No abstract

Inbred strains have been used to study genetic and physiological relationships among different aspects of circadian timekeeping, as well as relationships between circadian rhythmicity and other strain-specific traits. The present study characterized several features of circadian timekeeping in genetically hyperactive (WKHA) and genetically hypertensive (WKHT) inbred strains, derived from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. WKHAs and WKHTs differed in free-running period, steady-state entrainment to light-dark cycles, and photic phase shifting, and relationships among these measures were consistent with previous studies of species, strain, and individual differences. Because both WKHTs and SHRs show short circadian periods relative to their respective comparison strains, this trait may cosegregate genetically with hypertension. In contrast, because WKHAs and SHRs show similar photic entrainment and phase shifting, these circadian functions may cosegregate with open-field hyperactivity. Finally, because neither WKHAs nor WKHTs show the SHR's excessive levels of home-cage running wheel activity, this trait is not related to either hypertension or open-field activity. Further work would be required to elucidate specific genetic and/or physiological linkages among these variables.

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.

No abstract

Stimuli that evoke behavioral activation can phase-shift free-running circadian activity rhythms in Syrian hamsters. Activation-induced phase shifting is characterized by a phase-response curve (PRC) that is dissimilar to the PRC for photic phase shifting, and recent studies indicate that complex interactions may occur between photic and non-photic phase shifting. Since animals in the laboratory may be exposed to both photic and behaviorally activating stimulation during routine cage maintenance procedures, we performed a retrospective analysis of possible phase shifts associated with cage cleaning in individually housed hamsters maintained in either constant darkness (DD) or dim red light (RR) during the course of an ongoing study of drug-induced phase shifting. All cage cleanings were conducted under RR and were separated from drug treatments by at least one week. The results indicated that both photic and non-photic phase shifts could be induced by routine cage maintenance procedures, depending on the circadian timing of the procedure, on lighting conditions, and on the degree of evoked activity.