Tetrodotoxin-sensitivity of nicotine-evoked dopamine release from rat striatum

Marshall, David L.; Soliakov, L.; Redfern, P. H.; Wonnacott, Susan

doi:10.1016/s0028-3908(96)00117-7

Cited by 43 publications

(33 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…According to a recent study, at least two dierent subtypes of nicotinic AChRs control striatal DA release (Kaiser et al, 1998). The enhancement of DA metabolism seems to be linked to the activation of nicotinic AChRs in the somatodendritic region, because locally applied nicotine failed to increase the extracellular concentrations of DOPAC and HVA in the striatum and nucleus accumbens (Toth et al, 1992;Marshall et al, 1997). Also, the data presented here that the mechanisms controlling striatal DA release seem to be more readily aected by ambient temperature than those controlling the extracellular levels of DA metabolites, indicate the multiplicity of nicotinic AChRs involved in the control of striatal DA system.…”

Section: Discussionmentioning

confidence: 70%

“…Dopaminergic neurons innervating the striatum are thought to have nicotinic AChRs in somatodendritic regions as well as on nigral axons presynaptically and preterminally, a distinction based on tetrodotoxin sensitivity (Marshall et al, 1996;Wonnacott, 1997). According to a recent study, at least two dierent subtypes of nicotinic AChRs control striatal DA release (Kaiser et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of acute nicotine administration on striatal dopamine output and metabolism in rats kept at different ambient temperatures

Seppä

Ruotsalainen

Laakso

et al. 2000

British J Pharmacology

View full text Add to dashboard Cite

1 The eect of ambient temperature on the nicotine-induced (0.3, 0.5 or 0.8 mg kg 71 s.c.) changes of the striatal concentrations of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) was studied in freely-moving rats by in vivo microdialysis. 2 At the ambient temperature of 30 ± 338C, but not at 20 ± 238C, nicotine doses of 0.5 (P50.01) and 0.8 mg kg 71 (P50.05) signi®cantly increased the extracellular DA concentration. The nicotine doses of 0.5 and 0.8 mg kg 71 increased the DA metabolite levels similarly at both ambient temperatures studied (P40.0001), but the dose of 0.3 mg kg 71 only at 30 ± 338C (DOPAC: P50.05; HVA: P50.01).3 At 30 ± 338C, dihydro-b-erythroidine (DHbE 2.8 mg kg 71 i.p.) blocked the nicotine-induced (0.5 or 0.8 mg kg 71 ) increases of extracellular DA concentration but only tended to antagonize the increases of DA metabolites. Mecamylamine (5.0 mg kg 71 i.p.) blocked the increase of DA output induced by 0.5 mg kg 71 but not that induced by 0.8 mg kg 71 of nicotine and fully prevented the nicotine-induced elevations of DOPAC and HVA. 4 Elevation of ambient temperature did not aect the cerebral concentration of nicotine or the nicotine-induced elevation of serum corticosteroids. Also, the rectal temperatures of rats given nicotine at either ambient temperature did not signi®cantly change. 5 Our results show that the nicotine-induced output of striatal DA is enhanced at high ambient temperature. Further, our ®ndings suggest that the nicotinic cholinoceptors mediating the eects of nicotine on striatal DA release are dierent from those mediating nicotine's eects on DA metabolism.

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Effect of acute nicotine administration on striatal dopamine output and metabolism in rats kept at different ambient temperatures

Seppä

Ruotsalainen

Laakso

et al. 2000

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…It is therefore possible that, during the neonatal period, DA terminals have not acquired the necessary "machinery" for impulse-induced neurotransmitter release (e.g. voltage gated ion channels) which mediate nicotine's actions (Soliakov et al, 1995,Marshall et al, 1996,Prince et al, 1996,Kulak et al, 2001); however, this seems unlikely since K + -stimulated release was also significantly lower in fetal brain, whereas maximal levels of nicotine-stimulated transmitter release were similar to that obtained in mature brain. Thus, it seems likely that the early postnatal changes in nicotine actions reflect changes in nAChR properties.…”

Section: Early Postnatal Periodmentioning

confidence: 98%

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

2007

View full text Add to dashboard Cite

We have combined anatomical and functional methodologies to provide a comprehensive analysis of the properties of nicotinic acetylcholine receptors (nAChRs) on developing dopamine (DA) neurons. Double-labeling in situ hybridization was used to examine the expression of nAChR subunit mRNAs within developing midbrain DA neurons. As brain maturation progressed there was a change in the pattern of subunit mRNA expression within DA neurons, such that α3 and α4 subunits declined and α6 mRNA increased. Although there were strong similarities in subunit mRNA expression in substantia nigra (SNc) and ventral tegmental area (VTA), there was higher expression of α4 mRNA in SNc than VTA at gestational day (G)15, and of α5, α6 and β3 mRNAs during postnatal development. Using a superfusion neurotransmitter release paradigm to functionally characterize nicotine-stimulated release of [ 3 H]DA from striatal slices, the properties of the nAChRs on DA terminals were also found to change with age. Functional nAChRs were detected on striatal terminals at G18. There was a decrease in maximal release in the first postnatal week, followed by an increase in nicotine efficacy and potency during the second and third postnatal weeks. In the transition from adolescence (postnatal days (P) 30 and 40) to adulthood, there was a complex pattern of functional maturation of nAChRs in ventral, but not dorsal, striatum. In males, but not females, there were significant changes in both nicotine potency and efficacy during this developmental period. These findings suggest that nAChRs may play critical functional roles throughout DA neuronal maturation. Keywords adolescent; fetal; nicotine; sex; striatum; maternal smoking Maternal smoking during pregnancy has been correlated with a number of adverse outcomes in the offspring (Lichtensteiger et al., 1988,Lichtensteiger andSchlumpf, 1993), including cognitive deficits that are often manifested in early childhood as attention deficit hyperactivity disorder (ADHD) (Millberger et al., 1996). Though the underlying neurobiological mechanism * Correspondence to: Dr. Layla Azam Department of Biology, University of Utah 257 South 1400 East Salt Lake City, UT 84112 Tel.: (801) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ,Pliszka et al., 1996,Castellanos, 1997. In animal studies, maternal nicotine exposure produces sexdependent alterations in the development of DA neurochemical markers (Fung, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Muneoka et al., 1997, and induces hyperactivity in the offspring, which is believed...

show abstract

“…One recent functional study for example showed that while nicotine infused at a dose of 4.0 mg kg 71 day 71 desensitized nicotine-stimulated striatal dopamine release, a lower dose of 1.0 mg kg 71 day 71 showed no such desensitization of function (Benwell & Balfour, 1997). It should be noted however that an enhancement of function has also been associated with nAChR upregulation in vivo (see Marshall et al, 1997).…”

mentioning

confidence: 99%

“…As nAChR regulation and function in vivo are aected not only by nicotine dose but also the duration (acute versus chronic) and method (continuous versus intermittent) of treatment (see Marshall et al, 1997;Rowell & Li, 1997), these factors may potentially in¯uence the neuroprotective capacity of nicotine in vivo.…”

mentioning

confidence: 99%

Dose‐related neuroprotective effects of chronic nicotine in 6‐hydroxydopamine treated rats, and loss of neuroprotection in α4 nicotinic receptor subunit knockout mice

Ryan

Ross

Drago

et al. 2001

British J Pharmacology

178

151

View full text Add to dashboard Cite

1 The present study examined the eect of a range of doses of chronic nicotine (0.75, 1.5, 3.0 and 30.0 mg kg 71 day 71, s.c., 14 days) upon striatal dopaminergic nerve terminal survival following 6-hydroxydopamine (6-OHDA; 10 mg intrastriatal unilaterally) in rats; and the eects of acute nicotine (1 ) nicotine doses signi®cantly inhibited 6-OHDA-induced degeneration. 4 In wild-type mice, acute nicotine treatment produced signi®cant inhibition of methamphetamineinduced neurodegeneration. In a4 nAChR subunit knockout mice, acute nicotine treatment failed to inhibit methamphetamine-induced neurodegeneration. 5 Nicotine is capable of protecting dopaminergic neurons against Parkinsonian-like neurodegeneration in vivo. In rats, this neuroprotective eect is critically dependent upon nicotine dose and is consistent with the activation of nAChRs, as high, desensitizing doses of nicotine fail to be neuroprotective. Further, neuroprotection is absent in a4 nAChR subunit knockout mice. The current results therefore suggest that activation of a4 subunit containing nAChRs constitutes a major component of the neuroprotective eect of nicotine upon Parkinsonian-like damage in vivo.

show abstract

Tetrodotoxin-sensitivity of nicotine-evoked dopamine release from rat striatum

Cited by 43 publications

References 18 publications

Effect of acute nicotine administration on striatal dopamine output and metabolism in rats kept at different ambient temperatures

Effect of acute nicotine administration on striatal dopamine output and metabolism in rats kept at different ambient temperatures

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

Dose‐related neuroprotective effects of chronic nicotine in 6‐hydroxydopamine treated rats, and loss of neuroprotection in α4 nicotinic receptor subunit knockout mice

Contact Info

Product

Resources

About