Brain research
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We assessed the post-seizure effects on the seizure threshold and the seizure duration using low-frequency kindling technique. The number of stimulating pulses required for a triggering of epileptic afterdischarge (pulse-number threshold; PNT) was used for the indicator of seizure threshold. PNT increased significantly at 2 and 4 h inter-stimulation intervals, whereas it decreased significantly with an increase of seizure duration at 16 and 24 h intervals. It appears from these data that a post-seizure excitation occurs after a post-seizure inhibition.
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In rats, microinjection of the opioid agonist morphine (15-45 nmol/0.5 microliter) and the excitatory amino acid monosodium glutamate (30-60 nmol/0.5 microliter) into identical brainstem sites within the mesencephalic periaqueductal gray matter (PAG; 23 sites) and the rostral ventromedial medulla (RVM; 22 sites) produced an increase of tail flick and hot plate response latencies. At both PAG and RVM sites, there was a statistically significant relationship between the effect obtained with morphine and with glutamate on the two nociceptive responses. While morphine and glutamate produced indistinguishable inhibition of tail flick and hot plate response latencies in the PAG, the tail flick inhibition following RVM morphine, but not RVM glutamate, displayed a clear plateau. One parsimonious interpretation of these data is that (1) glutamate directly increases the activity in the bulbospinal pathway, and (2) morphine inhibits an evoked or tonic suppression of a bulbospinal projection.
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The selectivity of the neurotoxic lesion of Ricinus communis agglutinin I (RCAI) in rat dorsal root ganglia was examined. RCAI was injected in the sural nerve on one side. Two weeks later, the injected nerve, as well as the ipsilateral peroneal nerve, were examined in 1-micron-thick plastic embedded sections in the light microscope. ⋯ Three weeks after unilateral injections of RCAI in the sciatic nerve, the L4-L6 dorsal root ganglion cells were counted bilaterally. On average, relative neuronal numbers between injected and uninjected sides were 0.36, 0.15 and 0.64 for L4, L5 and L6 respectively. From these data we conclude that the sciatic nerve receives on average of 64%, 85% and 36%, respectively of its sensory contribution from these ganglia.
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Kainic acid was injected bilaterally (4.8 micrograms in 1.2 microliters each side) into the dorsolateral pontomesencephalic tegmentum of cats in order to destroy the cholinergic neurons located in that region and thus to study the effects of their destruction upon sleep-waking states. The kainic acid produced a large area of nerve cell loss and/or gliosis centered in the dorsolateral tegmentum-cholinergic cell area, that includes the pedunculopontine tegmental (PPT) and laterodorsal tegmental (LDT) nuclei rostrally (A1-P2), and the parabrachial (PB) and locus coeruleus (LC) nuclei caudally (P3-P5). The mean loss of choline acetyltransferase (ChAT)-immunoreactive neurons within this area was 60% with a range from 25% to 85% across 11 cats. ⋯ The percent of PS-like epochs, the rate of PGO spiking and the EMG amplitude on postlesion day 28 were found to be significantly correlated with the volume of the lesion within the dorsolateral pontine tegmentum-cholinergic cell area. The percent PS-like episodes and PGO spike rate were significantly correlated with the number of remaining ChAT-immunoreactive neurons, but not with the number of remaining TH-immunoreactive neurons within this region. These results suggest that cholinergic pontomesencephalic neurons may be critically involved in the generation of paradoxical sleep and its phasic events.
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A unilateral experimental inflammation of the hindlimb produces hyperalgesia to both mechanical and radiant thermal stimuli that is rapid in onset. During this period, parameters of dynorphin biosynthesis are elevated to a much greater degree than those of the enkephalin system. An increase in the content of the peptide dynorphin A(1-8) occurs in the spinal cord segments that receive sensory input from the affected limb. ⋯ Dorsal spinal cord preproenkephalin mRNA is elevated to a lesser degree (50-80%). However, the increase in preproenkephalin mRNA is apparently not enough to yield a measurable increase in the proenkephalin-derived peptide met5-enkephalin-Arg6-Gly7-Leu8, the levels of which showed no significant change during the 14-day inflammatory period. These data suggest the active participation of opioid neurons, especially those containing dynorphin, at the spinal level, in the modulation of sensory afferent input during peripheral inflammatory pain states.