic Interneurons via Protein Kinase G Activation

Distribution and chemical coding pattern of somatostatin immunoreactivity in the dorsal striatum of the guinea pig

Phasic Dopaminergic Transmission Increases NO Efflux in the Rat Dorsal Striatum via a Neuronal NOS and a Dopamine D1/5 Receptor-Dependent Mechanism

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