Neurokinin-1 receptors in cholinergic neurons of the rat ventral pallidum have a predominantly dendritic distribution that is affected by apomorphine when combined with startle-evoking auditory stimulation

Abstract

Cholinergic neurons of the basal forebrain are implicated in startle reflex inhibition by a prior weak stimulus often referred to as prepulse inhibition (PPI) and used as an index of sensorimotor gating deficits in schizophrenia. Gating deficits can be produced in rodent models by acute systemic administration of apomorphine, a non-selective dopamine D1 and D2 receptor agonist that also affects trafficking of neurokinin-1 (NK(1)) receptors induced by startle evoking auditory stimulation (AS) in midbrain neurons. We used electron microscopic immunolabeling of NK(1) receptors and the vesicular acetylcholine transporter (VAchT) to test the hypothesis that the subcellular distributions of these receptors in cholinergic neurons of the rat ventral pallidum are subject to a similar regulation. In vehicle controls, NK(1) immunogold was often seen near cytoplasmic endomembranes in somata and large dendrites, but was more equally distributed in cytoplasmic and plasmalemmal compartments of medium dendrites, and principally located on the plasma membrane of small dendrites. These labeling patterns appeared to be largely independent of whether the NK(1) receptor was co-expressed with VAchT, however only the medium and small VAchT-labeled dendrites showed significant treatment-specific differences in NK(1) immunogold distributions. The NK(1) receptor immunogold particle density on the plasma membrane of medium cholinergic dendrites was significantly enhanced by combined apomorphine and AS, while neither alone affected either the plasmalemmal density or the equality of the plasmalemmal and cytoplasmic distributions of NK(1) receptors in these dendrites. Small cholinergic dendrites showed a significant AS-induced increase in both the plasmalemmal and cytoplasmic density of NK(1) gold particles, and an apomorphine-induced disruption of the preferential plasmalemmal targeting of the NK(1) receptors. These results provide ultrastructural evidence that NK(1) receptors in cholinergic neurons of the ventral pallidum have subcellular locations and plasticity conducive to active involvement in dopamine-dependent sensorimotor processing.

Ultrastructural and antigenic properties of neural stem cells and their progeny in adult rat subventricular zone

“…The subcellular distribution of growth factor receptors was determined using the immunogold labeling technique (Armbruster et al, 1983;Carlemalm et al, 1982;D'Amico and Skarmoutsou, 2008;Ferreira et al, 2007;Mengual et al, 2008;Renno, 2001;Roth, 1982;Roth et al, 1978). Several lines of evidence confirmed the specificity of the EGFR and PDGFRa immunolabeling in our study.…”

Stress-induced dendritic internalization and nuclear translocation of the neurokinin-3 (NK3) receptor in vasopressinergic profiles of the rat paraventricular nucleus of the hypothalamus

“…Stress-induced trafficking of NK 3 receptor in AVP but not OC PVN neurons: Involvement in circuits relaying emotional information Quantitative electron microscopy is a valid method to measure trafficking of receptors in specific neuronal compartments, as demonstrated many times by our team and others (Lessard and Pickel, 2005;Hara and Pickel, 2007;Lane et al, 2008;Mengual et al, 2008;Misono and Lessard, 2012). In the present study, restraint stress increased the nuclear but not the cytoplasmic NK 3 R density in AVP cell bodies.…”

The Role of Substance P in the Marginal Division of the Neostriatum in Learning and Memory is Mediated Through the Neurokinin 1 Receptor in Rats

“…SP has excitatory effects in the hippocampus and is able to facilitate long term potentiation (LTP) via activation of NK1R in the hippocampus [4]. Anxiety and stress responses are modulated by SP released within the amygdale and self-regulatory capacity of SP-mediated neurotransmission that differs in the effect on basal and stress-induced release of SP via activation of NK1R [5]. NK1Rs may be important mediators of SP evoked excitation in the ventral pallidum, and specifically affecting the postsynaptic excitability of the cholinergic neurons in this brain region [6].…”