Adrenergic regulation of GABA release from presynaptic terminals in rat cerebral cortex.

The α1-adrenoceptor agonist phenylephrine and the ß-adrenoceptor agonist isoproterenol have opposite effects on evoked EPSPs (eEPSPs) in the cerebral cortex. The suppressive effects of phenylephrine on eEPSPs are mediated by modulation of postsynaptic glutamate receptors, whereas enhancement of eEPSPs by isoproterenol is due to facilitation of glutamate release from presynaptic terminals. The present study used whole-cell patch-clamp recordings from layer V pyramidal neurons in visuocortical slice preparations to assess the effects of phenylephrine and isoproterenol on the release probability of γ-aminobutyric acid (GABA). The present study recorded evoked inhibitory postsynaptic potentials (eIPSCs) by repetitive electrical stimulation (duration, 100 µs; 10 stimuli at 33 Hz) and miniature IPSCs (mIPSCs). The effects of phenylephrine (100 µM) depended on the amplitude of eIPSCs: phenylephrine decreased the paired-pulse ratios (PPRs) of eIPSCs with smaller amplitudes (<~600 pA) but increased PPRs of eIPSCs with larger amplitude. Phenylephrine also exhibited amplitude-dependent modulation of mIPSCs, i.e., an increase in the frequency of smaller mIPSC events (<~20 pA) and a decrease in the frequency of larger events. These findings suggest that α1-adrenoceptor activation facilitates GABA release from a subpopulation of GABAergic terminals that induce smaller-amplitude IPSCs in postsynaptic neurons. In contrast, isoproterenol (100 µM) consistently decreased the PPR of eIPSCs and increased the frequency of mIPSCs, suggesting that presynaptic ß-adrenoceptors increase release probability from most GABAergic terminals. The complexity of adrenoceptor modulations in GABAergic synaptic transmission by α1-adrenoceptor and ß-adrenoceptor activation may be due to the presence of pleiotropic subtypes of GABAergic interneurons in the cerebral cortex.

Apomorphine-induced modulation of neural activities in the ventrolateral striatum of rats.

The dopaminergic system in the ventrolateral portion of the striatum (Svl), part of the basal ganglia, regulates orofacial movements; bilateral co-stimulation of both dopamine D1 -like and D2 -like receptors elicits repetitive jaw movements in rats. However, how the activities of Svl neurons are modulated by the activation of dopaminergic receptors remains unknown. We systematically injected apomorphine, a non-selective dopamine receptor agonist that induced jaw movements under urethane anesthesia, and performed multi-channel unit recording from Svl neurons. The Svl neurons were classified into two subgroups: (1) the phasically active (PA) neurons represented by mainly the medium spiny neurons and the GABAergic interneurons in part, and (2) the tonically active (TA) neurons composed of mainly the cholinergic interneurons. Apomorphine modulated PA neuron firing frequency with wide variability; 33.3% of the PA neurons were facilitated, while 38.3% were suppressed. In the majority of TA neurons, the firing frequency was reduced by apomorphine (71.1%). The cross-correlations between PA and PA, PA and TA, and TA and TA neurons were analyzed, and pairs of PA neurons and pairs of PA and TA neurons, showed negligible apomorphine-induced effect on the number of synchronized spikes. In contrast, pairs between TA neurons showed a consistent decrease in the number of synchronized spikes. The apomorphine-induced suppression of TA neuron activities with decreased synchronized outputs is likely to reduce the amount of locally released acetylcholine, which may contribute to the induction of apomorphine-induced jaw movements in rats.

5-HT(1A) and 5-HT(1B) receptors in the ventrolateral striatum differentially modulate apomorphine-induced jaw movements in rats.

The ability of serotonin 5-HT(1A) and 5-HT(1B) receptors in the ventrolateral striatum to modulate dopamine receptor-mediated jaw movements was investigated in freely moving rats, using a magnet-sensing system combined with an intracerebral drug microinjection technique. Apomorphine (1 mg/kg i.v.) has been found to elicit repetitive jaw movements. Bilateral injections of the 5-HT(1A) receptor agonist 8-OH-DPAT (1 and 4 microg/0.2 microl in each side) into the ventrolateral striatum partially but significantly reduced apomorphine-induced repetitive jaw movements. The 5-HT(1A) receptor antagonist WAY-100635 (1 microg), which alone did not affect the effects of apomorphine, antagonized the inhibitory effects of 8-OH-DPAT (4 microg). Bilateral injections of the 5-HT(1B) receptor agonist CP93129 (1 and 10 microg) also reduced apomorphine-induced repetitive jaw movements in a dose-dependent manner. However, the 5-HT(1B) receptor antagonist GR55562 (1 and 10 microg) did not antagonize the inhibitory effects of CP93129 (10 microg). These results suggest that 5-HT(1A), but not 5-HT(1B), receptors in the ventrolateral striatum play a modulatory role in the production of dopamine receptor-mediated jaw movements.

[Anterior guidance reconstruction by fixed prosthesis containing bone anchored crown].

PATIENT: A 24-year-old female patient visited our dental office with esthetic complaint. Implant-supported fixed prostheses were placed on the upper right and left side canine area. The cusps of bone anchored crowns were made to contact with the lower canine cusps during mandibular translation. The patient was followed for 5 years with no surgical or prosthetic complications. DISCUSSION: Stability of the intercuspal position and reduction of lateral force are of importance when providing occlusal contacts for bone-anchored prosthesis in eccentrec relations. CONCLUSION: This case offers useful information on occlusal contact for implant-supported prostheses.