Brain research
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Intra-axonal recording and horseradish peroxidase (HRP) injection techniques were employed to define the response properties of periodontal mechanoreceptive afferents originating from the trigeminal mesencephalic nucleus (Vmes) and their morphological characteristics. The periodontal Vmes neurons were classified into two types: slowly adapting (SA) and fast adapting (FA) types. The central terminals of 7 SA and 4 FA afferents were recovered for detailed analyses. ⋯ The average size of somata and mean diameters of U fibers and main collaterals from C fiber were significantly larger in SA neurons than FA neurons. The average size of fiber varicosities became smaller in the following nuclei, Vmo, Vsup, Vp, Vint and Vo.r, but not significant between the two functional types. The functional role of the periodontal Vmes afferents to jaw reflexes was discussed particularly with respect to their central projection sites in the brainstem nuclei.
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We applied tests of antidromic activation to identify cells in the hamster intergeniculate leaflet (IGL) that project to either the suprachiasmatic nucleus (SCN) or the contralateral IGL. IGL cells projecting to these targets were tested for photic responses; most showed sustained activation, while a few were suppressed by retinal illumination. Stimulation of one IGL typically suppressed firing in contralateral IGL cells and inhibited responses to immediately succeeding photic stimulation.
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The highly mu-selective agonist Tyr-D-Ala-Gly-MePhe-Gly-ol-enkephalin (DAGO) produces potent, dose-dependent naloxone-reversible antinociception when microinjected into the ventrolateral periaqueductal gray (PAG) (ED50 = 0.72 nmol) or rostral ventromedial medulla (RVM) (ED50 = 0.05 nmol) as measured on the rat tail flick (TF) assay. In single-unit recording experiments, DAGO microinjected into the PAG also affected On- and Off-Cell firing in the RVM in the same way as previously demonstrated by our group for morphine. PAG-microinjected DAGO inhibits spontaneous and noxious-evoked On-Cell firing (attenuating the characteristic On-Cell burst) (n = 19), and excites spontaneous Off-Cell firing, preventing the characteristic Off-Cell pause (n = 12) at doses which suppress the TF. ⋯ In our experiments using BAM22P, an endogenous weakly mu-selective opioid peptide, we could not demonstrate a dose-dependent antinociceptive effect, whether the peptide was microinjected supraspinally into the PAG (n = 9) or RVM (n = 11), or intrathecally at the lumbar cord (n = 4). In two animals, a naloxone-reversible antinociceptive effect was observed following the microinjection of 10 nmol BAM 22P into the RVM; however, no effect was seen in 3 animals microinjected with 20 nmol. Dyn A(1-13), a putative endogenous ligand for the kappa receptor, had no antinociceptive effect when microinjected into the ventrolateral PAG, and no effect on the firing (spontaneous or noxious-evoked) of RVM On (n = 3)- or Off (n = 2)-Cells.
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Previous in vivo studies from our laboratory have consistently shown that iontophoretically applied norepinephrine (NE) can potentiate gamma-aminobutyric acid (GABA)-induced depressant responses of cerebrocortical, cerebellar and hypothalamic neurons. Additional experiments have further suggested that this noradrenergic facilitating action is specific for GABA and results from the activation of a beta-type adrenoceptor. The goal of the present studies was to determine if the cAMP second messenger system might also be a component of the mechanism responsible for this NE modulatory action on GABA-mediated inhibition. ⋯ As with NE, BcAMP was ineffective in enhancing P-cell inhibitory responses to beta-alanine, an agent which like GABA causes hyperpolarization, by increasing Cl conductance. In summary, these results indicate that a membrane permeant analog of cAMP, a phosphodiesterase inhibitor and an agent which directly activates adenyl cyclase can mimic the previously observed GABA-potentiating actions of NE. Thus, these findings provide further support for the contention that noradrenergic enhancement of GABA inhibition results from a cascade of transmembrane events which includes beta-receptor activation, adenyl cyclase stimulation and increased intracellular production of cAMP.
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In the present study, we have used a newly developed microdialysis system to perfuse the nucleus accumbens (NAC) of conscious rats during spontaneous intracranial self-stimulation of the medial forebrain bundle (MFB). Chromatographic (HPLC-ECD) analysis of the perfusates showed that dopamine (DA) release increased, but with an unstable pattern during the actual period of self-stimulation. ⋯ These findings indicate that self-stimulation of the MFB in rats induces increases in both DA and serotonin activities in the NAC. Such changes may be involved in mediating self-stimulation of the MFB.