About

Gene Block is a Distinguished Professor at UCLA, with a background in psychology. He earned his B.A. in Psychology from Stanford University in 1970, followed by an M.S. in Psychology from the University of Oregon in 1972, and a Ph.D. in Psychology from the University of Oregon in 1975. His research focus and key contributions are not detailed on the page, but his academic background indicates a strong foundation in psychological sciences.

Research topics

• Medicine
• Political Science
• Psychiatry
• Internal medicine
• Endocrinology
• Computer Science
• Business
• Geography
• Biology
• Psychology
• Economics
• Public relations
• Economic growth
• Neuroscience

Selected publications

• Bright Days Buffer Nighttime Light: Daytime Illumination Shapes Sex Differences in Sleep and Circadian Regulation

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-26

  articleOpen access

  Summary Sex differences in sleep and wakefulness are well documented in humans but remain inconsistent in rodent studies, suggesting strong sensitivity to experimental context. In prior work, we observed no sex differences in sleep-wake architecture under relatively bright daytime light, raising the possibility that daytime illumination is a critical but underappreciated variable shaping sex-dependent sleep regulation. Here, we tested the hypothesis that daytime light intensity modulates sex differences in sleep-wake architecture and vulnerability to dim light at night (DLaN). Male and female C57BL/6J mice were exposed to acute (one night) or chronic (two weeks) DLaN (10 lux) under three daytime light intensities (50, 100, 300 lux). Sleep was assessed using electroencephalographic-based measures of vigilance states and slow wave activity (SWA). Dim daytime light (50 lux) unmasked robust sex differences in dark-phase sleep-wake architecture that were absent under brighter daytime light (300 lux). Acute DLaN reduced early-night wakefulness in both sexes under low daytime light but had minimal effect under bright daytime conditions. Following chronic DLaN, males exhibited reduced dim light-phase wakefulness and dampened rhythm amplitude, whereas females showed pronounced phase shifts, rhythm attenuation, and altered timing of SWA under 50 and 100 lux. These changes were largely prevented under bright daytime light. Together, these findings identify daytime light intensity as a critical contextual factor governing sex-specific regulation of sleep and vulnerability to nighttime light, providing a unifying framework to reconcile inconsistencies in the rodent sleep literature. Highlights Daytime light intensity shapes sex differences in sleep–wake architecture Acute and chronic nighttime light elicit distinct sex-specific sleep responses Females exhibit greater circadian and slow-wave vulnerability to nighttime light Brighter daytime light buffers sleep and circadian disruption

  PublisherDOI

• Dissociating the Effects of Light at Night from Circadian Misalignment in a Neurodevelopmental Disorder Mouse Model Using Ultradian Light-Dark Cycles.

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-05

  preprintOpen access

  Individuals with neurodevelopmental disorders (NDDs) often experience sleep disturbances and are frequently exposed to light during nighttime hours. Our previous studies using the Cntnap2 knockout (KO) mouse model of NDDs demonstrated that nighttime light exposure increases behaviors such as excessive grooming, reduces social interactions, and disrupts daily locomotor rhythms. To further evaluate the effects of nighttime light exposure, we exposed wild-type (WT) and Cntnap2 KO mice to an ultradian lighting cycle (T7), which alternates 3.5 hours of light and 3.5 hours of darkness. Circadian rhythms in activity, corticosterone levels, and clock gene expression are maintained under T7 lighting despite the presence of light during the usual night phase, whilst animals display increased depressive-like behaviors and reduce performance on the novel object recognition test. Based on these observations, we hypothesized that T7 lighting would mimic the impact of nighttime light exposure seen in standard light-dark cycles with dim light at night (DLaN). However, in this study, adult WT and Cntnap2 KO mice held under the T7 cycle did not show the increased grooming behavior or reduced social interaction observed in Cntnap2 KO mice exposed to DLaN. Regarding locomotor activity rhythms, the T7 cycle lengthened the circadian period and weakened the rhythm amplitude but did not abolish rhythmicity in either genotype. Finally, opposite to DLaN, neither the T7 cycle nor constant darkness (DD) elicited an increase in cFos expression in the basolateral amygdala in WT and KO mice. These results demonstrate that the adverse behavioral and neurobiological effects of nighttime light exposure in a model of a neurodevelopmental disorder depend on circadian disruption rather than light exposure alone, highlighting the importance of circadian stability as a protective factor in NDDS.

  PublisherOA PDFDOI

• Dissociating the Effects of Light at Night from Circadian Misalignment in a Neurodevelopmental Disorder Mouse Model Using Ultradian Light–Dark Cycles

  Clocks & Sleep · 2025-09-15 · 1 citations

  articleOpen access

  Individuals with neurodevelopmental disorders (NDDs) often experience sleep disturbances and are frequently exposed to light during nighttime hours. Our previous studies using the Contactin-associated protein-like 2 (Cntnap2) knockout (KO) mouse model of NDDs demonstrated that nighttime light exposure adversely affected behavioral measures. In this study, we exposed wild-type (WT) and Cntnap2 KO mice to an ultradian lighting cycle (T7), which alternates 3.5 h of light and 3.5 h of darkness, hypothesizing that this lighting protocol would mimic the impact of nighttime light exposure seen in standard light–dark cycles with dim light at night (DLaN). However, adult WT and Cntnap2 KO mice held under the T7 cycle did not show the increased grooming behavior or reduced social interaction observed in Cntnap2 KO mice exposed to DLaN. The T7 cycle lengthened the circadian period and weakened the rhythm amplitude without abolishing rhythmicity in either genotype. Finally, opposite to DLaN, neither the T7 cycle nor constant darkness (DD) elicited an increase in cFos expression in the basolateral amygdala. These results demonstrate that the adverse effects of nighttime light exposure in an NDD model depend on the extent of the circadian disruption rather than light exposure alone, emphasizing the importance of circadian stability as a protective factor in NDDs.

  PublisherOA PDFDOI

• Dim light at night disrupts the sleep-wake cycle and exacerbates abnormal EEG activity in Cntnap2 knockout mice: implications for autism spectrum disorders

  Molecular Autism · 2025-12-18 · 3 citations

  articleOpen access

  Epilepsy is a common comorbidity in individuals with autism spectrum disorders (ASDs). Many patients with epilepsy as well as ASD experience disruptions in their sleep-wake cycle and daily fluctuations in symptom severity. Chronic exposure to light at nighttime can disrupt sleep and circadian rhythms. Contactin associated protein-like 2 knockout (Cntnap2 KO) mice, a model of ASD and epilepsy, exhibit sleep and circadian disturbances and abnormal events in the electroencephalogram (EEG). Here, we investigated how chronic dim light at night (DLaN) exposure affects sleep architecture, EEG power spectra, and abnormal EEG events in Cntnap2 KO and wildtype (WT) mice. Male and female Cntnap2 KO and WT mice were exposed to DLaN (5 lx) for 6 weeks. EEG recordings were collected and analyzed to assess sleep architecture, spectral power, and abnormal EEG events. A two-way repeated-measures analysis of variance (ANOVA) was used to evaluate the effects of DLaN across time and EEG frequencies, followed by Bonferroni-corrected post hoc tests where appropriate. DLaN exposure delayed wake onset and disrupted sleep patterns in a sex-dependent manner, with females being more affected. DLaN significantly increased slow-wave activity (SWA, 0.5–4 Hz) in both WT and KO mice, consistent with increased sleep pressure. Notably, DLaN markedly elevated the frequency of abnormal hypersynchronized EEG events in Cntnap2 KO mice and even induced such events in WT mice. Spectral analysis of abnormal EEG events revealed elevated theta power, suggesting hippocampal involvement. Chronic DLaN exposure disrupts sleep architecture in a sex-dependent fashion and increases the occurrence of abnormal EEG events in Cntnap2 KO mice. These findings highlight the potential risks of nighttime light exposure for individuals with ASD and epilepsy, underscoring the importance of managing light environments to improve sleep quality and neurological health.

  PublisherOA PDFDOI

• Dim Light at Night Disrupts the Sleep-Wake Cycle and Exacerbates Seizure Activity in <i>Cntnap2</i> Knockout Mice: Implications for Autism Spectrum Disorders

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-24 · 1 citations

  preprintOpen access

  Abstract Epilepsy is one of the most common comorbidities in individuals with autism spectrum disorders (ASDs). Many patients with epilepsy as well as ASD experience disruptions in their sleep-wake cycle and exhibit daily rhythms in expression of symptoms. Chronic exposure to light at nighttime can disrupt sleep and circadian rhythms. Contactin associated protein-like 2 knockout ( Cntnap2 KO) mice, a model for autism spectrum disorder (ASD) and epilepsy, exhibit sleep and circadian disturbances and seizure-like events. This study examines how chronic dim light at night (DLaN) exposure affects sleep architecture, EEG power spectra, and seizure activity in Cntnap2 KO and wildtype (WT) mice. Using electroencephalography (EEG) recordings, male and female Cntnap2 KO and WT mice were exposed to DLaN (5 lux) for 2 or 6 weeks. EEG recordings were analyzed to assess sleep architecture, power spectrum, and seizure-like events. DLaN exposure delays the wake onset and disrupts sleep patterns in a sex-dependent manner, with females being more affected. DLaN significantly increased slow-wave activity (SWA, 0.5–4 Hz) in both WT and KO mice, indicating increased sleep pressure. Finally, we found that DLaN dramatically increased the frequency of seizure-like events in the Cntnap2 KO mice and even increased the occurrence rate in the WT mice. Spectral analysis of seizure-like events revealed increased theta power, suggesting the involvement of hippocampus. Chronic DLaN exposure disrupts sleep and increases seizure-like events in Cntnap2 KO mice, with sex-specific differences. These findings emphasize the potential risks of nighttime light exposure for individuals with ASD and epilepsy, reinforcing the need to manage light exposure to improve sleep quality and reduce seizure risk.

  PublisherOA PDFDOI

• Pittendrigh Remembered

  Journal of Biological Rhythms · 2023-02-07 · 1 citations

  editorial1st author
  PublisherDOI

• Long wavelength light reduces the negative consequences of dim light at night in the <i>Cntnap2</i> mouse model of autism

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-06-12

  preprintOpen access

  Abstract Many patients with autism spectrum disorders (ASD) show disturbances in their sleep/wake cycles, and may be particularly vulnerable to the impact of circadian disruptors. We have previously shown that exposure to dim light at night (DLaN) in contactin associated protein-like 2 knock out ( Cntnap2 KO) mice disrupts diurnal rhythms, increases repetitive behaviors while reducing social interactions. These negative effects of DLaN may be mediated by intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing the photopigment melanopsin, which is maximally sensitive to blue light (480nm). In this study, we used a light-emitting diode (LED) array that enabled us to shift the spectral properties of the DLaN while keeping the intensity at 10 lx. First, using wild-type (WT) mice, we confirmed that the short-wavelength enriched lighting produced strong acute suppression of locomotor activity (masking), robust light-induced phase shifts, and c-Fos expression in the suprachiasmatic nucleus, while the long-wavelength enriched lighting evoked much weaker responses. Furthermore, exposure of WT mice to the short-wavelength light at night reduced the amplitude of locomotor activity rhythms and impaired social interactions. Mice lacking the melanopsin expressing ipRGCs ( Opn4 DTA mice) were resistant to these negative effects of DLaN. Importantly, the shift of the DLaN stimulus to longer wavelengths ameliorated the negative impact on the activity rhythms and autistic behaviors (i.e. reciprocal social interactions, repetitive grooming) of the Cntnap2 KO model. The short-, but not the long-wavelength enriched, DLaN triggered cFos expression in the peri-habenula region as well as in the basolateral amygdala (BLA). Finally, DLaN-driven c-Fos induction in BLA glutamatergic neurons was about 3-fold higher in the Cntnap2 KO mice, suggesting that these cells may be particularly vulnerable to the effects of photic disruption. Broadly, our findings suggest that the spectral properties of light at night should be considered in the management of ASD and other neurodevelopmental disorders.

  PublisherOA PDFDOI

• Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease

  Frontiers in Nutrition · 2022 · 18 citations

  • Medicine
  • Endocrinology
  • Internal medicine

  Disturbances in sleep/wake cycles are common among patients with neurodegenerative diseases including Huntington's disease (HD) and represent an appealing target for chrono-nutrition-based interventions. In the present work, we sought to determine whether a low-carbohydrate, high-fat diet would ameliorate the symptoms and delay disease progression in the BACHD mouse model of HD. Adult WT and BACHD male mice were fed a normal or a ketogenic diet (KD) for 3 months. The KD evoked a robust rhythm in serum levels of β-hydroxybutyrate and dramatic changes in the microbiome of male WT and BACHD mice. NanoString analysis revealed transcriptional changes driven by the KD in the striatum of both WT and BACHD mice. Disturbances in sleep/wake cycles have been reported in mouse models of HD and are common among HD patients. Having established that the KD had effects on both the WT and mutant mice, we examined its impact on sleep/wake cycles. KD increased daytime sleep and improved the timing of sleep onset, while other sleep parameters were not altered. In addition, KD improved activity rhythms, including rhythmic power, and reduced inappropriate daytime activity and onset variability. Importantly, KD improved motor performance on the rotarod and challenging beam tests. It is worth emphasizing that HD is a genetically caused disease with no known cure. Life-style changes that not only improve the quality of life but also delay disease progression for HD patients are greatly needed. Our study demonstrates the therapeutic potential of diet-based treatment strategies in a pre-clinical model of HD.

  PublisherDOI

• Long wavelength light reduces the negative consequences of dim light at night

  Neurobiology of Disease · 2022-12-06 · 14 citations

  articleOpen access

  Many patients with autism spectrum disorders (ASD) show disturbances in their sleep/wake cycles, and they may be particularly vulnerable to the impact of circadian disruptors. We have previously shown that a 2-weeks exposure to dim light at night (DLaN) disrupts diurnal rhythms, increases repetitive behaviors and reduces social interactions in contactin-associated protein-like 2 knock out (Cntnap2 KO) mice. The deleterious effects of DLaN may be mediated by intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing the photopigment melanopsin, which is maximally sensitive to blue light (480 nm). In this study, the usage of a light-emitting diode array enabled us to shift the spectral properties of the DLaN while keeping the intensity of the illumination at 10 lx. First, we confirmed that the short-wavelength enriched lighting produced strong acute suppression of locomotor activity (masking), robust light-induced phase shifts, and cFos expression in the suprachiasmatic nucleus in wild-type (WT) mice, while the long-wavelength enriched lighting evoked much weaker responses. Opn4DTA mice, lacking the melanopsin expressing ipRGCs, were resistant to DLaN effects. Importantly, shifting the DLaN stimulus to longer wavelengths mitigated the negative impact on the activity rhythms and ‘autistic’ behaviors (i.e. reciprocal social interactions, repetitive grooming) in the Cntnap2 KO as well as in WT mice. The short-, but not the long-wavelength enriched, DLaN triggered cFos expression in in the basolateral amygdala (BLA) as well as in the peri-habenula region raising that possibility that these cell populations may mediate the effects. Broadly, our findings are consistent with the recommendation that spectral properties of light at night should be considered to optimize health in neurotypical as well as vulnerable populations.

  PublisherDOI

• Chronic methamphetamine uncovers a circadian rhythm in multiple-unit neural activity in the dorsal striatum which is independent of the suprachiasmatic nucleus

  Neurobiology of Sleep and Circadian Rhythms · 2021-06-25 · 9 citations

  articleOpen access

  The dorsal striatum forms part of the basal ganglia circuit that is a major regulator of voluntary motor behavior. Dysfunction in this circuit is a critical factor in the pathology of neurological (Parkinson's and Huntington's disease) as well as psychiatric disorders. In this study, we employed in vivo real-time monitoring of multiple unit neural activity (MUA) in the dorsal striatum of freely moving mice. We demonstrate that the striatum exhibits robust diurnal and circadian rhythms in MUA that peak in the night. These rhythms are dependent upon the central circadian clock located in the suprachiasmatic nucleus (SCN) as lesions of this structure caused the loss of rhythmicity measured in the striatum. Nonetheless, chronic treatment of methamphetamine (METH) makes circadian rhythms appear in MUA recorded from the striatum of SCN-lesioned mice. These data demonstrate that the physiological properties of neurons in the dorsal striatum are regulated by the circadian system and that METH drives circadian rhythms in striatal physiology in the absence of the SCN. The finding of SCN-driven circadian rhythms in striatal physiology has important implications for an understanding of the temporal regulation of motor control as well as revealing how disease processes may disrupt this regulation.

  PublisherDOI

Recent grants

• NIH Grant R01NS055361

  NIH · $883k · 2010

• NIH Grant R01NS015264

  NIH · $3.2M · 2002

• NIH Grant R01MH062517

  NIH · $805k · 2004

• NIH Grant R01HL071510

  NIH · $642k · 2006

Frequent coauthors

• Shin Yamazaki

  The University of Texas Southwestern Medical Center

  49 shared

• Michael Menaker

  University of Virginia

  47 shared

• Christopher S. Colwell

  University of California, Los Angeles

  46 shared

• Erik D. Herzog

  36 shared

• Hajime Tei

  Kanazawa University

  32 shared

• Takahiro J. Nakamura

  Meiji University

  27 shared

• Stephan Michel

  Leiden University Medical Center

  27 shared

• Yoshiyuki Sakaki

  24 shared

Education

• Ph.D., Molecular, Cellular, and Developmental Biology

  University of California, Los Angeles

  1984

• M.S., Molecular, Cellular, and Developmental Biology

  University of California, Los Angeles

  1981

• B.S., Molecular, Cellular, and Developmental Biology

  University of California, Los Angeles

  1978