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H Q Yan

Publications and source records attributed to H Q Yan.

At least 19 recordsLinked to original sources
PubMed2001

Tyrosine hydroxylase, but not dopamine beta-hydroxylase, is increased in rat frontal cortex after traumatic brain injury.

Chronic frontal lobe functional deficits after traumatic brain injury (TBI) may be associated with altered catecholamine systems in the frontal cortex. To test this, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) levels were examined by immunohistochemistry and Western blot at 1, 7, 14, and 28 days after TBI or sham surgery. No alterations in DBH levels were observed by Western blot at any time point examined, but there was a significant increase in TH expression 28 days after TBI (optical density 334 +/- 68% or 3.3-fold, ipsilateral and 218 +/- 39% or 2.2-fold, contralateral) relative to the sham controls. The increase in TH may reflect a compensatory response of dopaminergic neurons to upregulate their synthesizing capacity and increase the efficiency of dopamine neurotransmission chronically after TBI.

Animals↗
PubMed2001

Adenovirus-mediated transfer and expression of beta-gal in injured hippocampus after traumatic brain injury in mice.

In models of focal cerebral ischemia, adenoviral gene transfer is often attenuated or delayed versus naive. After controlled cortical impact (CCI)-induced traumatic brain injury in mice, CA1 and CA3 hippocampus exhibit delayed neuronal death by 3 days, with subsequent near complete loss of hippocampus by 21 days. We hypothesized that adenoviral-mediated expression of the reporter gene beta-Galactosidase (beta-Gal) in hippocampus would be attenuated after CCI in mice. C57BL6 mice (n = 16) were subjected to either CCI to left parietal cortex or sham (burr hole). Adenovirus carrying the beta-Gal gene (AdlacZ; 1 x 10(9) plaque-forming units [pfu]/mL) was then injected into left dorsal hippocampus. At 24 or 72 h, beta-Gal expression was quantified (mU/mg protein). Separate mice (n = 10) were used to study beta-Gal spatial distribution in brain sections. Beta-Gal expression in left hippocampus was similar in shams at 24 h (48.4 +/- 4.1) versus 72 h (68.8 +/- 8.8, not significant). CCI did not reduce beta-Gal expression in left hippocampus (68.8 +/- 8.8 versus 88.1 +/- 7.0 at 72 h, sham versus CCI, not significant). In contrast, CCI reduced beta-Gal expression in right (contralateral) hippocampus versus sham (p < 0.05 at both 24 and 72 h). Beta-Gal was seen in many cell types in ipsilateral hippocampus, including CA3 neurons. Despite eventual loss of ipsilateral hippocampus, adenovirus-mediated gene transfer was surprisingly robust early after CCI providing an opportunity to test novel genes targeting delayed hippocampal neuronal death.

Adenoviridae↗
PubMed2000

Evaluation of combined fibroblast growth factor-2 and moderate hypothermia therapy in traumatically brain injured rats.

Both the exogenous administration of fibroblast growth factor-2 (FGF-2) or the induction of moderate hypothermia have been shown to attenuate histopathology and improve functional outcome after traumatic brain injury (TBI). Since combined therapeutic strategies may be more beneficial than single therapies, we examined the potential synergistic effect of FGF-2 combined with moderate hypothermia treatment induced 10 min after TBI on functional and histological outcome following controlled cortical impact (CCI) injury. Fifty male Sprague-Dawley rats were randomized to one sham and four CCI treatment groups: Sham+vehicle (VEH); FGF-2 (45 microg/kg/h for 3 h i.v.)+Normothermia (37+/-0.5 degrees C); FGF-2+Hypothermia (32+/-0.5 degrees C for 3 h); VEH+Norm; VEH+Hypo. Vestibulomotor performance on the beam balance and beam-walk (BW) tasks on post-operative days 1-5 and spatial memory acquisition in the Morris water maze (MWM) on days 14-18 were assessed. After 4 weeks survival, histological evaluations (CA(1) and CA(3) cell counts and lesion volume) were performed. MWM performance improved in all treatment groups, but combined treatment was not more efficacious than either alone. The FGF-2+Hypo group performed significantly better than the other injured treatment groups in the BW task. Lastly, no significant group differences in beam balance or histological outcome were observed. These data suggest a suboptimal and incomplete synergy of combined FGF-2 and hypothermia treatment. These data may indicate that either our dose of FGF-2 or combination therapy was not optimized in our model.

Animals↗
PubMed2000

Chronic methylphenidate treatment enhances water maze performance following traumatic brain injury in rats.

Methylphenidate (MPH), a central nervous system stimulant with dopaminergic activity, facilitates neurobehavioral outcome following cortical suction ablation injury, but its potential efficacy following experimental traumatic brain injury (TBI) is unknown. Thus, beginning 24 h after controlled cortical impact injury or sham surgery, male Sprague-Dawley rats were injected (i.p.) once daily for 18 days with either MPH (5 mg/kg) or saline vehicle (VEH) and motor function assessed on post-operative days 1-4, followed by Morris water maze training to find a hidden platform on days 14-18. The MPH treatment regimen was ineffective in accelerating beam-balance or beam-walk recovery, but did significantly decrease swim latencies when compared to VEH-treated controls. The results are consistent with published studies showing improved outcome with MPH therapy. Furthermore, this positive finding with delayed treatment suggests that strategies that enhance catecholamine neurotransmission during the chronic post injury phase may be a useful adjunct in ameliorating some of the neurobehavioral sequelae following TBI in humans.

Analysis of Variance↗
PubMed1999

Vascular angiotensin II receptor and calcium signaling in toadfish.

The renin-angiotensin system evolved during the early evolution of vertebrates and regulates blood pressure/blood volume homeostasis in nonmammalian and mammalian vertebrates. Properties of vascular angiotensin (ANG) receptors and signal pathways in primitive animals are, however, not well understood. We aimed to determine whether vascular ANG II receptors in the toadfish, Opsanus tau, an aglomerular teleost, pharmacologically resemble either the ANG subtype 1 receptor (AT1) or the subtype 2 receptor (AT2) by examining (i) the effects of selective ANG receptor antagonists on ANG II-induced vasopressor action and binding and (ii) ANG II's effect on cytosolic Ca2+ signaling. [Asn1, Val5]ANG II (native teleost ANG II) dose-dependently increased the mean arterial pressure of conscious toadfish. ANG II-induced pressor responses (100-500 ng/kg) were inhibited substantially (79-83%) by [Sar1, Ile8]ANG II (5 microg x kg-1 + 5 microg x kg-1 x min-1) and moderately (34-53%) by losartan (AT1 antagonist, 10 mg/kg + 20 mg x kg-1 x h-1) and by PD 123319 (AT2 antagonist, 10 mg/kg + 20 mg x kg-1 x h-1) (36-60%). Likewise, the [Asp1, Val5, His9]ANG I-induced pressor effect was completely eliminated by an ANG I-converting enzyme inhibitor, SQ 14,225. Specific 125I-ANG II binding to vascular smooth muscle (VSM) membrane fractions was displaced completely by [Asn1, Val5]ANG II and [Sar1, Ile8]ANG II. Losartan, but not PD 123319, partly displaced ANG II binding at 10(-10)-10(-6) M. Furthermore, ANG II (10(-7) or 10(-8) M) caused a rapid, transient increase in the cytosolic Ca2+ signal (fluorescence ratio (FR) of 340/380 nm) of isolated VSM tissues measured by fura-2 and a dual wavelength fluorospectrometer, whereas extracellular K+ induced sustained, dose-dependent (P < 0.01) increases in FR. The results indicate that toadfish VSM tissues possess a rather nonselective ANG receptor; partial inhibition of ANG II binding by losartan and stimulation of cytosolic Ca2+ signaling by ANG II suggest that the receptor has some resemblance to AT1 homologous receptors.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1999

One-year study of spatial memory performance, brain morphology, and cholinergic markers after moderate controlled cortical impact in rats.

Persistent cognitive deficits are one of the most important sequelae of head injury in humans. In an effort to model some of the structural and neuropharmacological changes that occur in chronic postinjury brains, we examined the longitudinal effects of moderate vertical controlled cortical impact (CCI) on place learning and memory using the Morris water maze (MWM) test, morphology, and vesicular acetylcholine (ACh) transporter (VAChT) and muscarinic receptor subtype 2 (M2) immunohistochemistry. Vertical CCI (left parietal cortex, 4 m/sec, 2.5 mm; n = 10) or craniotomy (sham) was produced in male Sprague-Dawley rats (n = 10). Place learning was tested at 2 weeks, 4 weeks, 3 months, 6 months, and 12 months postinjury with the escape platform in a different maze quadrant for each time point. At each interval, rats received 5 days of water maze acquisition (latency to find hidden platform), a probe trial to measure place memory, and 2 days of visible platform trials to control for nonspecific deficits. At 3 weeks, half the animals were sacrificed for histology. At these injury parameters, CCI produced no significant differences in place learning between injured and sham rats at 2 weeks, 4 weeks, or 6 months after injury. However, at 3 and 12 months, the injured rats took significantly longer to find the hidden platform than the sham rats. Probe trial performance differed only at 12 months postinjury between injured (25.73+/-2.1%, standard error of the mean) and sham rats (44.09+/-7.0%, p < 0.05). The maze deficits at 1 year were not due to a worsening of performance, but may have resulted from a reduced ability of injured rats to benefit from previous water maze experience. Hemispheric loss of 30.4+/-5.5 mm3 was seen at 3 weeks after injury (versus respective sham). However, hemispheric loss almost doubled by 1 year after injury (51.5+/-8.5 mm3, p < 0.05 versus all other groups). Progressive tissue loss was also reflected by a three- to fourfold increase in ipsilateral ventricular volume between 3 weeks and 1 year after injury. At 1 year after injury, immunostaining for VAChT was dramatically increased in all sectors of the hippocampus and cortex after injury. Muscarinic receptor subtype 2 (M2) immunoreactivity was dramatically decreased in the ipsilateral hippocampus. This suggests a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission. Moderate CCI in rats produces subtle MWM performance deficits accompanied by persistent alteration in M2 and VAChT immunohistochemistry and progressive tissue atrophy. The inability of injured rats to benefit from repeated exposures to the MWM may represent a deficit in procedural memory that is independent of changes in hippocampal cholinergic systems.

Analysis of Variance↗
PubMed1999

Effect of traumatic brain injury in mice deficient in intercellular adhesion molecule-1: assessment of histopathologic and functional outcome.

Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule of the immunoglobulin family expressed on endothelial cells that is upregulated in brain as part of the acute inflammatory response to traumatic brain injury (TBI). ICAM-1 mediates neurologic injury in experimental meningitis and stroke; however, its role in the pathogenesis of TBI is unknown. We hypothesized that mutant mice deficient in ICAM-1 (-/-) would have decreased neutrophil accumulation, diminished histologic injury, and improved functional neurologic outcome versus ICAM-1 +/+ wild type control mice after TBI. Anesthetized ICAM-1 -/- mice and wild-type controls were subjected to controlled cortical impact (CCI, 6 m/sec, 1.2 mm depth). Neutrophils in brain parenchyma and ICAM-1 on vascular endothelium were assessed by immunohistochemistry in cryostat brain sections from the center of the contusion 24 h after TBI (n = 4/group). Separate groups of wild-type and ICAM-1-deficient mice (n = 9-10/group) underwent motor (wire grip test, days 1-5) and cognitive (Morris water maze [MWM], days 14-20) testing. Lesion volume was determined by image analysis 21 days following TBI. Robust expression of ICAM-1 was readily detected in choroid plexus and cerebral endothelium at 24 h in ICAM-1 +/+ mice but not in ICAM-1 -/- mice. No differences between groups were observed in brain neutrophil accumulation (9.4 +/- 2.2 versus 11.1 +/- 3.0 per x100 field, -/- versus +/+), wire grip score, MWM latency, or lesion volume (7.24 +/- 0.63 versus 7.21 +/- 0.45 mm3, -/- versus +/+). These studies fail to support a role for ICAM-1 in the pathogenesis of TBI.

Acute-Phase Reaction↗
PubMed1999

Differential effects of traumatic brain injury on vesicular acetylcholine transporter and M2 muscarinic receptor mRNA and protein in rat.

Experimental traumatic brain injury (TBI) produces cholinergic neurotransmission deficits that may contribute to chronic spatial memory deficits. Cholinergic neurotransmission deficits may result from presynaptic alterations in the storage and release of acetylcholine (ACh) or from changes in the receptors for ACh. The vesicular ACh transporter (VAChT) mediates accumulation of ACh into secretory vesicles, and the M2 muscarinic receptor subtype can modulate cholinergic neurotransmission via a presynaptic inhibitory feedback mechanism. We examined the effects of controlled cortical impact (CCI) injury on hippocampal VAChT and M2 muscarinic receptor subtype protein and medial septal mRNA levels at 4 weeks following injury. Rats were anesthetized and surgically prepared for CCI injury (4 m/sec, 2.5 to 2.9 mm in depth) and sham surgery. Animals were sacrificed, and coronal sections (35 microm thick) were cut through the dorsal hippocampus for VAChT and M2 immunohistochemistry. Semiquantitative measurements of VAChT and M2 protein in hippocampal homogenates from injured and sham rats were assessed with Western blot analysis. Changes in VAChT and M2 mRNA levels were evaluated by reverse transcriptase polymerase chain reaction (RT-PCR). At 4 weeks after injury, both immunohistochemical and Western blot methods demonstrated an increase in hippocampal VAChT protein. An increase in VAChT mRNA was also observed. Immunohistochemistry demonstrated a loss of M2; however, there was no significant change in M2 mRNA levels in comparison with sham controls. These changes may represent a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission chronically after TBI through differential transcriptional regulation.

Acetylcholine↗
PubMed1999

[Forensic pathology studies of sudden death caused by pulmonary embolism].

The analytic result of 50 sudden death cases caused by pulmonary embolism showed that their main causes were trauma (42%), heart diseases (32%), surgical operation (20%) and so on. In majority of these cases (80%), thrombus embolus came from deep veins of lower limbs, in some cases (20%) came from cardiac cavity. These cases occurred most frequently in the period of October to December and rarely in the period of April to June. Finally, some problems in forensic examination in this sort of sudden death were discussed in this article.

Adolescent↗
PubMed1998

Chronic effects of traumatic brain injury on hippocampal vesicular acetylcholine transporter and M2 muscarinic receptor protein in rats.

Experimental traumatic brain injury (TBI) produces cholinergic neurotransmission deficits that may contribute to chronic spatial memory deficits. Cholinergic neurotransmission deficits may be due to presynaptic alterations in the storage and release of acetylcholine (ACh) or from changes in the receptors for ACh. The vesicular ACh transporter (VAChT) mediates accumulation of ACh into secretory vesicles, and M2 receptors can modulate cholinergic neurotransmission via a presynaptic inhibitory feedback mechanism. We examined the effects of controlled cortical impact (CCI) injury on hippocampal VAChT and M2 muscarinic subtype receptor protein levels at four time points: 1 day, 1 week, 2 weeks, and 4 weeks following injury. Rats were anesthetized and surgically prepared for controlled cortical impact injury (4 m/s, 2.5- to 2.9-mm depth) and sham surgery. Animals were sacrificed and coronal sections (35 micro(m) thick) were cut through the dorsal hippocampus for VAChT and M2 immunohistochemistry. Semiquantitative measurements of VAChT and M2 protein in hippocampal homogenates from injured and sham rats were assessed using Western blot analysis. Immunohistochemistry showed no obvious changes in VAChT and M2 immunoreactivity at 1 day and 1 week postinjury. At 2 and 4 weeks postinjury, an increase in hippocampal VAChT protein and a corresponding loss of hippocampal M2 protein was observed compared to sham controls. Consistent with these results, Western blot analyses at 4 weeks postinjury demonstrated a 40-50% increase in VAChT and a 25-30% decrease in M2. These changes may represent a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission chronically after TBI, by upregulating the storage capacity and subsequent release of ACh and downregulating presynaptic inhibitory receptors.

Acetylcholine↗
PubMed1998

Control of vascular smooth muscle cell growth in fowl.

In adult domestic fowl, angiotensin (ANG) receptors are present in the vascular smooth muscles (VSM) and in the endothelium, mediating vasorelaxation via endothelium-derived relaxing factor/cGMP. ANG II-induced relaxation is minor in chicks and becomes more marked as they mature but diminishes in adult birds, whereas ANG II neither relaxes nor contracts endothelium-denuded aortae from mature chickens. The present study examines in cultured fowl aortic SM cells whether (1) ANG II stimulates or inhibits VSM cell growth and, if so, whether this growth-stimulatory or -inhibitory effect changes with maturation/aging, and (2) S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, and cGMP attenuate the basal or stimulated VSM cell growth. [Asp1, Val5]ANG II (native fowl ANG II, 10(-6) M) markedly increased (increase from vehicle control, 226.5%; P < 0.01) [3H]thymidine (Thd) incorporation into DNA of quiescent VSM cells (first subculture) from 6-week-old chicks. This growth-stimulating effect was reduced with age (41.4, 29.6, and 3.2% at 9, 19, and 43 weeks of age, respectively). In contrast, platelet-derived growth factor (PDGF, 20 ng/ml) increased [3H]Thd incorporation similarly in chicks, pullets, and hens. Furthermore, ANG II significantly (45.9%, P < 0.01) attenuated the growth-promoting effect of fetal calf serum in cultured VSM cells from 6-week-old chicks. This inhibitory effect also decreased in older birds. ANG II showed neither a growth-stimulatory nor -inhibitory effect in cultured neointimal cells. SNAP attenuated dose dependently (20-60 microM) the basal and PDGF-induced VSM cell growth, whereas cGMP inhibited basal growth only at a high dose (100 microM). These results indicate that in fowl VSM cells, ANG II is mitogenic and antimitogenic in chicks but not in mature birds, suggesting that phenotypic modulation occurs in the ANG receptors/signaling mechanism with maturation/age or in neointimal cells, whereas the mitogenic mechanism via PDGF remains in both young and mature birds.

Anesthesia↗
PubMed1998

New challenges of psychiatry: the development of mental health service in Shanghai.

Shanghai has a population of 13 million. In past two decades, three levels of the mental health service have been developed. It was to meet the needs of the city. Acute cases were hospitalized in time. Chronic cases were rehabilitated in community bases. All these are under the system of planning economics. In recent years, China conducted an economic reform. Shanghai was facing rapid development, psychological problems increased, the mental health service system was challenged by the market economics, insurance policy will practised. The reform of the health service system was performed in some areas. The economic constraints became the main problem for mental health facilities. In order to meet the needs of a variety of social strata, it will be necessary to develop different services: 'The hot line', 'crises intervention', 'family member association', 'psychological consulting', 'self-help groups', liaison-consultation psychiatry in general health care etc. Augment services will adapt to the development. The drive will be for healthy living styles to raise public awareness of mental health.

China↗
PubMed1996

Increased expression of brain-derived neurotrophic factor but not neurotrophin-3 mRNA in rat brain after cortical impact injury.

Levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) mRNA expression were measured in a rodent model of traumatic brain injury (TBI) following unilateral injury to the cerebral cortex. To obtain reliable data on the co-expression of neurotrophin genes, adjacent coronal sections from the same rat brains were hybridized in situ with BDNF and NT3 cRNA probes. BDNF mRNA increased at 1,3, and 5 hr after unilateral cortical injury in the cortex ipsilateral to the injury site and bilaterally in the dorsal hippocampus. NT3 mRNA did not change significantly following injury. Our results suggest that TBI produces rapid increases in BDNF mRNA expression in rat brain without changes in NT3 mRNA expression, a finding which differs from studies of ischemia and seizures. It is possible that increased levels of BDNF mRNA rather than NT3 are important components of pathophysiological responses to TBI.

Analysis of Variance↗
PubMed1996

NGF prevents the changes induced by monocular deprivation during the critical period in rats.

Photic evoked responses were recorded from the striate cortex of Long-Evans hooded intact, monocular visual deprivation (MD) and MD treated with NGF rats. The averaged visual evoked responses (AVER) were obtained from both hemispheres and provided comparison after binocular photic stimuli between the contralateral and the ipsilateral striate cortex with relation to the MD eye. One month of monocular visual deprivation at the critical period of development resulted in marked reduction of the amplitudes of AVER components as compared to the control recordings (P < 0.001). These changes of the AVER could be prevented by NGF infusion to lateral ventricle at the dosage of 2.0-2.4 micrograms/day for four weeks during the monocular deprivation. In conclusion, the change of AVER amplitudes induced by monocular visual deprivation during the critical period of development can be prevented by NGF infusion to lateral ventricle.

Animals↗
PubMed1995

Monocular visual deprivation at the critical period modulates photic evoked responses.

Photic evoked responses were recorded from the striate cortex of Long-Evans hooded normal (control) rats and from monocular visual deprivation (MD) rats. The averaged visual evoked responses (AVER) were obtained from both hemispheres and provide comparison between the contralateral and the ipsilateral striate cortex with relation to the monocular deprived eye. The AVER recorded following binocular photic stimulation after 1 month of monocular deprivation demonstrated that the two visual cortexes responded differently. In the contralateral hemisphere of the visual cortex (related to the MD eye), all three components (P2, N2 and P3) of the AVER of the MD rats had significant increases in their peak amplitude as compared to the control recordings. In the ipsilateral cortex, the amplitude of component P2 and N2 was significantly reduced as a result of 1 month of MD. Comparing the AVER amplitudes of the two homotopic sites of the visual cortex obtained from the control group reveals no differences between the two hemispheres but markedly significant differences in P2, N2 and P3 components for the MD group. Based on the literature, the possibility that the monocular visual deprivation at the critical period in early developmental stage modulates the AVER as a result from the neurocytological alteration from altering of GABA and ACh within the striate cortex was discussed. In conclusion, the AVER is a reliable and practical method for studying the effects of monocular deprivation and neuroplasticity in the rat visual cortex.

Animals↗
PubMed1995

Visual deprivation at the critical period modulates photic evoked responses.

Average visual evoked responses (AVER) were recorded from the striate cortex of normal (control) and monocular visually deprived Long-Evans hooded rats. One month of monocular visual deprivation (MD) at the critical period of development resulted in marked reduction of all the three AVER components (i.e., components P2, N2 and P3) as compared to the control recording (P < 0.001). In control animals, the AVER amplitudes of the two hemispheres were identical, while in MD rats, the P2 and N2 components of the AVER obtained from the hemisphere ipsilateral to the MD eye were markedly smaller than those of the AVER obtained from the contralateral hemisphere (P < 0.001). The latencies of the late components (N2 and P3) obtained from the hemisphere ipsilateral to the MD eyes were significantly delayed as compared to those from the contralateral hemisphere (P < 0.05 for N2, P < 0.01 for P3). The AVER following paired photic stimuli with various time intervals between the stimuli were used to study the neuronal recovery function of control animals compared to MD animals. The AVER to the second stimulus obtained from the MD rats exhibited greater attenuation in their amplitude responses than the AVER obtained from the control group, i.e., slower neuronal recovery. The neurophysiological changes observed in this study may relate to the neurocytological alteration occurring in the striate cortex following monocular visual deprivation at the critical period. In conclusion, AVER recorded from monocular visually deprived rats during the critical period is a simple and reliable electrophysiological animal model to study neuroplasticity during postnatal development.

Animals↗
PubMed1992

Expression of interleukin (IL)-1 beta, IL-6 and their respective receptors in the normal rat brain and after injury.

The expression of interleukin (IL)-1 beta, IL-6 and their respective receptors has been studied in the rat brain before and up to 24 h after injury. Messenger RNA transcripts of these four genes were detected by in situ hybridization (ISH) in different structures of the intact brain. The distribution was very similar for IL-1 beta, IL-6 and IL-6 receptor (IL-6R). The expression of IL-1R was more widespread. Within hours after injury, an increased expression of IL-1 beta, and thereafter of IL-6 was documented. The expression of IL-1R and IL-6R was also increased. This expression was bilateral and not restricted to the injured area. Within 24 h, all ISH patterns had returned to normal. The molecular data were confirmed by protein data. Indeed, the distribution of IL-6 (detected by immunocytochemistry) agreed with the ISH patterns for IL-6. Furthermore, extracellular fluid was collected by microdialysis at the site of the lesion during 12 h and successive fractions were assayed for the presence of bioactive IL-1 and IL-6. Increases in IL-1 and later in IL-6 levels were detected. The rapid and concomitant increased expression of IL-1 beta, IL-6 and their receptors after injury stresses their possible early role in inflammatory mechanisms also in the brain, before any recruitment of inflammatory cells from remote nervous and not nervous areas.

Animals↗