Cyclic compression of the intracranial optic nerve: patterns of visual failure and recovery.
(9/1964)
A patient with a cystic craniopharyngioma below the right optic nerve had several recurrences requiring surgery. Finally the cyst was connected with a subcutaneous reservoir by means of a fine catheter. Symptoms of optic nerve compression recurred more than 50 times during the following year, and were relieved within seconds upon drainage of the reservoir. In each cycle, a drop in visual acuity preceded a measurable change in the visual field. The pattern of field changes was an increasingly severe, uniform depression. Optic nerve ischaemia induced by compression was probably the most important factor causing visual failure in this case. (+info)
A case of septo-optic dysplasia.
(10/1964)
A child was reported here who has the hypoplastic optic nerve, absent septum pellucidum and endocrinological disorders. Growth hormone deficiency, antidiuretic hormone deficiency and mild hypothyroidism were observed. He has been treated with thyroid hormone and DDAVP. (+info)
Link between optic nerve regrowth failure and macrophage stimulation in mammals.
(11/1964)
The adult mammalian central nervous system (CNS) fails to regenerate its axons following injury. A comparison between its postinjury response and that of axons of nervous systems capable of regeneration reveals major differences with respect to inflammation. In regenerative systems, a large number of macrophages rapidly invade the injured site during the first few hours and days after the injury. Following their activation/differentiation through interaction with the host tissue, they play a central role in tissue healing through phagocytosis of cell debris and communication with cellular and molecular elements of the damaged tissue. Relative to the peripheral nervous system (PNS), macrophage recruitment in the adult mammalian CNS is delayed and is restricted in amount and activity. It was recently proposed that in injured mammalian CNS tissue, implantation of macrophages stimulated by prior co-culture with segments of peripheral (sciatic) nerves can compensate, at least in part, of the restricted postinjury inflammatory reaction. In the present study, this experimental paradigm is further explored and shows that there is no conflict between the systemic use of anti-inflammatory compounds and treatment with stimulated macrophages to promote regrowth of neuronal tissue. (+info)
5-HT1B receptor-mediated presynaptic inhibition of retinal input to the suprachiasmatic nucleus.
(12/1964)
The suprachiasmatic nucleus (SCN) receives glutamatergic afferents from the retina and serotonergic afferents from the midbrain, and serotonin (5-HT) can modify the response of the SCN circadian oscillator to light. 5-HT1B receptor-mediated presynaptic inhibition has been proposed as one mechanism by which 5-HT modifies retinal input to the SCN (Pickard et al., 1996). This hypothesis was tested by examining the subcellular localization of 5-HT1B receptors in the mouse SCN using electron microscopic immunocytochemical analysis with 5-HT1B receptor antibodies and whole-cell patch-clamp recordings from SCN neurons in hamster hypothalamic slices. 5-HT1B receptor immunostaining was observed associated with the plasma membrane of retinal terminals in the SCN. 1-[3-(Trifluoromethyl)phenyl]-piperazine HCl (TFMPP), a 5-HT1B receptor agonist, reduced in a dose-related manner the amplitude of glutamatergic EPSCs evoked by stimulating selectively the optic nerve. Selective 5-HT1A or 5-HT7 receptor antagonists did not block this effect. Moreover, in cells demonstrating an evoked EPSC in response to optic nerve stimulation, TFMPP had no effect on the amplitude of inward currents generated by local application of glutamate. The effect of TFMPP on light-induced phase shifts was also examined using 5-HT1B receptor knock-out mice. TFMPP inhibited behavioral responses to light in wild-type mice but was ineffective in inhibiting light-induced phase shifts in 5-HT1B receptor knock-out mice. The results indicate that 5-HT can reduce retinal input to the circadian system by acting at presynaptic 5-HT1B receptors located on retinal axons in the SCN. (+info)
Unilateral papilledema after bone marrow transplantation.
(13/1964)
We describe a patient who developed unilateral papilledema after allogeneic BMT. This is a rare manifestation of pseudotumor cerebri, which results from elevated intracranial pressure caused by cyclosporin A. The papilledema usually involves the fundi bilaterally, but unilateral involvement has been described. Congenital anomalies, compression and adhesion of the optic nerve sheath are its causes. In this patient, the right optic fundus was spared although leukemic infiltration was present on this side and high-dose irradiation (72 Gy) was given. Although papilledema is a sensitive marker of elevated intracranial pressure, this sign may be masked by constriction of the optic sheath in patients who suffer from leukemic infiltration of the central nervous system and receive high doses of cranial irradiation. (+info)
Mice deficient for tenascin-R display alterations of the extracellular matrix and decreased axonal conduction velocities in the CNS.
(14/1964)
Tenascin-R (TN-R), an extracellular matrix glycoprotein of the CNS, localizes to nodes of Ranvier and perineuronal nets and interacts in vitro with other extracellular matrix components and recognition molecules of the immunoglobulin superfamily. To characterize the functional roles of TN-R in vivo, we have generated mice deficient for TN-R by homologous recombination using embryonic stem cells. TN-R-deficient mice are viable and fertile. The anatomy of all major brain areas and the formation and structure of myelin appear normal. However, immunostaining for the chondroitin sulfate proteoglycan phosphacan, a high-affinity ligand for TN-R, is weak and diffuse in the mutant when compared with wild-type mice. Compound action potential recordings from optic nerves of mutant mice show a significant decrease in conduction velocity as compared with controls. However, at nodes of Ranvier there is no apparent change in expression and distribution of Na+ channels, which are thought to bind to TN-R via their beta2 subunit. The distribution of carbohydrate epitopes of perineuronal nets recognized by the lectin Wisteria floribunda or antibodies to the HNK-1 carbohydrate on somata and dendrites of cortical and hippocampal interneurons is abnormal. These observations indicate an essential role for TN-R in the formation of perineuronal nets and in normal conduction velocity of optic nerve. (+info)
A true neuronal consensual pupillary reflex in chicks.
(15/1964)
The existence of a true neuronal consensual pupillary reflex (CPR) in birds has long been debated. In this century Noll (Noll, A. (1915). Archiv fur Physiologie (Leipzig), 350-372.) claimed to observe a neuronal CPR in a pigeon, but this was contradicted by Levine (Levine, J. (1955). Science, 122, 699.), who observed a direct transillumination effect (Durchleuchtungs-effekt) due to the retinas of the two eyes of the pigeon being in close apposition. To determine if a neuronal CPR exists, we transected the optic nerves of 28 chicks and observed and videotaped the direct and indirect pupillary responses. Twenty-one of the chicks exhibited no direct response in the operated eye but did exhibit an indirect pupillary response. The non-operated eye showed a direct but no indirect response. These results conclusively demonstrate for the first time that a true neuronal CPR does exist in chickens. (+info)
Effects of adenosinergic agents on the vascular resistance and on the optic nerve response in the perfused cat eye.
(16/1964)
The function of A1- and A2a-adenosine receptors in the control of vascular resistance and in the modulation of light-evoked neuronal activity was investigated in the isolated perfused cat eye. The A1 agonist CCPA, the A1 antagonist CPT, the A2a agonist CGS 21680 and the A2 antagonist DMPX were used. The agents were applied intra-arterially at concentrations in the low nanomolar to micromolar range during rod-selective photic stimulation. The flow rate of perfusate, reflecting vascular resistance and the light-evoked optic nerve response (ONR) were recorded. Our results show a vasodilating effect of both A1 and A2 agonists and a vasoconstricting effect of the respective antagonists. The dose-effect relationships are suggestive, however, of an A2a receptor-mediated mechanism. The amplitude of the ONR-ON component was decreased during application of both adenosine-agonists. Analysis of the dose-effect relationships and the blockade of the CCPA-induced decrease by CPT suggests that inhibition is mediated by A1 receptors. However, CGS 21680-mediated inhibition cannot be explained by unspecific binding at A1 receptors alone and suggests the involvement of inhibitory A2a receptors. (+info)