Noradrenergic innervation of the substantia innominata: A light and electron microscopic analysis of dopamine β-hydroxylase immunoreactive elements in the rat
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Ventral pallidum cellular and pathway specificity in drug seeking
2021, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Thus, the glutamate released in the VP originates in both local and external sources, affects VP activity and may be relevant to relapse behavior. The VP receives projections releasing all three major monoamine neurotransmitters – dopamine, noradrenaline and serotonin (Semba et al., 1988; Chang, 1989; Klitenick et al., 1992). Serotonin and noradrenaline fibers are quite abundant while dopamine input to the VP is relatively sparse (Klitenick et al., 1992; Root et al., 2015) and dopamine extracellular levels are low (Napier and Potter, 1989).
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2004, Brain Research ReviewsCitation Excerpt :Noradrenaline may regulate cortical cholinergic transmission through an action at presynaptic alpha2-adrenergic heteroreceptors on basalocortical cholinergic terminals [267], or at the level of the cholinergic nerve cell bodies within the basal forebrain. A noradrenergic modulation at this latter level is supported by studies showing that (1) dopamine-beta-hydroxylase immunoreactive terminals make close contact with ChAT-immunoreactive neurons in the nbM [87,564], (2) moderate to high densities of alpha2-adrenoceptors exist in the basal forebrain regions of the rat brain [23,283], (3) alpha2-adrenoceptor immunoreactivity is observed in ChAT-immunopositive neurons of the rat basal forebrain at both light and electron microscopic levels [565], (4) alpha2-adrenoceptor agonists inhibit acetylcholine release from slices of the nbM [490], and (5) alpha1- and beta-adrenoceptors mediate excitatory effects of noradrenaline in basal forebrain cholinergic neurons in vitro [187]. A role for alpha2-adrenoceptors in modulating the release of acetylcholine in the cerebral cortex has been suggested largely from in vivo studies in rodents showing that cortical acetylcholine release is modified by selective alpha2-adrenoceptor ligands [522–524].