The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 +/- 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 microM) did not change in amplitude during in vitro ischemia. In a normoxic medium, a pair of fast EPSCs was elicited by paired-pulse stimulation (40-ms interval), and the amplitude of the second fast EPSC increased to 156 +/- 24% of the first EPSC amplitude. The ratio of paired-pulse facilitation (PPF ratio) increased during in vitro ischemia. Pretreatment of the slices with adenosine 1 (A1) receptor antagonist, 8-cyclopenthyltheophiline (8-CPT) antagonized the depression of the fast EPSCs, in a concentration-dependent manner: in the presence of 8-CPT (1-10 microM), the amplitude of the fast EPSCs decreased by only 20% of the control during in vitro ischemia. In addition, 8-CPT antagonized the enhancement of the PPF ratio during in vitro ischemia. A pair of presynaptic volleys and excitatory postsynaptic field potentials (fEPSPs) were extracellularly recorded in a proximal part of the stratum radiatum in the CA1 region. The PPF ratio for the fEPSPs also increased during in vitro ischemia. On the other hand, the amplitudes of the first and second presynaptic volley, which were abolished by TTX (0.5 microM), did not change during in vitro ischemia. The maximal slope of the Ca(2+)-dependent action potential of the CA3 neurons, which were evoked in the presence of 8-CPT (1 microM), nifedipine (20 microM), TTX (0.5 microM), and tetraethyl ammonium chloride (20 mM), decreased by 12 +/- 6% of the control 4 min after the onset of in vitro ischemia. These results suggest that in vitro ischemia depresses the evoked fast EPSCs mainly via the presynaptic A1 receptors, and the remaining 8-CPT-resistant depression of the fast EPSCs is probably due to a direct inhibition of the Ca(2+) influx to the axon terminals.

Direct and indirect actions of dopamine on the membrane potential in medium spiny neurons of the mouse neostriatum. J Neurophysiol 87: 1234 -1243, 2002; 10.1152/jn.00514.2001. Many studies have shown dopamine (DA) to have a modulatory effect on neuronal excitability, which cannot be simply classified as excitatory or inhibitory in the neostriatum. To clarify whether the responses to DA (10 -30 M) are excitatory or inhibitory in the mouse medium spiny neurons, we examined the effects of DA agonists on the synchronous potential trajectory from the resting potential to the subthreshold potential. The DA-induced potential changes, which were estimated at the subthreshold potential (approximately Ϫ60 mV), were summarized as the combination of three kinds of responses: an initial hyperpolarization lasting approximately 1 min and a slow depolarization and/or hyperpolarization lasting more than 20 min. A D 1 -like receptor agonist, R(ϩ) -6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3benzazepine hydrobromide (SKF81297, 1 M) mainly induced the initial hyperpolarization and slow depolarization. A D 2 -like receptor agonist, trans-(Ϫ)- 4aR-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrazolo[3,4-g]quinoline hydrochloride (quinpirole, 1 M), mainly induced the initial hyperpolarization and slow hyperpolarization. D 1 -like receptor antagonist R(ϩ)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH23390, 1 M) depressed both the initial hyperpolarization and slow depolarization. D 2 -like receptor antagonist sulpiride (1 M) depressed all the DA-induced responses except for the slow depolarization. TTX (0.5 M) abolished all the DA-induced responses. Bicuculline (20 M) and atropine (1 M) abolished the DA-induced initial hyperpolarization and slow depolarization, respectively. Either DL-2-amino-5-phosphonopentanoic acid (AP5; 100 M) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20 M) blocked both the initial hyperpolarization and slow depolarization. The application of exogenous glutamate (Glu) mimicked the initial hyperpolarization and slow depolarization. These results suggest that the initial hyperpolarization is mainly due to GABA release via the cooperative action of D 1 -and D 2 -like receptors and Glu receptors in GABAergic interneurons, whereas the slow depolarization is mediated by acetylcholine (ACh) release via the cooperative action of mainly D 1 -like receptors and Glu receptors in cholinergic interneurons. The potential oscillation was generated at the subthreshold level in a Ba 2ϩ -, AP5-, CNQX-, bicuculline-, and atropine-containing medium. The oscillation depressed after the addition of TTX, Co 2ϩ , or DA. In DA agonists, quinpirole rather than SKF81297 had a more depressive effect on the potential oscillation. These results indicate that the slow hyperpolarization is due to the suppression of noninactivating Na ϩ -Ca 2ϩ conductances via mainly D 2 -like receptors in the medium spiny neurons. In conclusion, the DA actions on the medium spiny neurons show a transient i...

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Percutaneous endoscopic lumbar discectomy PELD is a minimally invasive spinal technique. PELD can be performed using the transforaminal TF or interlaminar IL approach. The TF approach is a well-established modality in the treatment of patients with a herniated lumbar disc. This technique makes the most of the space within the intervertebral foramen, where Kambin s triangle permits a safe approach to the lesion. Knowledge of the anatomy of the lumbar artery and its branches and the ligaments of the intervertebral foramen is necessary to perform successful surgery and avoid complications.