Circadian Rhythms in Neurotransmitter Receptors in Discrete Rat Brain Regions

Abstract

Circadian rhythms were measured in alpha 1-, alpha 2- and beta-adrenergic, acetylcholine muscarinic (ACh), and benzodiazepine (BDZ) receptor binding in small regions of rat brain. Rhythms in alpha 1-receptor binding were measured in olfactory bulb, frontal, cingulate, piriform, parietal, temporal and occipital cortex, hypothalamus, hippocampus, pons-medulla, caudate-putamen and thalamus-septum. No rhythm was found in cerebellum. Rhythms in alpha 2-receptor binding were measured in frontal, parietal and temporal cortex, and pons-medulla. No rhythm was found in cingulate, piriform or occipital cortex, or hypothalamus. Rhythms in binding to beta-receptors were measured in olfactory bulb, piriform, insular, parietal and temporal cortex, hypothalamus and cerebellum. No rhythms were found in frontal, entorhinal, cingulate, or occipital cortex, hippocampus, caudate-putamen, or pons-medulla. Rhythms in ACh receptor binding were measured in olfactory bulb, parietal cortex and caudate-putamen. No rhythms were found in frontal or occipital cortex, nucleus accumbens, hippocampus, thalamus-septum, pons-medulla or cerebellum. Rhythms in BDZ receptor binding were measured in olfactory bulb, olfactory and occipital cortex, olfactory tubercle, nucleus accumbens, amygdala, caudate-putamen, hippocampus and cerebellum. No rhythms were found in parietal cortex, pons-medulla or thalamus-septum. The 24-hr mean binding to receptors varied between 3- and 10-fold, the highest in cortex and the lowest, usually, in cerebellum. The piriform cortex was particularly high in alpha 1- and alpha 2-adrenergic receptors; the nucleus accumbens and caudate, in ACh receptors; and the amygdala, in BDZ receptors. Most adrenergic and ACh receptor rhythms peaked in subjective night (the period when lights were off under L:D conditions), whereas most BDZ receptor rhythms peaked in subjective day (the time lights were on in L:D). Perhaps in the rat, a nocturnal animal, the adrenergic and ACh receptors mediate activity and the functions that accompany it, and the BDZ receptors mediate rest, and with it, sleep.

Circadian genes, rhythms and the biology of mood disorders

“…Indeed some of the major neurotransmitters that have been implicated in mood regulation, including serotonin, norepinephrine and dopamine, have a circadian rhythm in their levels, release, and synthesis-related enzymes (Weiner et al, 1992;Shieh et al, 1997;Aston-Jones et al, 2001;Barassin et al, 2002;Khaldy et al, 2002;Castaneda et al, 2004;Weber et al, 2004;Malek et al, 2005). There are also circadian rhythms in the expression and activity of several of the receptors that bind these neurotransmitters, suggesting that these entire circuits are under circadian control (Kafka et al, 1983;Wesemann and Weiner, 1990;Witte and Lemmer, 1991;Coon et al, 1997;Akhisaroglu et al, 2005). It seems likely that disruptions in the normal rhythms in these circuits (either continuous or abrupt) could have major effects on mood and motivational states.…”

Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence

“…While spontaneous activity has often been associated with the mesolimbic dopaminergic system, an examination of circadian changes has indicated that dark-phase increases in several indices of CS function including dopamine receptors (36), content (37), turnover (38) and in vitro release (39) are associated with dark-phase increases in behavioral activity (38,40). Moreover, a significant correlation between striatal dopamine and spontaneous motor activity in both male and female rats has been reported (41) and there is also a strong positive correlption between in vivo striatal dopamine output as Dopamine release/locomotor behavior-intact vs castrate rats determined by detection of the dopamine metabolite, homovanillac acid (42,43), and dopamine biosynthesis (44) with circadian changes in spontaneous behavioral activity.…”

Coactivation of M1Muscarinic and α1 Adrenergic Receptors Stimulates Extracellular Signal-Regulated Protein Kinase and Induces Long-Term Depression at CA3–CA1 Synapses in Rat Hippocampus

“…Interestingly, hippocampal ACh and NE levels can vary in vivo, so that combined activation of G␣q-coupled signaling may be important physiologically to allow induction of plasticity even when ACh and/or NE are present at low levels. For example, ACh and NE levels fluctuate across the sleep-wake cycle, as hippocampal function alternates between memory encoding during wakefulness and consolidation during sleep (Hobson et al, 1975;Kafka et al, 1986;Aston-Jones et al, 1991;Hasselmo, 1999). Cholinergic and/or noradrenergic signaling can also be reduced in hippocampus during aging and neurodegenerative diseases (Carlsson et al, 1980;Tomlinson et al, 1981;Collerton, 1986;Springer et al, 1987;Bickford-Wimer et al, 1988;ChanPalay and Asan, 1989;German et al, 1992;Kasa et al, 1997).…”