Effects of noradrenaline on the responsiveness of cultured cerebellar neurons to excitatory amino acids

Differential regulations of vestibulo-ocular reflex and optokinetic response by β- and α2-adrenergic receptors in the cerebellar flocculus

“…Previous studies showed that activation of β-adrenergic receptor enhances the Purkinje neuron activity 26 , parallel fiber synaptic or glutamate responses of Purkinje neurons 31, 32 , and inhibitory synaptic or GABA responses of Purkinje neurons 33, 34 , and that α2-adrenergic activity decreases the Purkinje neuron activity 26 , and parallel fiber or inhibitory synaptic responses of Purkinje neurons 32, 35 . It has also been reported that stimulation of the locus coeruleus enhances the Purkinje neuron response to climbing fiber activation 14 , and that α2-adrenergic receptor activity decreases the glutamate release from climbing fibers 36 .…”

Catecholaminergic Modulation of Corticotropin-Releasing Factor and Adrenocorticotropin Secretion

“…On the other hand, blockade of catecholaminergic input to the PVN by a variety of means is associated with reduced HPA secretory tone and a reduction of central catecholamine turnover or release is highly correlated with decreased HPA activity. The apparent discrepancies among data obtained from in vivo experiments might arise from: 1) differences in sites of injection, stimulation, or lesion; 2) variations in the hormonal milieu in different experiments; 3) the proposed conditional nature of catecholaminergic neurotransmission (243); 4) the ability of the catecholamines to alter the responsiveness of target cells to other neurotransmitters (244,245).…”

Neuron specific α-adrenergic receptor expression in human cerebellum: Implications for emerging cerebellar roles in neurologic disease

“…The synchronized release of NE by LC neurons throughout the neuraxis can be either tonic (steady, low to high levels of NE, depending on state of vigilance), or phasic (additional bursts of high levels of NE during stimulus-evoked activity; Aston- Jones et al, , 1999. LC stimulation and iontophoretical applications of NE to rat cerebellar slices or cells increase spontaneous Purkinje cell firing at low concentrations (0.5-10 μM), increase the frequency of spontaneous firing of stellate cells at > 16 μM, resulting in depression of Purkinje cell spontaneous activity, and cause consistent depression of Purkinje cell spontaneous activity at higher concentrations (25-100 μM; Basile and Dunwiddie, 1984;Mori-Okamoto and Tatsuno, 1988;Kondo and Marty, 1998). Furthermore, 10 mM NE has been reported to potentiate the inhibitory activity of stellate and basket cells (Llano and Gerschenfeld, 1993;Saitow and Konishi, 2000), while application of 100 mM NE for 30 min causes both a short-term enhancement of GABAergic inhibition and prolonged inhibition lasting more than 2 h. This is suggestive of the long-term depression involved in motor learning that occurs after simultaneous stimulation of climbing fibers (CF) and parallel fibers (PF) (Mitoma and Konishi, 1999;Gao et al, 2003).…”

“…Thus, NE enhances stimulus-evoked signals, i.e. increases the "signal-to-noise ratio" of firing for both glutamatergic excitatory and GABAergic inhibitory synapses of cerebellar interneurons (Freedman et al, 1977;Moises et al, 1979Moises et al, , 1990Mori-Okamoto and Tatsuno, 1988;Woodward et al, 1991). In contrast, depletion of cerebellar NE impairs motor performance (Watson and McElligott, 1984).…”

“…In contrast, depletion of cerebellar NE impairs motor performance (Watson and McElligott, 1984). Activation of specific ARs has been reported for some NE concentrations: α 2a AR for > 16 μM NE, αAR below that range, α 2 AR at 10 mM and α 1 AR at 0.5 M (Yeh and Woodward, 1983;Basile and Dunwiddie, 1984;Mori-Okamoto and Tatsuno, 1988;Kondo and Marty, 1998). Thus, modulation of cerebellar neuron activity appears to be regulated by specific AR subtypes that selectively respond to certain levels or exposure times of NE.…”