Detailed knowledge of the inhibitory input to trigeminal motoneurons is needed to understand better the central mechanisms of jaw movements. Here a quantitative analysis of terminals contacting somata of jaw-closing (JC) and jaw-opening (JO) alpha-motoneurons, and of JC gamma-motoneurons, was performed by use of serial sectioning and postembedding immunogold cytochemistry. For each type of motoneuron, the synaptic boutons were classified into four groups, i.e., immunonegative boutons or boutons immunoreactive to glycine only, to gamma-aminobutyric acid (GABA) only, or to both glycine and GABA. The density of immunolabeled boutons was much higher for the alpha- than for the gamma-motoneurons. In the alpha-motoneuron populations, the immunolabeled boutons were subdivided into one large group of boutons containing glycine-like immunoreactivity only, one group of intermediate size harboring both glycine- and GABA-like immunoreactivity, and a small group of boutons containing GABA-like immunoreactivity only. The percentage of immunolabeled boutons was higher for JC than JO alpha-motoneurons, the most pronounced difference being observed for glycine-like immunoreactivity. In contrast, on the somatic membrane of gamma-motoneurons, the three types of immunoreactive bouton occurred at similar frequencies. These results indicate that trigeminal motoneurons are strongly and differentially controlled by premotoneurons containing glycine and/or GABA and suggest that these neurons play an important role for the generation of masticatory patterns.
Previous studies provide evidence that a structure/function correlation exists in the distinct zones of the trigeminal sensory nuclei. To evaluate this relationship, we examined the ultrastructure of afferent terminals from the tooth pulp in the rat trigeminal sensory nuclei: the principalis (Vp), the dorsomedial part of oral nucleus (Vdm), and the superficial layers of caudalis (Vc), by using transganglionic transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). A total of 93 labeled boutons were serially sectioned, in which some sections were incubated with gamma-aminobutyric acid (GABA) antiserum. Almost all labeled boutons formed asymmetric contact with nonprimary dendrites, in which more than half of labeled boutons in the Vc made synapses with their spines. The labeled boutons could be divided into two types on the basis of numbers of dense-cored vesicles (DCVs) in a boutons: S-type and DCV-type. Almost all labeled boutons in the Vp and Vdm were S-type, whereas two types were distributed evenly in the Vc. In contrast to DCV-type boutons, the S-type was frequently postsynaptic to unlabeled axon terminals containing a mixture of round, oval, and flattened vesicles (p-endings) and forming symmetrical synapses. Most p-endings examined were immunoreactive to GABA. The frequency of axoaxonic contacts was higher for labeled boutons in the Vp than in the Vdm and Vc. These results suggest that the three structures of trigeminal sensory nuclei serve distinct functions in nociceptive processing.
Recent progress in brain imaging has revealed a high frequency of cortical malformations in childhood epilepsy. 1,2) However, very little is knownregarding the pathophysiological mechanisms of epileptogenicity in the malformed cortex, partly because of the rarity of experimental studies with animal models.3) In rats, the application of methylazoxymethanol (MAM) in utero (E15) results in the formation of dysplastic regions in the neocortex and the CA1 region of the hippocampus, as well as in the heterotopic clusters of neurons in the subcortical white matter.4,5) Some MAM-treated pups, with both neocortical and hippocampal dysgenesis, have a lower threshold for seizure activity.6) Heterotopic neurons in the MAM model lack potassium channels and exhibit burster firing properties 7,8) and heterotopia received abundant GABAergic innervations in the MAM exposed rats. 9) Heterotopic CA1 pyramidal neurons appear to have atypical electrophysiological and morphological characteristics 10) and may form abnormal connections with neocortical regions. 11) Although it is well established that these models mimic the structural aspects of human early-onset epilepsy syndrome, there were few behavioral changes regarding spontaneous and recurrent seizures in the MAM rats. When MAM animals were examined specifically for spontaneous seizures, no activity was detected, although some EEG and sleep-cycle irregularities exist. [12][13][14][15] Behavioral changes are considered to be important factors in evaluating the usefulness of epilepsy animal models. [16][17][18] Spontaneous electrographic and behavioral seizures have been observed in pilocarpine-induced status epilepticus (SE), [19][20][21] although spontaneous epileptic seizures have not yet been observed in MAM-exposed rats. This indicates that the MAM rats were resistant to the development of spontaneous and recurrent seizures. Since spontaneous and recurrent seizures are typical characteristics of epilepsy, developing a similar seizure model in the MAM rats is important in the study of pathophysiological mechanisms that contribute to epileptogenesis.In the present study, we examined the facilitated effect of MAM-treated animals on seizure induced by pilocarpine. MATERIALS AND METHODS AnimalsFemale rats (Sprague-Dawley) with known insemination times were obtained. Pregnant rats were injected with 25 mg/kg MAM dissolved in 0.9% saline. Intraperitoneal injections were made on embryonic 15 d. Experimental procedures were performed in accordance with the animal care guidelines of NIH and the Korean Academy of Medical Sciences. All animals were maintained in a 12-h light-dark cycle and were provided with food and water ad libitum.In Vivo Recording Sprague-Dawley rats were anesthetized with urethane (1.3 g/kg), according to procedures reported elsewhere.22) Briefly, the recording electrode was located in the hippocampus (AP: Ϫ3.8 mm from bregma; L: 2.5 mm). A concentric bipolar stimulating electrode was inserted into the contralateral fimbria-fornix (AP: Ϫ1.3, L: 1.0, V: 4.8 mm) to s...
The GABA(B) receptor-mediated presynaptic inhibition of glycinergic transmission was studied from young rat substantia gelatinosa (SG) neurons using a conventional whole-cell patch clamp technique. Action potential-dependent glycinergic inhibitory postsynaptic currents (IPSCs) were recorded from SG neurons in the presence of 3 mM kynurenic acid and 10 microM SR95531. In these conditions, baclofen (30 microM), a selective GABA(B) receptor agonist, greatly reduced the amplitude of glycinergic IPSCs and increased the paired-pulse ratio. Such effects were completely blocked by 3 microM CGP55845, a selective GABA(B) receptor antagonist, indicating that the activation of presynaptic GABA(B) receptors decreases glycinergic synaptic transmission. Glycinergic IPSCs were largely dependent on Ca2+ influxes passing through presynaptic N- and P/Q-type Ca2+ channels, and these channels contributed equally to the baclofen-induced inhibition of glycinergic IPSCs. However, the baclofen-induced inhibition of glycinergic IPSCs was not affected by either 100 microM SQ22536, an adenylyl cyclase inhibitor, or 1 mM Ba2+, a G-protein coupled inwardly rectifying K+ channel blocker. During the train stimulation (10 pulses at 20 Hz), which caused a marked synaptic depression of glycinergic IPSCs, baclofen at a 30 microM concentration completely blocked glycinergic synaptic depression, but at a 3 microM concentration it largely preserved glycinergic synaptic depression. Such GABA(B) receptor-mediated dynamic changes in short-term synaptic plasticity of glycinergic transmission onto SG neurons might contribute to the central processing of sensory signals.
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