Magnetic resonance imaging assessment of the lateral geniculate nucleus volume and height in patients with glaucoma:a Meta-analysis

AIM:To evaluate the lateral geniculate nucleus(LGN)volume and height using magnetic resonance imaging(MRI)in glaucoma patients.METHODS:Literatures retrieval was carried out through Pub Med,Web of Science,Embase,and Cochrane Library.Studies that compared the volume and height of LGN in glaucoma patients with that in control subjects were included.The volume and height of LGN were extracted from the included studies.The Review Manager 5.4.1 software was used for the Meta-analysis.RESULTS:This Meta-analysis included 10 crosssectional studies,including the eyes of 223 glaucoma patients and 185 healthy controls.Compared with the control subjects,the volume and height of LGN in glaucoma patients measured by MRI were significantly reduced{-29.13 mm3,95%[confidence interval(CI):-44.82 to-13.43,P=0.0003;-0.61 mm,95%CI:-0.78 to-0.44,P<0.00001,respectively]}.Subgroup analysis demonstrated that the differences of LGN volume and height between glaucoma patients and control subjects in the older group were smaller than that in the younger group,and LGN volume decreased with the increase of glaucoma severity.CONCLUSION:The results demonstrate that the volume and height of LGN are decreased in glaucoma patients,and LGN volume can be considered a parameter of glaucoma severity.

Heat shock protein 72 confers protection in retinal ganglion cells and lateral geniculate nucleus neurons via blockade of the SAPK/JNK pathway in a chronic ocular-hypertensive rat model

Optic nerve transection increased the expression of heat shock protein 72 （HSP72） in the lateral geniculate body, indicating that this protein is involved in the prevention of neuronal injury. Zinc sulfate and quercetin induced and inhibited the expression of HSP72, respectively. Intraperitoneal injections of zinc sulfate, SP600125 （c-Jun N-terminal kinase inhibitor）, or quercetin were performed on retinal ganglion cells in a Wistar rat model of chronic ocular hypertension. Our results showed that compared with the control group, the expression of HSP72 in retinal ganglion cells and the lateral geniculate body was increased after the injection of zinc sulfate, but was decreased after the injection of quercetin. The expression of phosphorylated c-Jun N-terminal kinases and phosphorylated c-Jun were visible 3 days after injection in the control group, and reached apeak at 7 days. Zinc sulfate and SP600125 significantly decreased the expression of p-c-Jun, whereas quercetin significantly enhanced the expression of this protein. These results suggest that HSP72 protects retinal ganglion cells and lateral geniculate body in a rat model of chronic ocular hypertension from injury by blocking the activation of the stress-activated kinase/c-Jun N-terminal kinase apoptotic pathway.

Neuronal apoptosis and neurofilament protein expression in the lateral geniculate body of cats following acute optic nerve injuries

The visual pathway have 6 parts, involving optic nerve, optic chiasm, optic tract, lateral geniculate body, optic radiation and cortical striatum area. Corresponding changes may be found in these 6 parts following optic nerve injury. At present, studies mainly focus on optic nerve and retina, but studies on lateral geniculate body are few. OBJECTIVE： To prepare models of acute optic nerve injury for observing the changes of neurons in lateral geniculate body, expression of neurofilament protein at different time after injury and cell apoptosis under the optical microscope, and for investigating the changes of neurons in lateral geniculate body following acute optic nerve injury. DESIGN： Completely randomized grouping design, controlled animal experiment. SETTING： Department of Neurosurgery, General Hospital of Ji＇nan Military Area Command of Chinese PLA. MATERIALS： Twenty-eight adult healthy cats of either gender and common grade, weighing from 2.0 to 3.5 kg, were provided by the Animal Experimental Center of Fudan University. The involved cats were divided into 2 groups according to table of random digit： normal control group （n=3） and model group （n=25）. Injury 6 hours, l, 3, 7 and 14 days five time points were set in model group for later observation, 5 cats at each time point. TUNEL kit （Bohringer-Mannheim company ）and NF200＆ Mr 68 000 mouse monoclonal antibody （NeoMarkers Company） were used in this experiment. METHODS： This experiment was carded out in the Department of Neurosurgery, General Hospital of Ji＇nan Military Area Command of Chinese PLA between June 2004 and June 2005.① The cats of model group were developed into cat models of acute intracranial optic nerve injury as follows： The anesthetized cats were placed in lateral position. By imitating operation to human, pterion approach was used. An incision was made at the joint line between outer canthus and tragus, and deepened along cranial base until white optic nerve via optic nerve pore and further to brain tissue. Optic nerve about 3 mm was liberated and occluded by noninvasive vascular clamp for 20 s. After removal of noninvasive vascular clamp, the area compressed by optic nerve was hollowed and narrowed, but non-fractured. Skull was closed when haemorrhage was not found. Bilateral pupillary size, direct and indirect light reflect were observed. Operative side pupil was enlarged as compared with opposite side, direct light reflect disappeared and indirect light reflect existed, which indicated that the models were successful. Animals of control group were not modeled .② The animals in the control group and model group were sacrificed before and 6 hours, 1, 3, 7 and 14 days after modeling respectively. Lateral geniculate body sample was taken and performed haematoxylin ＆ eosin staining. Immunohistochemical staining showed lateral geniculate body neurofilament protein expression, and a comparison of immunohistochemial staining results was made between experimental group and control group. Terminal deoxynucleo-tidyl transferase （TdT）-mediated dUTP-biotin nick end labeling （TUNEL） was used to label apoptotic cells in lateral geniculate body. MAIN OUTCOME MEASURES： Neuronal morphological change, neurofilament protein expression and cell apoptosis in lateral geniculate body following acute optic nerve injury. RESULTS： Twenty-eight involved cats entered the final analysis. ① Histological observation results： In the control group, cell processes were obviously found, which were few or shortening in the model group. ② Neuronal neurofilament protein expression： Cells in lateral geniculate body in the control group and at 6 hours after injury presented clear strip-shaped staining, and those at 7 and 14 days presented irregular distribution without layers and obviously decreasing staining intensity. The positive rate of neurofilament protein in lateral geniculate body in control group and 6 hours, l, 3, 7 and 14 days after injury was （ 10.22±0.42） %, （10.03±0.24） %, （9.94±0.14） %, （9.98±0.22） %, （8.18±0.34） % and （6.37±0.18）%, respectively. Positive rate of neurofilament protein in control group, at 6 hours, 1 or 3 days after injury was significantly different from that at 7 days after injury （P 〈 0.05）; Positive rate of neurofilament protein in control group, at 6 hours, 1, 3 or 7 days after injury was significantly different from that at 14 days after injury （P 〈 0.05）. It indicated that neuronal injury in lateral geniculate body was not obvious within short term after optic nerve injury, but obvious at 7 days after injury and progressively aggravated until at 14 days after injury.③ Neuronal apoptosis： TUNEL staining showed that neuronal apoptosis in lateral geniculate body appeared at 7 days after injury, and a Lot of neuronal apoptosis in lateral geniculate body was found at 14 days after injury. It indicated that neuronal injury in lateral geniculate body was related to apoptosis. CONCLUSION： In short term after optic nerve injury （within 7 days）, nerve injury of lateral geniculate body is not obvious, then, it will aggravate with the elongation of injury time. The occurrence of neuronal iniury of lateral geniculate body is related to the apoptosis of nerve cells.

Temporal properties of pattern adaptation of relay cells in the lateral geniculate nucleus of cats

The temporal properties of pattern adaptation of relay cells induced by repeated sinusoidal drifting grating were investigated in the dorsal lateral geniculate nucleus (dLGN) of cats. The results showed that the response amplitude declined and the response latency prolonged when relay cells were pattern-adapted in dLGN, like the similar findings in visual cortex. However, in contrast to the result in cortex, the response phase of relay cells advanced. This implies that an inhibition with relatively long latency may participate in the pattern adaptation of dLGN cells and the adaptation in dLGN may be via a mechanism different from that of visual cortex.

Characterization of Rebound Depolarization in Neurons of the Rat Medial Geniculate Body In Vitro

Rebound depolarization （RD） is a response to the offset from hyperpolarization of the neuronal mem- brane potential and is an important mechanism for the synaptic processing of inhibitory signals. In the present study, we characterized RD in neurons of the rat medial geniculate body （MGB）, a nucleus of the auditory thala- mus, using whole-cell patch-clamp and brain slices. RD was proportional in strength to the duration and magnitude of the hyperpolarization; was effectively blocked by Ni2＋ or Mibefradil; and was depressed when the resting membrane potential was hyperpolarized by blocking hyperpolarization-activated cyclic nucleotide-gated （HCN） channels with ZD7288 or by activating G-protein-gated inwardly-rectifying K＋ （GIRK） channels with baclofen. Our results demonstrated that RD in MGB neurons, which is carried by T-type Ca2＋ channels, is critically regulated by HCN channels and likely by GIRK channels.

Time-dependent changes in eye-specific segregation in the dorsal lateral geniculate nucleus and superior colliculus of postnatal mice

Eye-specific segregation in the dorsal lateral geniculate nucleus(dLGN) and superior colliculus(SC) starts from the embryonic stage and continues to develop postnatally until eye-opening in mice. However, there have been few systematic studies on the details of this developmental process. Here, we carried out time-dependent studies of eye-specific segregation in the dLGN and SC. Our results demonstrated that the development of eye-specific segregation in the SC is completed before postnatal day 12(P12), which is earlier than in the dLGN(P20). During the whole period, ipsilateral and overlapping axonal projections decreased continuously in both the dLGN and SC. On the other hand, contralateral axonal projections showed little change, except for a slight decrease between P8 and P20 in the dLGN.

Perigeniculate arachnoid cysts and CSF fistulae of the fallopian canal:Histopathologic correlates of a rare clinical entity

Cerebrospinal fluid(CSF)fistulae originating from the fallopian canal of the facial nerve is hypothesized to arise due to atypical patterns of subarachnoid space extension into the geniculate ganglion or more distal regions along the intratemporal course of the facial nerve,but its pathogenesis remains poorly understood.Although a rare etiology of CSF fistulae of the temporal bone,there are significant clinical ramifications due to the risk of recurrent meningitis,difficulty in identifying the anatomic location of the CSF leak,and technical challenges associated with surgical repair.We present three clinical cases of arachnoid cysts within the geniculate fossa with or without CSF fistulization and provide histopathologic correlates of this rare clinical phenomenon from a human temporal bone collection.The pediatric and adult patients presented suggest differential pathophysiologic mechanisms associated with CSF fistulae.Temporal bone histology reveals atypical patterns of subarachnoid space extension in the fallopian canal that may underlie arachnoid cyst formation and overt CSF leak from the geniculate region.

After hyperpolarization of relay neurons in lateral geniculate nucleus of cat

The action potential （Na+ spike） of neurons is often followed by a compound after hyperpolarization （AHP） which is mediated by Ca2+-dependent K+ channels. Pyramidal cells in the cerebral cortex are known to have fast, medium and slow AHPs. It is commonly accepted that the fast AHP （fAHP） is mediated by a kind of C- or BK-K+ channels. The fAHP is characterized by a short duration of about 20 ms, its remarkable voltage dependence and sensitivity to low concentration （【1 mmol/L） of Tetraethylammonium （TEA）.The mAHP results from activation of AHP- or SK-K+ channels and has a long duration over 200 ms. It is poorly voltage-dependent and blocked by Apamin, but not by TEA.

IPSP-EPSP interactions in lateral geniculate neurons of rat

It has been demonstrated that the lateral geniculate nucleus (LGN) of the cat possesses two types of inhibitory circuits: feedforward and recurrent inhibitory circuits. The results obtained from brain slice experiments have shown that the rat LGN also has the feedforward inhibitory circuit, which mediates an inhibitory postsynaptic potential (IPSP)

Kinetics of low threshold calcium channels of relay cells in cat lateral geniculate nucleus

Kinetics of the low threshold T-type Ca2+ channel is studied with single electrode voltage damp technique on brain slices of the cat lateral geniculate nucleus (LGN). Space damp is dramatically improved by blocking various K+ and Na+ channels, decreasing Ca2+ current and selecting proper holding potentials. Results from this study are similar to those obtained from acutely dissociated LGN neurons of the rat, indicating that the kinetics of T-Ca2+ channels of the cat LGN neurons is the same as that of the rat LGN. The result reported previously on the cat LGN may result from a defect in space damp.

A new anterograde trans-synaptic tracer based on Sindbis virus

Mapping neural circuits is critical for understanding the structure and function of the nervous system.Engineered viruses are a valuable tool for tracing neural circuits.However,current tracers do not fully meet the needs for this approach because of various drawbacks,such as toxicity and characteristics that are difficult to modify.Therefore,there is an urgent need to develop a new tracer with low toxicity and that allows for long-term studies.In this study,we constructed an engineered Sindbis virus(SINV)expressing enhanced green fluorescent protein(EGFP)reporter gene(SINV-EGFP)and found that it had no significant difference in biological characterization compared with the wild-type Sindbis virus in BHK-21 cells and neurons in vitro.We injected the virus into the visual circuit of mouse brain and found that the virus infected neurons in the local injected site and anterogradely spread in the neural circuits.Although the efficiency of transmission was limited,the findings demonstrate that SINV can be used as a new anterograde tracer to map neural circuits in mouse brain and that it spreads exclusively in the anterograde direction.Further,use of SINV in mouse brain research will provide longer time windows for circuit tracing than is possible with herpes simplex virus and vesicular stomatitis virus tracers.

Role of BDNF in the taste system

Neurotrophins are a family of proteins that regulate neural survival, development, function and plasticity in the central and the peripheral nervous system. There are four neurotrophins： NGF, BDNF, NT-3 and NT-4. Among them, BDNF is mostly studied in the taste system due to its high expression. Recent studies have shown BDNF play an important role in the developmental and mature taste system, by regulating survival of taste cells and geniculate ganglion neurons, and maintaining and guiding taste nerve innervations. These studies imply BDNF has great potentialities for therapeutic usage to enhance sensory regeneration following nerve injury, with aging, and in some neurodegenerative diseases.