The nucleus accumbens (NAc) core is critical in the control of motivated behaviors. The muscarinic acetylcholine receptors (mAChRs) modulating the excitatory inputs into the NAc core have been reported to impact such behaviors. Recent studies suggest that ventral and dorsal regions of the NAc core seem to be innervated by distinct popula tions of glutamatergic projection neurons. To further examine mAChRs modulation of these glutamatergic inputs to the NAc core, we employed intracellular recordings in rat NAc coronal slice preparation to characterize: 1) the effects of muscarine, an mAChRs agonist, on membrane properties of the NAc core neurons; 2) depolarizing synaptic potentials (DPSP) elicited by ventral and dorsal focal electrical stimuli; and 3) paired-pulse response with paired-pulse stimulation. Here we report that the paired-pulse ratio (PPR) elicited by dorsal stimuli was grea ter than that elicited by ventral stimuli. Bath application of muscarine (1-30 μ M) decreased both ventral and dorsal DPSP in a concentration-dependent manner, with no effect on electrophysiological properties of NAc core neurons. Muscarine at 30 μ M also elicited larger depression of dorsal DPSP than ventral DPSP. Moreover, muscarine increased the PPR of both dorsal and ventral DPSP. These data indicate that the glutamatergic afferent fibers traversing the dorsal and ventral NAc are separate, and that differential decrease of distinct afferent excitatory neurotransmission onto NAc core neurons may be mediated by presynaptic mechanisms., X. Jiang ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Galanin and galanin receptors (GalRs) have been reported to be
involved in the transmission and modulation of nociceptive
information in the central nervous system (CNS). However, the
underlying mechanism of the antinociception of GalRs in
neuropathic pain remains unclear. This study investigated the
antinociception induced by galanin receptor 1 (GalR1) via protein
kinase A (PKA) signaling pathway in the nucleus accumbens
(NAc) of rats with neuropathic pain. A mononeuropathy model
was replicated by ligation of the left sciatic nerve, following which
the expression of phospho-PKA (p-PKA) in the NAc were
markedly up-regulated at 14th and 28th day after ligation of sciatic
nerve, and p-PKA expression was down-regulated by intra-NAc
injection of GalR1 agonist M617, but the GalR1 antagonist M35
did not have an effect. We also found that M35 in the NAc
blocked the M617-induced increase in the hind paw withdrawal
latencies (HWLs) of rats with mononeuropathy, but M35 alone
had no effect on HWLs, and PKA inhibitor H-89 attenuated the
M617-induced an increase in the HWLs. These results suggested
that GalR1 induced an antinociception via inhibiting PKA
activation, implying that GalR agonists may be potential and
potent therapeutic options to treat chronic neuropathic pain.