Parvalbumin (PV)-expressing perisoma-inhibiting interneurons (PIIs) of the dentate gyrus integrate rapidly correlated synaptic inputs and generate short-duration action potentials that propagate along the axon to their output synapses, supporting fast inhibitory signaling onto their target cells. Here we show that PV-PIIs in rat and mouse dentate gyrus (DG) integrate their intrinsic activity over time and can turn into a persistent firing mode characterized by the ability to generate long-lasting trains of action potentials at ϳ50 Hz in the absence of additional inputs. Persistent firing emerges in the axons remote from the axon initial segment and markedly depends on hyperpolarization-activated cyclic nucleotide-gated channel (HCNC) activation. Persistent firing properties are modulated by intracellular Ca 2ϩ levels and somatic membrane potential. Detailed computational single-cell PIIs models reveal that HCNC-mediated conductances can contribute to persistent firing during conditions of a shift in their voltage activation curve to more depolarized potentials. Paired recordings from PIIs and their target granule cells show that persistent firing supports strong inhibitory output signaling. Thus, persistent firing may emerge during conditions of intense activation of the network, thereby providing silencing to the circuitry and the maintenance of sparse activity in the dentate gyrus.

Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. However, arterial thrombosis has been only rarely observed. We describe a young patient with heterozygous protein C deficiency who experienced a severe stroke due to thrombotic occlusion of the left middle cerebral artery. (Stroke 1990;21:1077-1080) P rotein C is a plasmaglycoprotein with a molecular weight of 62 kDa. Its synthesis by the liver depends on vitamin K. The inactive form of protein C is converted to the active protein C a by thrombin in the presence of Ca . Combination of thrombin with the cofactor thrombomodulin on the surface of endothelial cells greatly accelerates the activation rate of protein C.1 Protein C a acts as an anticoagulant by inactivating factors V a and VIII a . Protein C a also exerts profibrinolytic properties by inactivating plasminogen activator inhibitor 1. Protein S, which is also a vitamin K-dependent plasma protein synthesized by the liver and the endothelium, enhances the activity of protein Ca. 23Protein C deficiency is inherited as an autosomal dominant trait with incomplete penetrance. Heterozygous individuals have an increased risk of venous thrombosis and thromboembolism at a young age. 4 Homozygous protein C deficiency is rare and leads to a purpura fulminans-like syndrome in neonates. Homozygous individuals usually die within the first months of life unless treated with replacement of protein C during the acute phase, followed by lifelong anticoagulation. 55 Two types of protein C deficiency are known. Most common is type I, in which both the absolute concentration of protein C and its functional activity are reduced. In type II protein C deficiency the activity is reduced whereas the concentration of protein C is normal. 3 We describe a young patient with heterozygous protein C deficiency. Occlusion of the left middle cerebral artery led to a severe ischemic stroke. Received December 11, 1989; accepted February 28, 1990. Case ReportAfter suffering from a headache for several days, a 32-year-old mechanic acutely developed a brachiofacial hemiparesis of his right side and global aphasia. Cranial computed tomography showed an extensive ischemic infarct in the territory of the left middle cerebral artery (Figure 1). Occlusion of the left middle cerebral artery at its proximal stem was demonstrated by transtemporal Doppler sonography (Figure 2). Duplex scanning of the extracranial carotid arteries did not show arteriosclerotic lesions but revealed reduced blood flow velocities on the left. Since the Doppler sonographic data were unequivocal, cerebral angiography was not done.The patient had been healthy until this event, and there were no obvious precipitants of thrombosis (i.e., no trauma, intoxication, or dehydration). His on...

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We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis.