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Neuropeptide Y-deficient mice show altered circadian response to simulated natural photoperiod.

ABSTRACT: Circadian rhythms, endogenously generated by the suprachiasmatic nucleus (SCN), can be synchronized to a variety of photic and non-photic environmental stimuli. Neuropeptide Y (NPY) is produced in the intergeniculate leaflet (IGL) and known to mediate both photic and non-photic influences on the SCN. We recently found that npy-/- mice were slower to shift their locomotor activity onset to the new time of light offset when photoperiod was abruptly changed from light/dark (LD) cycle 18:6 to LD 6:18. In the present study, we measured the locomotor response of npy-/- mice to gradual changes in photoperiod (4 min a day) for 141 days (LD 16:8 changing to LD 8:16), mimicking external LD cycles in nature. When the photoperiod approached LD 8:16, npy-/- mice showed a significantly delayed onset of activity compared to wild-type mice. Activity patterns disintegrated into multiple bouts and intensity of activity decreased as the photoperiod changed and these changes were more pronounced in npy-/- mice. Our results lend further support to the idea that NPY is involved in circadian entrainment responses to seasonal photoperiod changes.

SUBMITTER: Kim HJ

PROVIDER: S-EPMC2673519 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature

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Neuropeptide Y-deficient mice show altered circadian response to simulated natural photoperiod.

Kim Hyun Jung HJ Harrington Mary E ME

Brain research 20080924

Circadian rhythms, endogenously generated by the suprachiasmatic nucleus (SCN), can be synchronized to a variety of photic and non-photic environmental stimuli. Neuropeptide Y (NPY) is produced in the intergeniculate leaflet (IGL) and known to mediate both photic and non-photic influences on the SCN. We recently found that npy-/- mice were slower to shift their locomotor activity onset to the new time of light offset when photoperiod was abruptly changed from light/dark (LD) cycle 18:6 to LD 6:1 ...[more]

PMID: 18926801

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Project description:Epilepsy is a neurological disease that is caused by abnormal hypersynchronous activities of neuronal ensembles leading to recurrent and spontaneous seizures in human patients. Enhanced neuronal excitability and a high level of synchrony between neurons seem to trigger these spontaneous seizures. The molecular mechanisms, however, regarding the development of neuronal hyperexcitability and maintenance of epilepsy are still poorly understood. Here, we show that pumilio RNA-binding family member 2 (Pumilio2; Pum2) plays a role in the regulation of excitability in hippocampal neurons of weaned and 5-month-old male mice. Almost complete deficiency of Pum2 in adult Pum2 gene-trap mice (Pum2 GT) causes misregulation of genes involved in neuronal excitability control. Interestingly, this finding is accompanied by the development of spontaneous epileptic seizures in Pum2 GT mice. Furthermore, we detect an age-dependent increase in Scn1a (Nav1.1) and Scn8a (Nav1.6) mRNA levels together with a decrease in Scn2a (Nav1.2) transcript levels in weaned Pum2 GT that is absent in older mice. Moreover, field recordings of CA1 pyramidal neurons show a tendency towards a reduced paired-pulse inhibition after stimulation of the Schaffer-collateral-commissural pathway in Pum2 GT mice, indicating a predisposition to the development of spontaneous seizures at later stages. With the onset of spontaneous seizures at the age of 5?months, we detect increased protein levels of Nav1.1 and Nav1.2 as well as decreased protein levels of Nav1.6 in those mice. In addition, GABA receptor subunit alpha-2 (Gabra2) mRNA levels are increased in weaned and adult mice. Furthermore, we observe an enhanced GABRA2 protein level in the dendritic field of the CA1 subregion in the Pum2 GT hippocampus. We conclude that altered expression levels of known epileptic risk factors such as Nav1.1, Nav1.2, Nav1.6 and GABRA2 result in enhanced seizure susceptibility and manifestation of epilepsy in the hippocampus. Thus, our results argue for a role of Pum2 in epileptogenesis and the maintenance of epilepsy.

Dataset Information

Neuropeptide Y-deficient mice show altered circadian response to simulated natural photoperiod.

Publications

Neuropeptide Y-deficient mice show altered circadian response to simulated natural photoperiod.

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