A problem of gendered injustice? Objective and subjective poverty among older women and men across European welfare regimes.

Using European Social Survey data, this article studies the prevalence of objective and subjective poverty among older women and men (60+ years) in 21 European countries. Objective poverty refers to whether one's disposable income falls below the poverty line, whereas subjective poverty relates to the capacity to make ends meet. It analyzes gender differences in these two dimensions of poverty and the role of gender as an explanation to these phenomena while controlling for other individual-level variables as well as the role of welfare state regimes. The results show that older women are more exposed to objective poverty than men, and that female gender remains strongly and positively correlated with this kind of poverty even when controlling for other variables. They also show that other individual-level variables, such as partnership, paid work and education curbs objective poverty, while the type of welfare regime does not matter. As to subjective poverty, on the other hand, there is no significant association with female gender, nor with the type of welfare regime, while individual-level variables such as subjective health, partnership and paid work are negatively correlated with this dimension of poverty. Subjective poverty is somewhat more influenced by contextual factors than objective poverty although the type of welfare state regime is not significantly associated with subjective or objective poverty.

A Cross-Sectional Study on the Associations between Economic, Social, and Political Resources and Subjective Caregiver Burden among Older Spousal Caregivers in Two Nordic Regions.

Inspired by the caregiver stress process model emphasising the role of resources for caregiving outcomes, the aim of this study was to investigate the prevalence of subjective caregiver burden (SCB) and its associations with individual social, economic, and political resources among older spousal caregivers in a Nordic regional setting. Cross-sectional survey data collected in 2016 in the Bothnia region of Finland and Sweden were used, where 674 spousal caregivers were identified and included in the analyses. The descriptive results showed that about half of the respondents experienced SCB. SCB was more common among Finnish-speaking caregivers. Results from the multivariate logistic regression analysis showed that none of the assessed political resources were significantly associated with SCB when controlling for other variables. Experiencing financial strain was associated with SCB, while personal income was not. Frequent contact with family members was statistically significantly associated with SCB. Future research could use longitudinal data to determine causal relationships, and when data allow, test the full caregiver stress process model to investigate the role of mediating factors in different comparative settings. Accumulated evidence on risk factors for negative outcomes of informal caregiving can contribute to effective screening tools for identifying and supporting vulnerable caregivers, which is becoming increasingly important with the ageing population.

Morale in Old Age and Its Association with Sociodemographic, Social, and Health-Related Factors in Different Age Groups.

Morale can be viewed as a future-oriented optimism or pessimism regarding challenges associated with aging and is closely related to subjective well-being. Promoting morale in old age could be considered to have important implications for aging well, and increased knowledge about morale in different stages of old age is needed. Hence, the aim of this study was to investigate factors associated with morale in different age groups among old people. Data were derived from a survey conducted in 2016, as a part of the Gerontological Regional Database (GERDA). The sample consisted of 9,047 individuals aged between 65 and 86 years from Ostrobothnia and Southern Ostrobothnia in Finland, and Västerbotten in Sweden. Morale was measured with the Philadelphia Geriatric Center Morale Scale (PGCMS) and regressed upon a number of sociodemographic, social, and health-related factors using linear regression analyses. The results showed that older age was an independent factor explaining lower level of morale. Additionally, the sociodemographic, social, and health-related variables could explain a large proportion of the variance in morale. Perceived loneliness, having gone through a crisis in life, poor self-rated health, and depression were associated with lower morale, and sleeping well with higher morale, in all age groups. Furthermore, the oldest age groups seem to be more exposed to several risk factors of lower morale identified in this study. Multidimensional interventions targeting especially social and mental health and the oldest-old could therefore be recommended.

Risk factors for a decrease in high morale in very old people over a 5-year period: data from two Nordic countries.

High morale could be considered to be an essential part of aging well and increased knowledge of how to prevent a decrease in high morale in very old age could have important implications for policy, and social and health care development. The objective was to identify social and health-related risk factors for a decrease in morale over 5 years in very old people among those with high morale at baseline. The study is based on data derived from the Umeå85+/GERDA study conducted in Northern Sweden and Western Finland. The final sample consisted of 174 individuals who were 85 years and older at baseline and who had completed the follow-up 5 years later. Morale was measured with The Philadelphia Geriatric Center Morale Scale (PGCMS). A set of social and health-related variables were used to test which factors were associated with a decrease in morale over 5 years. Linear regression was used for the multivariable analyses. The sample had a mean change of - 1.3 (SD = 2.5) in PGCMS scores from T1 to T2. The results from the regression analyses showed that development of depressive disorders, increased feelings of loneliness and the death of a child during the follow-up period were associated with a decrease in morale. The results from our study indicate that preventing the development of depressive disorders and increasing loneliness are key factors in preventing a decrease in high morale. Additionally, very old people who have recently lost an adult child should receive adequate psychosocial support.

Loneliness amongst older people in Europe: a comparative study of welfare regimes.

Previous research implies that the extent of welfare state regime provision plays an important indirect role in the prevalence of loneliness in later life. The aim of this study was therefore to assess the association between quality of living conditions and level of social integration indicators and the absence of loneliness in five different welfare regimes. By incorporating welfare state regimes as a proxy for societal-level features, we expanded the micro-level model of loneliness suggesting that besides individual characteristics, welfare state characteristics are also important protective factors against loneliness. The data source was from the European Social Survey round 7, 2014, from which we analysed 11,389 individuals aged 60 and over from 20 countries. The association between quality of living conditions, level of social integration variables and the absence of loneliness was analysed using multivariate logistic regression treating the welfare regime variable as a fixed effect. Our study revealed that the absence of loneliness was strongly associated with individual characteristics of older adults, including self-rated health, household size, feeling of safety, marital status, frequency of being social, as well as number of confidants. Further, the Nordic as well as Anglo-Saxon and Continental welfare regimes performed better than the Southern and Eastern regimes when it comes to the absence of loneliness. Our findings showed that different individual resources were connected to the absence of loneliness in the welfare regimes in different ways. We conclude that older people in the Nordic regime, characterised as a more socially enabling regime, are less dependent on individual resources for loneliness compared to regimes where loneliness is to a greater extent conditioned by family and other social ties.

Five-year change in morale is associated with negative life events in very old age.

OBJECTIVES: The objectives were to study changes in morale in individuals 85 years and older, and to assess the effect of negative life events on morale over a five-year follow-up period. METHOD: The present study is based on longitudinal data from the Umeå85+/GERDA-study, including individuals 85 years and older at baseline (n = 204). Morale was measured with the Philadelphia Geriatric Center Morale Scale (PGCMS). Negative life events were assessed using an index including 13 negative life events occurring during the follow-up period. Linear regression was used for the multivariate analyses. RESULTS: The majority of the sample (69.1%) had no significant changes in morale during the five-year follow-up. However, the accumulation of negative life events was significantly associated with a greater decrease in PGCMS. A higher baseline PGCMS score did not attenuate the adverse effect negative life events had on morale. CONCLUSION: Morale seemed to be mainly stable in a five-year follow-up of very old people. It seems, nonetheless, that individuals are affected by negative life events, regardless of level of morale. Preventing negative life events and supporting individuals who experience multiple negative life events could have important implications for the care of very old people.

Leisure Engagement: Medical Conditions, Mobility Difficulties, and Activity Limitations-A Later Life Perspective.

Objectives. This study aims to investigate the impact of medical conditions, mobility difficulties, and activity limitations on older people's engagement in leisure activities. Methods. The analyses are based on a cross regional survey carried out in 2010 in the Bothnia region (Northern Sweden and Western Finland). A posted questionnaire, which included questions on different aspects of leisure engagement, medical history, and health, was sent out to older persons in the region. The final sample consisted of 5435 persons aged 65, 70, 75, and 80 years. The data was analyzed by using ordinary least squares (OLS) multivariate regression. Results. The most important predictor of leisure engagement abstention among older people is the prevalence of activity limitations, whereas mobility difficulties and medical conditions play less important roles. The strong negative association between activity limitations and leisure engagement remains significant even after we control for individual, sociodemographic characteristics, and country. Discussion. This study provides a window into leisure engagement in later life and factors influencing the magnitude of engagement in leisure activities.

Social capital and self-rated health amongst older people in Western Finland and Northern Sweden: a multi-level analysis.

BACKGROUND: Social capital can be conceptualised as an individual resource residing in relationships between individuals or as a collective resource produced through interactions in neighbourhoods, communities or societies. Previous studies suggest that social capital is, in general, good for health. However, there is a shortage of studies analysing the association between individual and collective social capital in relation to health amongst older people. PURPOSE: The purpose of this study was to assess the relationship between municipal- and individual-level social capital and self-rated health amongst older people in Western Finland and Northern Sweden. METHOD: Data were retrieved from a cross-sectional postal questionnaire survey conducted in 2010. The study included, in total, 6,838 people aged 65, 70, 75 and 80 years living in the two Bothnia regions, Västerbotten, Sweden and Pohjanmaa, Finland. The association between social capital and self-rated health was tested through multi-level logistic regression analyses with ecometric tests. Social capital was measured by two survey items: interpersonal trust and social participation. RESULTS: Individual-level social capital including social participation and trust was significantly associated with self-rated health. A negative association was found between municipal-level trust and health. However, almost all variation in self-rated health resided on the individual level. CONCLUSIONS: We conclude that contextual-level social capital on a municipal level is less important for understanding the influence of social capital on health in the Bothnia region of Finland and Sweden. On the other hand, our study shows that individual-level social participation and trust have a positive and significant association with self-rated health. We suggest that other ways of defining social capital at the collective level, such as the inclusion of neighbourhood social capital, could be one direction for future research.

Social participation, interpersonal trust, and health: a study of 65- and 75-year-olds in western Finland.

AIM: To study the association between social participation, interpersonal trust, and self-rated health among 65- and 75-year-olds. METHODS: The data originates from a cross-sectional postal questionnaire survey conducted among 1577 persons aged 65 and 75 years in western Finland (response rate 67%). Logistic regression analyses were performed in order to investigate the association between social capital--in terms social participation and interpersonal trust--and health while controlling for sociodemographic variables. RESULTS: The results showed that the social participation indicator ("active membership in organisations") was positively associated with health among 75-year-olds, but not among 65-year-olds. By contrast, interpersonal trust was positively associated with health in both age groups. CONCLUSIONS: The results imply that social participation and its association with health is moderated by age, whereas interpersonal trust is not.

Glial transcripts and immune-challenged glia in the suprachiasmatic nucleus of young and aged mice.

Biological rhythms are frequently disturbed with advancing age, and aging-related changes of glia in the hypothalamic suprachiasmatic nucleus (SCN), the master circadian pacemaker, require special attention. In particular, astrocytes contribute to SCN function, and aging is associated with increased inflammatory activity in the brain, in which microglia could be especially implicated. On this basis, we investigated in the SCN of young and old mice glial transcripts and cell features, and the glial cell response to a central inflammatory challenge. Quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) was used to analyze the expression of mRNAs encoding the astrocytic glial fibrillary acidic protein and the microglial antigen CD11b. Both these transcripts, here investigated in the SCN for the first time, were significantly increased in the old SCN. Glial cell phenotyping with immunohistochemistry revealed hypertrophic and intensely stained astrocytes and microglia in the aged SCN. In both age groups, microglia were scattered throughout the SCN and astrocytes were prominent in the ventral portion, where retinal fibers are densest; in the aged SCN, astrocytes were also numerous in the dorsal portion. After intracerebroventricular injections of a mixture of interferon-gamma and tumor necrosis factor-alpha, or phosphate-buffered saline as control, immunolabeling was evaluated with stereological cell counts and confocal microscopy. Phenotypic features of astrocyte and microglia activation in response to cytokine injections were markedly enhanced in the aged SCN. Subregional variations in glial cell density were also documented in the aged compared to the young SCN. Altogether, the findings show increases in the expression of glial transcripts and hypertrophy of astrocytes and microglia in the aged SCN, as well as age-dependent variation in the responses of immune-challenged SCN glia. The data thus point out an involvement of glia in aging-related changes of the biological clock.

Clock gene expression during chronic inflammation induced by infection with Trypanosoma brucei brucei in rats.

African sleeping sickness is characterized by alterations in rhythmic functions. It is not known if the disease affects the expression of clock genes, which are the molecular basis for rhythm generation. We used a chronic rat model of experimental sleeping sickness, caused by the extracellular parasite Trypanosoma brucei brucei (Tb brucei), to study the effects on clock gene expression. In tissue explants of pituitary glands from Period1-luciferase (Per1-luc) transgenic rats infected with Tb brucei, the period of Per1-luc expression was significantly shorter. In explants containing the suprachiasmatic nuclei (SCN), the Per1-luc rhythms were flat in 21% of the tissues. We also examined the relative expression of Per1, Clock, and Bmal1 mRNA in the SCN, pineal gland, and spleen from control and infected rats using qPCR. Both Clock and Bmal1 mRNA expression was reduced in the pineal gland and spleen following Tb brucei infection. Infected rats were periodic both in core body temperature and in locomotor activity; however, early after infection, we observed a significant decline in the amplitude of the locomotor activity rhythm. In addition, both activity and body temperature rhythms exhibited decreased regularity and "robustness." In conclusion, although experimental trypanosome infection has previously been shown to cause functional disturbances in SCN neurons, only 21% of the SCN explants had disturbed Per1-luc rhythms. However, our data show that the infection overall alters molecular clock function in peripheral clocks including the pituitary gland, pineal gland, and spleen.

Regulation of cytokine signaling and T-cell recruitment in the aging mouse brain in response to central inflammatory challenge.

Aging is often accompanied by increased levels of inflammatory molecules in the organism, but age-related changes in the brain response to inflammatory challenges still require clarification. We here investigated in mice whether cytokine signaling and T-cell neuroinvasion undergo age-related changes. We first analyzed the expression of molecules involved in T-cell infiltration and cytokine signaling regulation in the septum and hippocampus of 2-3 months and 20- to 24-month-old mice at 4h after intracerebroventricular injections of tumor necrosis factor (TNF)-alpha or interferon-gammaversus saline injections. Transcripts of the chemokine CXCL9, intercellular adhesion molecule (ICAM)-1 and suppressor of cytokine signaling molecules (SOCS) 1 and 3 were increased in both age groups after cytokine injection; microglia-derived matrix metalloproteinase (MMP) 12 mRNA was induced in old mice also after control saline injections. Age-related changes in ICAM-1 protein expression and T-cell infiltration were then analyzed in mice of 3-4, 8-9 and 15-16 months at 48h after TNF-alpha injections. ICAM-1 immunoreactivity, and Western blotting in striatum, septum, hippocampus and hypothalamus showed progressive age-related enhancement of TNF-alpha-elicited ICAM-1 upregulation. Double immunofluorescence revealed ICAM-1 expression in microglia and astrocytic processes. CD3(+), CD4(+) and CD8(+) T-cells exhibited progressive age-related increases in brain parenchyma and choroid plexus after cytokine exposure. The findings indicate that the brain responses to inflammatory challenges are not only preserved with advancing age, but also include gradual amplification of ICAM-1 expression and T-cell recruitment. The data highlight molecular and cellular correlates of age-related increase of brain sensitivity to inflammatory stimuli, which could be involved in altered brain vulnerability during aging.

African trypanosome infections of the nervous system: parasite entry and effects on sleep and synaptic functions.

The extracellular parasite Trypanosoma brucei causes human African trypanosomiasis (HAT), also known as sleeping sickness. Trypanosomes are transmitted by tsetse flies and HAT occurs in foci in sub-Saharan Africa. The disease, which is invariably lethal if untreated, evolves in a first hemo-lymphatic stage, progressing to a second meningo-encephalitic stage when the parasites cross the blood-brain barrier. At first, trypanosomes are restricted to circumventricular organs and choroid plexus in the brain outside the blood-brain barrier, and to dorsal root ganglia. Later, parasites cross the blood-brain barrier at post-capillary venules, through a multi-step process similar to that of lymphocytes. Accumulation of parasites in the brain is regulated by cytokines and chemokines. Trypanosomes can alter neuronal function and the most prominent manifestation is represented by sleep alterations. These are characterized, in HAT and experimental rodent infections, by disruption of the sleep-wake 24h cycle and internal sleep structure. Trypanosome infections alter also some, but not all, other endogenous biological rhythms. A number of neural pathways and molecules may be involved in such effects. Trypanosomes secrete prostaglandins including the somnogenic PGD2, and they interact with the host's immune system to cause release of pro-inflammatory cytokines. From the sites of early localization of parasites in the brain and meninges, such molecules could affect adjacent brain areas implicated in sleep-wakefulness regulation, including the suprachiasmatic nucleus and its downstream targets, to cause the changes characteristic of the disease. This raises challenging issues on the effects of cytokines on synaptic functions potentially involved in sleep-wakefulness alterations.

Plasma levels of interferon-gamma correlate with age-related disturbances of circadian rhythms and survival in a non-human primate.

Aging can be associated with changes in circadian rhythms and reduction in adaptive immune responses accompanied by expansion of memory T cells and elevated levels of pro-inflammatory cytokines. Recent findings suggest the cytokine interferon-gamma (IFN-gamma) can affect the function of the hypothalamic suprachiasmatic nucleus (SCN), the master mammalian circadian pacemaker, both in vitro and in vivo. We studied the correlation of plasma levels of IFN-gamma and changes in circadian rhythms in a non-human primate species, the nocturnal mouse lemur (Microcebus murinus). Plasma IFN-gamma and dehydroepiandrosterone sulfate (DHEA-S), a known biomarker of aging, were determined in middle- to old-age animals by immunoenzymoassay. Daily rhythms of locomotor activity and body temperature as well as survival time of the lemurs were recorded. With aging, mean levels of DHEA-S decreased whereas IFN-gamma increased. Aged animals showed biological rhythm alterations characterized by a high percentage of diurnal activity, anticipation of the activity onset relative to lights-off, short free-running period, and delayed occurrence of minimal body temperature. The magnitude of these disturbances was correlated with the plasma level of IFN-gamma but not DHEA-S. Most remarkably, in contrast to DHEA-S, increased levels of IFN-gamma correlated with duration of the lifetime of the lemurs. These results show the degree of circadian rhythm alterations in an individual is correlated with plasma IFN-gamma level during aging, and that plasma IFN-gamma level may predict survival, at least in this non-human primate.

Rapid nitric oxide-dependent effects of tumor necrosis factor-alpha on suprachiasmatic nuclei neuronal activity.

The effect of tumor necrosis factor-alpha (TNF-alpha) on excitability and synaptic function was analyzed in slice preparations of the suprachiasmatic nuclei (SCN), the major mammalian circadian pacemaker. TNF-alpha caused a rapid increase in the spontaneous firing rate in most SCN neurons examined that was paralleled by an increase of inhibitory postsynaptic currents. The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester abolished these effects. No effect of TNF-alpha was found on miniature synaptic currents. The lack of effect on miniature synaptic currents indicates that TNF-alpha primarily affects neuronal membrane properties to cause the changes in spontaneous firing. TNF-alpha, levels of which show circadian variation in the brain and increase during inflammatory conditions and aging, may thus through nitric oxide induction modulate SCN electrical output to affect downstream circadian rhythms.

Decline of the presynaptic network, including GABAergic terminals, in the aging suprachiasmatic nucleus of the mouse.

Biological rhythms, and especially the sleep/wake cycle, are frequently disrupted during senescence. This draws attention to the study of aging-related changes in the hypothalamic suprachiasmatic nucleus (SCN), the master circadian pacemaker. The authors here compared the SCN of young and old mice, analyzing presynaptic terminals, including the gamma-aminobutyric acid (GABA)ergic network, and molecules related to the regulation of GABA, the main neurotransmitter of SCN neurons. Transcripts of the alpha3 subunit of the GABAA receptor and the GABA-synthesizing enzyme glutamic acid decarboxylase isoform 67 (GAD67) were analyzed with real-time RT-PCR and GAD67 protein with Western blotting. These parameters did not show significant changes between the 2 age groups. Presynaptic terminals were identified in confocal microscopy with synaptophysin immunofluorescence, and the GABAergic subset of those terminals was revealed by the colocalization of GAD67 and synaptophysin. Quantitative analysis of labeled synaptic endings performed in 2 SCN subregions, where retinal afferents are known to be, respectively, very dense or very sparse, revealed marked aging-related changes. In both subregions, the evaluated parameters (the number of and the area covered by presynaptic terminals and by their GABAergic subset) were significantly decreased in old versus young mice. No significant differences were found between SCN tissue samples from animals sacrificed at different times of day, in either age group. Altogether, the data point out marked reduction in the synaptic network of the aging biological clock, which also affects GABAergic terminals. Such alterations could underlie aging-related SCN dysfunction, including low-amplitude output during senescence.

Suppressors, receptors and effects of cytokines on the aging mouse biological clock.

During aging, levels of inflammatory cytokines increase and circadian rhythms are frequently altered. We here investigated neurobiological correlates of neuroinflammation and its age-related variation in the hypothalamic suprachiasmatic nucleus (SCN), the master circadian pacemaker. Day/night variations of transcripts encoding cytokine receptors and suppressors of cytokine signaling (SOCS) were correlated in groups of mice of different ages with Fos induction elicited by intracerebroventricular injections of tumor necrosis factor-alpha and interferon-gamma. Cytokine-elicited Fos induction was high at early night, when SOCS1 and SOCS3 levels were low. Such Fos induction was significantly reduced in the older SCN at early night, and paralleled by reduced expression of interferon-gamma receptor transcripts as compared to the younger SCN. In addition, Fos induction at early night exhibited marked sub-regional differences in the SCN between the age groups. The study shows that SOCS1 and SOCS3 are expressed in the biological clock with a day/night variation that may regulate SCN responsiveness to cytokine exposure, and indicates that effects of pro-inflammatory cytokines on the SCN are markedly altered during senescence.

The GABAergic network in the suprachiasmatic nucleus as a key regulator of the biological clock: does it change during senescence?

GABA is the main neurotransmitter of the hypothalamic suprachiasmatic nucleus (SCN) and plays a key role in the function of this master circadian pacemaker. Despite the evidence that disturbances of biological rhythms are common during aging, little is known about the GABAergic network in the SCN of the aging brain. We here provide a brief overview of the GABAergic structures and the role of GABA in the SCN. We also review some age-related changes of the GABAergic system occurring in the brain outside the SCN. Finally, we present preliminary data on the GABAergic system within the SCN comparing young and aging mice. In particular, our study on age-related changes in the SCN focused on the daily expression of the alpha3 subunit of the GABA(A) receptor and on the density of GABAergic axon terminals. Interestingly, our preliminary findings point to alterations of the GABAergic network in the biological clock during senescence.

The aging suprachiasmatic nucleus and cytokines: functional, molecular, and cellular changes in rodents.

The aging process brings about a switch to a low-grade chronic inflammatory condition in the periphery and brain, a condition which may prime brain cells, including those of the hypothalamic suprachiasmatic nucleus (SCN). Little information is available, however, on the responses of the SCN to neuroinflammation and immune-related challenges, and such responses have not been hitherto investigated during aging. We here provide an overview of these issues and summarize data we obtained in the study of the SCN of young and aged mice. In particular, we analyzed: i) the electrophysiological properties of the SCN core (the retino-recipient region) in tissue slices; ii) expression and day/night variation of transcripts encoding the receptors for the cytokines interferon-gamma and tumor necrosis factor-alpha, as well as the expression of transcripts encoding the proteins "suppressors of cytokine signaling" SOCS1 and SOCS3, by means of quantitative real-time polymerase chain reaction; levels of mRNAs were correlated with neuronal activation, revealed by Fos induction, elicited in the SCN by intracerebroventricular injections of a mixture of interferon-gamma and tumor necrosis factor-alpha during the daytime and nighttime; and iii) response of astrocytes and microglia in the SCN to the same paradigm of cytokine administration. Marked changes of all the above-mentioned parameters were found in the aged SCN, indicating that the circadian pacemaker is a target of the aging process. In addition, the findings indicate that neurons and glial cells of the biological clock are sensitive to inflammatory signals, and that the response to such signals is altered during senescence.

Age-related changes in electrophysiological properties of the mouse suprachiasmatic nucleus in vitro.

Endogenous biological rhythms are altered at several functional levels during aging. The major pacemaker driving biological rhythms in mammals is the suprachiasmatic nucleus of the hypothalamus. In the present study we used tissue slices from young and old mice to analyze the electrophysiological properties of the retinorecipient ventrolateral part of the suprachiasmatic nucleus. Loose patch and whole-cell recordings were performed during day and night. Both young and old mice displayed a significant variation between day and night in the mean firing rate of suprachiasmatic nucleus neurons. The proportion of cells not firing spontaneous action potentials showed a clear day/night rhythm in young but not in old animals, that had an elevated number of such silent cells during the day compared to young animals. Analysis of firing patterns revealed a more regular spontaneous firing during the day than during the night in the old mice, while there was no difference between day and night in young animals. The frequency of spontaneous inhibitory postsynaptic currents was reduced in ventrolateral suprachiasmatic nucleus neurons in the old animals. Since the inhibitory input to these neurons is mainly derived from within the suprachiasmatic nucleus, this reduction most likely reflects the greater proportion of silent cells found in old animals. The results show that the suprachiasmatic nucleus of old mice is subject to marked electrophysiological changes, which may contribute to physiological and behavioral changes associated with aging.