Brain research
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Comparative Study
Blockade of GABAA receptors disrupts isoperiodic neuronal oscillations in the intergeniculate leaflet of the rat.
The intergeniculate leaflet of the thalamus is, besides the suprachiasmatic nucleus of the hypothalamus, the other important neuronal element of the mammalian biological clock. The extracellularly recorded activity of neurons constituting the intergeniculate leaflet, recorded in vivo, is characterized by distinct, very regular ultradian oscillations. The majority of neurons in the circadian timing system are GABAergic. ⋯ During the recording of isoperiodic oscillations, bicuculline or picrotoxin were stereotaxically injected at different concentrations into the lateral ventricle of rat brain. In all the experiments, injection of GABA(A) receptor antagonists transiently disrupted the isoperiodic phasic discharge recorded from the intergeniculate leaflet. These data suggest that GABA(A) receptors are involved in the generation of ultradian rhythmical neuronal oscillations in rat intergeniculate leaflet.
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Microinjections of morphine into the basolateral (BLa) and medial (MEa) nuclei of the amygdala differentially affect rostral ventromedial medulla (RVM) neuronal activity and nocifensive behaviors. PAG lesions attenuated or blocked the effects of both BLa and MEa morphine on RVM cell activity, and interfered with the behavioral antinociception produced by BLa infusions. These results demonstrate that the influences from both the BLa and MEa to the RVM are relayed via the PAG.
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The present study is aimed to systematically investigate wind-up and after-discharge of the spinal withdrawal reflex assessed by recording single motor unit (SMU) electromyographic (EMG) response to different intensities [0.5-1.5xreflex threshold (T)] of repetitive [frequencies (0.5-200 Hz)] transcutaneous electrical stimuli for 5 s. The role of central glutamate receptors in modulation of the withdrawal reflex facilitation was observed and evaluated in order to explore the potential central mechanism. Stimulus intensities below reflex threshold, such as 0.8xT, but not 0.5xT, could by repetition elicit and facilitate withdrawal reflex. ⋯ In conclusion, for the first time, the present study clearly demonstrates that, following the wind-up phase, the spinal withdrawal reflex pathways continue to fire spontaneously in a stimulus frequency- and intensity-dependent way (temporal and/or spatial summation). This inherited memory and the central non-N-methyl-d-aspartate (non-NMDA) receptor, but not the NMDA receptor, mainly involving pharmacological mechanisms, may play an important role in pathological conditions with spontaneous nociceptive firing. Furthermore, the after-discharge of the spinal reflex may be an important indicator for studies on central sensitization in many pathological pain conditions.
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Comparative Study
Differential action potentials and firing patterns in injured and uninjured small dorsal root ganglion neurons after nerve injury.
The profile of tetrodotoxin sensitive (TTX-S) and resistant (TTX-R) Na(+) channels and their contribution to action potentials and firing patterns were studied in isolated small dorsal root ganglion (DRG) neurons after L5/L6 spinal nerve ligation (SNL). Total TTX-R Na(+) currents and Na(v) 1.8 mRNA were reduced in injured L5 DRG neurons 14 days after SNL. In contrast, TTX-R Na(+)currents and Na(v) 1.8 mRNA were upregulated in uninjured L4 DRG neurons after SNL. ⋯ In the presence of TTX, only 26% of injured neurons could generate action potentials that had smaller amplitude, higher threshold, and higher rheobase compared with sham rats. In contrast, action potentials and firing patterns in uninjured L4 DRG neurons after SNL, in the presence or absence of TTX, were not affected. These results suggest that TTX-R Na(+) channels play important roles in regulating action potentials and firing patterns in small DRG neurons and that downregulation in injured neurons and upregulation in uninjured neurons confer differential roles in shaping electrogenesis, and perhaps pain transmission, in these neurons.
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It has been previously shown that the peptidergic nerve fibers are present in the anterior pituitary of monkeys, dogs and rats. In our study, which is reported here, thick nerve fiber bundles, large numbers of peptidergic nerve fibers and their varicosities, which are substance P (SP)-, calcitonin gene-related peptide (CGRP)- and galanin (GAL)-immunoreactive (ir), are found in the human pituitary stalk. All these peptidergic nerve fibers run along the pituitary stalk and enter the pars distalis, and some GAL-ir nerve fibers even reach the center of the human anterior pituitary as well as in parenchyma of adenohypophysis. ⋯ Furthermore, same SP-ir and CGRP-ir cells have been demonstrated in the pars distalis of the anterior pituitary. More or less, these peptidergic nerve fibers came also from the meningeal shell and enter the parenchyma of the anterior pituitary. Whatever the function of peptidergic nerve fibers in the human anterior pituitary might be, the concept that the adenohypophysis is regulated only hormonally by way of the portal system could be challenged.