Alcohol-Induced c-Fos Expression in the Edinger-Westphal Nucleus: Pharmacological and Signal Transduction Mechanisms

Bachtell, Ryan K.; Tsivkovskaia, Natalia O.; Ryabinin, Andrey E.

doi:10.1124/jpet.102.036046

Cited by 84 publications

(100 citation statements)

References 37 publications

(49 reference statements)

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“…However, in vivo exposure data are more consistent, revealing an ethanol-induced decrease in npg ERK activation [13][14][15] , except in the report from Bachtell et al [32] . Our data are in agreement with previous reports in which chronic ethanol exposure in vivo decreased ERK phosphorylation.…”

Section: Discussionmentioning

confidence: 70%

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Cui

Wang

et al. 2011

Acta Pharmacol Sin

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Aim:The dorsal striatum has been proposed to contribute to the formation of drug-seeking behaviors, leading to excessive and compulsive drug usage, such as addiction. The current study aimed to investigate the involvement of extracellular signal-regulated kinase (ERK) pathway in the modification of striatal synaptic plasticity. Methods: Ethanol was administered to rats in drinking water at concentration of 6% (v/v) for 30 days. Rats were sacrificed on day 10, 20, or 30 during ethanol intake or on withdrawal day 1, 3, or 7 following 30-d ethanol intake. The striata were removed either for electrophysiological recording or for protein immuno-blot analysis. Extracellular recording technique was used to record population spikes (PS) induced by high-frequency stimulation (HFS) in the dorsolateral striatum (DLS). Results: Corticostriatal long-term depression (LTD) was determined to be dependent upon ERK signaling. Chronic ethanol intake (CEI) attenuated ERK phosphorylation and LTD induction, whereas withdrawal for one day (W1D) potentiated ERK phosphorylation and LTD induction. These results showed that the impact of chronic ethanol intake and withdrawal on corticostriatal synaptic plasticity was associated with ethanol's effect on ERK phosphorylation. In particular, pharmacological inhibition of ERK hyper-phosphorylation by U0126 prevented LTD induction in the DLS and attenuated ethanol withdrawal syndrome as well. Conclusion: In rat DLS, chronic ethanol intake and withdrawal altered LTD induction via ERK signaling pathway. Ethanol withdrawal syndrome is mediated, at least partly, by ERK hyper-phosphorylation in the DLS.

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Section: Discussionmentioning

confidence: 70%

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Cui

Wang

et al. 2011

Acta Pharmacol Sin

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“…A possible explanation may be that diazepam potentiates the GABAergic inhibition not only of the locus coeruleus but also of the preganglionic parasympathetic neurones in the Edinger-Westphal nucleus, which mediate the pupillary light reflex (pupil constriction). Indeed, inhibitory GABA A receptors have been identified on the Edinger-Westphal nucleus [60]. Thus a reduction in sympathetic pupil dilatation may be masked by a reduction in parasympathetic pupil constriction.…”

Section: Discussionmentioning

confidence: 99%

Relationship between sedation and pupillary function: comparison of diazepam and diphenhydramine

Hou

Scaife

Freeman

et al. 2006

Brit J Clinical Pharma

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AimsTo examine the relationship between sedation and pupillary function by comparing the effects of diazepam and diphenhydramine on arousal and pupillary activity. MethodsFifteen male volunteers participated in three weekly sessions in which they received (i) diazepam 10 mg, (ii) diphenhydramine 75 mg and (iii) placebo, according to a balanced, double-blind protocol. Pupil diameter was measured with infrared pupillometry under four luminance levels. Alertness was assessed by visual analogue scales (VAS) and by critical flicker fusion frequency (CFFF). Blood pressure, heart rate and skin conductance were recorded by conventional methods. Data were analysed with analysis of variance ( ANOVA ) with multiple comparisons. ResultsThere were significant effects of ambient luminance ( F 3,42 = 305.7, P < 0.001) and treatment condition ( F 2,28 = 9.0, P < 0.01) on pupil diameter; diphenhydramine caused miosis at all luminance levels ( P < 0.05). The light reflex response was not affected. Both active drugs reduced the pre-post treatment changes compared with placebo [mean difference from placebo (95% confidence interval)]: in CFFF (Hz), diazepam − 0.73 ( − 1.63, 0.17), diphenhydramine − 1.46 ( − 2.40, − 0.52); and VAS alertness (mm), diazepam − 11.49 ( − 19.19, − 3.79), diphenhydramine − 19.83 ( − 27.46, − 12.20). There were significant effects of both session ( F 2,26 = 145.1, P < 0.001) and treatment ( F 2,26 = 5.5, P < 0.01) on skin conductance; skin conductance was reduced by both drugs ( P < 0.05). ConclusionsThe miosis by diphenhydramine and the reduction in skin conductance by both drugs may indicate central sympatholytic effects. A lack of a sympatholytic effect of diazepam on the pupil may be due to the masking of the miosis by mydriasis resulting from the inhibition of the parasympathetic output to the iris. IntroductionIt is generally accepted that there is a close relationship between the level of arousal of the central nervous system and pupil diameter: any decrease in arousal is accompanied by a decrease in pupil diameter. In fact, it has been stated that sedative drugs 'all decrease pupillary diameter in proportion to their sedative-hypnotic effects: the closer the recipient drifts toward somnolence, the smaller the pupils' [1]. This relationship may not hold in the case of drugs which, apart from causing sedation, may directly influence, by a separate pharmacological action, the pupil control mechanism. An example of such a class of drug may be the firstgeneration antihistamines. Many of these drugs, apart from causing sedation, presumably due to the blockade of central H1 histamine receptors, also have anticholinergic effects, due to their affinity for muscarinic cholinoceptors. Thus the sedation caused by these drugs is expected to induce miosis, whereas their atropine-like effect on the iris is predicted to lead to mydriasis. Another class of drug not conforming to the general rule of an association between sedation and miosis are the benzodiazepines. These drugs, although highly sedative, have been r...

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“…Our understanding of the structure of EW has been further challenged by studies that indicate that this nucleus also contains neurons projecting to central targets, instead of the ciliary ganglion (cat: Loewy et al, 1978;monkey: Burde, 1988), and that these centrally projecting neurons use neuropeptides, not acetylcholine as their transmitter (Maciewicz et al, 1983). This has recently been reinforced by discovery of a population of neurons that use urocortin, a neuropeptide tied to stress responses and ingestive behavior, within the rodent EW (Bachtell et al, 2002;Kozicz et al, 2001;Vaughan et al, 1995).…”

Section: Introductionmentioning

confidence: 96%

Defining the pupillary component of the perioculomotor preganglionic population within a unitary primate Edinger–Westphal nucleus

May

Sun

Erichsen

2008

Progress in Brain Research

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The primate Edinger-Westphal nucleus (EW) contains perioculomotor preganglionic (pIII PG ) motoneurons that control the lens and pupil. Separate subdivisions have been described in EW and termed visceral columns, with the lateral visceral column (lvc) reportedly receiving pretectal inputs for the pupillary light reflex. However, choline acetyl transferase staining reveals a single paired column of cells dorsal to the oculomotor nucleus, suggesting the EW is not subdivided. We investigated this issue by transneuronal retrograde labeling of pIII PG neurons in three monkey species. In all three, pIII PG neurons were contained in a single column. We have also examined which part of the macaque pIII PG population receives pretectal input. Injections of biocytin into the pretectum anterogradely labeled terminals that lay in close association with pIII PG motoneurons retrogradely labeled by ciliary ganglion injections of WGA-HRP. These close associations were concentrated in the ventromedial portion of the middle third of EW , suggesting this pIII PG region mediates pupillary control. In other cases, pretectal WGA-HRP injections, in addition to labeling terminals in the EW, produced a circular field of labeled neurons and terminals in the periaqueductal gray, dorsolateral to EW. This region may represent the previously designated lvc, but it does not contain pIII PG motoneurons.

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Alcohol-Induced c-Fos Expression in the Edinger-Westphal Nucleus: Pharmacological and Signal Transduction Mechanisms

Cited by 84 publications

References 37 publications

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Relationship between sedation and pupillary function: comparison of diazepam and diphenhydramine

Defining the pupillary component of the perioculomotor preganglionic population within a unitary primate Edinger–Westphal nucleus

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