Expression of alpha 2 adrenoceptors during rat brain development – I. Alpha 2A messenger RNA expression
ABSTRACT The distribution of alpha 2A adrenoceptor messenger RNA expression in developing rat brain was characterized using in situ hybridization with 35S-labeled riboprobes. Intense hybridization signal was detected as early as embryonic day 14 in several areas adjacent to the forebrain and hindbrain germinal zones and in central noradrenergic neurons. A marked increase in messenger RNA expression was observed throughout the brain during late prenatal development, consistent with the migration and maturation of neurons in developing brain structures. In embryonic brain, there was a temporal and spatial correspondence in the appearance of alpha 2A messenger RNA expression and binding sites labeled with [3H]idazoxan or p-[125I]iodoclonidine, indicating translation into receptor protein at an early stage of development. Whereas the presynaptic expression remained constant throughout development, there was an early postnatal decline of alpha 2A receptor expression in many brain regions, including the olfactory bulb, cortex, caudate-putamen, hippocampus, thalamus, hypothalamus and medulla. Thereafter, messenger RNA expression increased, establishing an adult-like pattern during the second postnatal week, but remained low in areas such as the caudate-putamen, thalamus and hippocampus, which do not exhibit extensive expression in the adult. The transient perinatal expression of this alpha 2 adrenoceptor type, which coincides with a period of hyperreactivity to sensory stimuli in the locus coeruleus, may indicate a specific functional role for the alpha 2A receptor in the developing rat brain. The early and intense expression in olfactory structures suggests an involvement in early olfactory learning. The pattern of widespread, transient expression of alpha 2A receptors in the fetal brain is in marked contrast to the postnatal development of the alpha 2C receptor type.
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- "Although LC fibers project differentially into the different layers of the bulb, adrenoceptors are expressed in all layers of the bulb. Both MCs and granule cells express a-adrenoceptors , including a 1 and a 2 subtypes (Day et al., 1997; Hayar et al., 2001; McCune et al., 1993; Nai et al., 2010; Pieribone et al., 1994; Winzer-Serhan and Leslie, 1999; Winzer-Serhan et al., 1997a,b). Both b 1 -and b 2 -adrenoceptors have also been reported, using radioautographic techniques, in the granule cell, internal plexiform, and glomerular layers, with only b 2 -adrenoceptors occurring in the external plexiform layer (Woo and Leon, 1995). "
ABSTRACT: Early odor preference training in rat pups produces behavioral preferences that last from hours to lifetimes. Here, we discuss the molecular and circuitry changes we have observed in the olfactory bulb (OB) and in the anterior piriform cortex (aPC) following odor training. For normal preference learning, both structures are necessary, but learned behavior can be initiated by initiating local circuit change in either structure. Our evidence relates dynamic molecular and circuit changes to memory duration and storage localization. Results using this developmental model are consistent with biological memory theories implicating N-methyl-D-aspartate (NMDA) receptors and β-adrenoceptors, and their associated cascades, in memory induction and consolidation. Finally, our examination of the odor preference model reveals a primary role for increases in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor synaptic strength, and in network strength, in the creation and maintenance of preference memory in both olfactory structures.Progress in brain research 01/2014; 208:115-56. DOI:10.1016/B978-0-444-63350-7.00005-X · 5.10 Impact Factor
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- "Most of the available electrophysiological data concerning the NA effect in different cell types of the olfactory bulb are limited to the granule and mitral cell layer. As for the glomerular layer, despite the fact that all NA receptor types have been localized in this region –, no data concerning possible modulation roles of NA inputs are available. Our observation, therefore, would be the first reporting an NA action in a specific subpopulation of glomerular cells, and is well in line with the general effect of NA: dopamine released by glomerular dopaminergic cells is known to inhibit glutamate release from olfactory nerve terminals . "
ABSTRACT: The properties of the hyperpolarization-activated cation current (I h) were investigated in rat periglomerular dopaminergic neurons using patch-clamp recordings in thin slices. A reliable identification of single dopaminergic neurons was made possible by use of a transgenic line of mice expressing eGFP under the tyrosine hydroxylase promoter. At 37 uC and minimizing the disturbance of the intracellular milieu with perforated patches, this current shows a midpoint of activation around 282.7 mV, with a significant level of opening already at rest, thereby giving a substantial contribution to the resting potential, and ultimately playing a relevant function in the control of the cell excitability. The blockage of I h has a profound influence on the spontaneous firing of these neurons, which result as strongly depressed. However the effect is not due to a direct role of the current in the pacemaker process, but to the I h influence on the resting membrane potential. I h kinetics is sensitive to the intracellular levels of cAMP, whose increase promotes a shift of the activation curve towards more positive potentials. The direct application of DA and 5-HT neurotransmitters, physiologically released onto bulbar dopaminergic neurons and known to act on metabotropic receptors coupled to the cAMP pathway, do not modifythe I h amplitude. On the contrary, noradrenaline almost halves the I h amplitude. Our data indicate that the HCN channels do not participate directly to the pacemaker activity of periglomerular dopaminergic neurons, but influence their resting membrane potential by controlling the excitability profile of these cells, and possibly affecting the processing of sensory information taking place at the entry of the bulbar circuitry. Citation: Pignatelli A, Borin M, Fogli Iseppe A, Gambardella C, Belluzzi O (2013) The h-Current in Periglomerular Dopaminergic Neurons of the Mouse Olfactory Bulb. PLoS ONE 8(2): e56571. doi:10.1371/journal.pone.0056571PLoS ONE 02/2013; 8(2):e56571. DOI:10.1371/journal.pone.0056571 · 3.23 Impact Factor
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- "Our physiological findings are consistent with the expression of both α1 and α2 receptors in the GCL, including GCs (Young and Kuhar 1979, 1980; Jones et al. 1985; McCune et al. 1993; Pieribone et al. 1994; Talley et al. 1996; Day et al. 1997; Domyancic and Morilak 1997; Winzer-Serhan et al. 1997a,b). Responses of single GCs to both PE and Clon suggest that some GCs express both α1 and α2 receptor subtypes as observed for brainstem neurons (Grudt et al., 1995; Fukada et al., 1987; Vaughn et al., 1996). "
ABSTRACT: The mammalian main olfactory bulb (MOB) receives a dense noradrenergic innervation from the pontine nucleus locus coeruleus that is important for neonatal odor preference learning and odor processing in mature animals. Modulation of GABAergic granule cells (GCs) is thought to play a key role in the net functional impact of norepinephrine (NE) release in the MOB, yet there are few direct studies of the influence of NE on these cells. In the present study we investigated noradrenergic modulation of GC excitability using electrophysiological approaches in rat MOB slices. A moderate concentration of NE (10 microM) and the alpha1 receptor agonist phenylephrine (10 microM) depolarized and increased spontaneous or current injection-evoked spiking in GCs. By contrast, low NE concentrations (0.1-1.0 microM) or the alpha2 receptor agonist clonidine (Clon, 10 microM) hyperpolarized and decreased the discharge of GCs. The effects of NE (10 microM) were blocked by antagonism of alpha1 and alpha2 receptors. Inhibitory effects of low NE concentrations were blocked or converted to excitatory responses by alpha2 receptor blockade, whereas excitatory effects of the moderate NE concentration were converted to inhibitory responses after alpha1 receptor blockade. NE (10 microM) and phenylephrine elicited inward currents that reversed near the potassium equilibrium potential. The effects of NE and phenylephrine were associated with increased membrane input resistance. Clonidine elicited an outward current associated with decreased membrane input resistance that reversed near the potassium equilibrium potential. These results indicate that alpha1 and alpha2 receptor activation exert opposing effects on GC excitability. Low concentrations of NE acting via alpha2 receptors suppress GC excitability, while higher concentrations of NE acting at alpha1 receptors increase GC excitability. These findings are consistent with recent findings that alpha1 and alpha2 receptor activation increase and decrease, respectively, GABAergic inhibition of mitral cells. The differential affinities of alpha1 and alpha2 noradrenergic receptor subtypes may allow for differential modulation of GABA release and olfactory processing as a function of the level of NE release, which in turn, is regulated by behavioral state.Neuroscience 05/2010; 169(2):882-92. DOI:10.1016/j.neuroscience.2010.05.010 · 3.33 Impact Factor