A phase-response curve to the benzodiazepine chlordiazepoxide and the effect of geniculo-hypothalamic tract ablation

Meyer, Edson L.; Harrington, Mary E.; Rahmani, Tayebeh

doi:10.1016/0031-9384(93)90199-p

Cited by 48 publications

(19 citation statements)

References 39 publications

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“…These effects are not systematically related to phase shift magnitude or direction, but were related to circadian time, showing "period-response" curves quite different from the corresponding PRCs. More similar to the present results, acute chlordiazepoxide treatment was reported to induce both period shortening and lengthening (Meyer et al, 1993), but these effects were not related to either circadian time or phase shifting. While the mechanisms underlying long-lasting period alterations following acute stimulation have not been specified, it appears that such effects may be related to temporal redistribution of activity within the subjective night for both acute and chronic (Duncan et al, 1988) drug treatments.…”

Section: Discussionsupporting

confidence: 91%

“…Long-term alterations in free-running period following acute stimulation have been reported previously for photic (Pittendrigh and Daan, 1976), pharmacological (Joy et al, 1989;Edgar et al, 1993;Meyer et al, 1993), and arousal-related stimuli (Mrosovsky, 1993). In the present study, we noted a tendency for phase delays to be associated with period lengthening and for phase advances to be associated with period shortening, for both clonidine and saline treatments.…”

Section: Discussionsupporting

confidence: 55%

“…These shifts did not differ between saline and clonidine, and were seen only in RR-housed animals. Previous studies have also reported saline-induced phase advances during the late subjective day Meyer et al, 1993), and this effect has been attributed to handling and arousal since similar shifts were not seen when saline was delivered by a remote infusion system . Furthermore, a recent study showed that several nonphotic stimuli, including saline injections, produced daytime phase advances in constant light but not in constant darkness (Cutrera et al, 1994), as seen in the Downloaded by [North Carolina State University] at 06:22 10 April 2015 present study.…”

Section: Discussionmentioning

confidence: 83%

“…Thus the dark-pulse type PRC is commonly referred to as the "non-photic" PRC. A number of pharmacological agents, including serotonergic agonists (Medanic and Gillette, 1992;Tominaga et al, 1992;Edgar et al, 1993;Prosser et al, 1993;Cutrera et al, 1994), benzodiazepines (Turek and Losee-Olson, 1986;Wee and Turek, 1989a;Biello et al, 1991;Morin, 1991;Meyer et al, 1993), and neuropeptide Y (NPY) (Albers et al, 1991) can also induce phase shifts mimicking the non-photic PRC, either in behaving animals or in vitro preparations, or both. For some of these agents, phase shifts seen in behaving animals may be mediated by drug-induced behavioral activation (Van Reeth and Turek, 1989), but this does not appear true of all such agents .…”

Section: Introductionmentioning

confidence: 98%

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Circadian phase shifting induced by clonidine injections in Syrian hamsters

Rosenwasser

Vogt

Pellowski

1995

Biological Rhythm Research

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The mammalian circadian pacemaker can be phase shifted by photic, pharmacological, and behaviorally-derived stimuli. The phase-response curves (PRCs) characterizing these diverse stimuli may comprise two distinct families; a photic PRC typified by the response to brief light pulses, and a nonphotic PRC, typified by the response to dark pulses and to behavioral activation. The present study examined the phase shifting effects of acute systemic treatment with the alpha2-adrenoceptor agonist, clonidine, in Syrian hamsters. Clonidine injections (0.25 mg/kg, ip) delivered during subjective night mimicked the phase shifting effects of light pulses in animals housed in both constant darkness (DD) and constant red light (RR), but similar effects were not seen in saline-treated controls. Both clonidine and saline injections resulted in phase advances during subjective day, but only in RRhoused animals. Clonidine-induced phase shifting was dose-dependent, but rather high doses were required to induce phase shifts. Pretreatment with the selective noradrenergic neurotoxin, DSP-4, blocked clonidine-induced phase shifting. These results suggest that clonidine acts at presynaptic alpha2-adrenergic autoreceptors to disinhibit spontaneous and/or evoked activity in the photic entrainment pathway.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 98%

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Circadian phase shifting induced by clonidine injections in Syrian hamsters

Rosenwasser

Vogt

Pellowski

1995

Biological Rhythm Research

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“…Lesions of the hamster geniculohypothalamic tract block nonphotic phase shifts (Johnson et al, 1988;Biello et al, 1991;Meyer et al, 1993;Janik and Mrosovsky, 1994). NPY can induce nonphotic-type phase shifts in rats and hamsters in vivo (Albers and Ferris, 1984;Huhman and Albers, 1994;Biello and Mrosovsky, 1996) and in vitro (Shibata and Moore, 1993;Golombek et al, 1996;Biello et al, 1997; but see Medanic and Gillette, 1993).…”

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confidence: 99%

Circadian Phase Shifts to Neuropeptide YIn Vitro: Cellular Communication and Signal Transduction

et al. 1997

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Mammalian circadian rhythms originate in the hypothalamic suprachiasmatic nuclei (SCN), from which rhythmic neural activity can be recorded in vitro. Application of neurochemicals can reset this rhythm. Here we determine cellular correlates of the phase-shifting properties of neuropeptide Y (NPY) on the hamster circadian clock in vitro. Drug or control treatments were applied to hypothalamic slices containing the SCN on the first day in vitro. The firing rates of individual cells were sampled on the second day in vitro. Control slices exhibited a peak in firing rate in the middle of the day. Microdrop application of NPY to the SCN phase advanced the time of peak firing rate. This phase-shifting effect of NPY was not altered by block of sodium channels with tetrodotoxin or block of calcium channels with cadmium and nickel, consistent with a direct postsynaptic site of action. Pretreatment with the glutamate receptor antagonists (DL-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione disodium) also did not alter phase shifts to NPY. Blocking GABA A receptors with bicuculline (Bic) had effects only at very high (millimolar) doses of Bic, whereas blocking GABA B receptors did not alter effects of NPY. Phase shifts to NPY were blocked by pretreatment with inhibitors of protein kinase C (PKC), suggesting that PKC activation may be necessary for these effects. Bathing the slice in low Ca 2ϩ /high Mg 2ϩ can block phase shifts to NPY, possibly via a depolarizing action. A depolarizing high K ϩ bath can also block NPY phase shifts. The results are consistent with direct action of NPY on pacemaker neurons, mediated through a signal transduction pathway that depends on activation of PKC.

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Interconnections among nuclei of the subcortical visual shell: The intergeniculate leaflet is a major constituent of the hamster subcortical visual system

Morin

Blanchard

1998

J. Comp. Neurol.

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The intergeniculate leaflet (IGL), a major constituent of the circadian visual system, is one of 12 retinorecipient nuclei forming a "subcortical visual shell" overlying the diencephalic-mesencephalic border. The present investigation evaluated IGL connections with nuclei of the subcortical visual shell and determined the extent of interconnectivity between these nuclei. Male hamsters received stereotaxic, iontophoretic injections of the retrograde tracer, cholera toxin beta fragment, or the anterograde tracer, Phaseolus vulgaris-leucoagglutin, into nuclei of the pretectum (medial, commissural, posterior, olivary, anterior, nucleus of the optic tract, posterior limitans), into the superior colliculus, or into the visual thalamic nuclei (lateral posterior, dorsal lateral geniculate, intergeniculate leaflet, ventral lateral geniculate). Retrogradely labeled cell bodies identified nuclei with afferents projecting to the site of injection, whereas the presence of anterogradely labeled fibers with terminals revealed brain nuclei targeted by neurons at the site of injection. The IGL projects bilaterally to all nuclei of the visual shell except the lateral posterior and dorsal lateral geniculate nuclei. The IGL also has afferents from the same set of nuclei, except the nucleus of the optic tract. The extensive bilateral efferent projections distinguish IGL from the ventral lateral geniculate nucleus. The superior colliculus, commissural pretectal, olivary pretectal, and posterior pretectal nuclei also project bilaterally to the majority of subcortical visual nuclei. The IGL has a well-established role in circadian rhythm regulation, but there is as yet no known function for it in the larger context of the subcortical visual system, much of which is involved in oculomotor control.

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A phase-response curve to the benzodiazepine chlordiazepoxide and the effect of geniculo-hypothalamic tract ablation

Cited by 48 publications

References 39 publications

Circadian phase shifting induced by clonidine injections in Syrian hamsters

Circadian phase shifting induced by clonidine injections in Syrian hamsters

Circadian Phase Shifts to Neuropeptide YIn Vitro: Cellular Communication and Signal Transduction

Interconnections among nuclei of the subcortical visual shell: The intergeniculate leaflet is a major constituent of the hamster subcortical visual system

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