Abstract T MP2: Infarct Pattern After Reperfusion: A Voxel Based Analysis

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Daniel Antoniello ◽  
Jon Rosenberg
Keyword(s):  
Infarct Volume ◽  
Brain Regions ◽  
Endovascular Recanalization ◽  
Statistical Map ◽  
Mca Occlusion ◽  
Unsuccessful Treatment ◽  
Lesion Mapping ◽  
Lesion Topography ◽  
Group A ◽  
Unexplored Area

Background and purpose: Recanalization reduces final infarct volume, an important predictor of clinical outcome. Lesion location is also a determinant of outcome, however, the extent to which recanalization affects lesion topography has yet to be explored. Are there brain regions more likely to be spared if recanalization occurs? We investigated this question by using voxel-based lesion mapping to examine the effect of recanalization on infarct topography in middle cerebral artery (MCA) occlusion. Methods: Consecutive patients with acute stroke from MCA occlusion were examined to identify brain regions characteristically spared with recanalization (R+) (TICI 2a to 3), but damaged in patients with persistent occlusions (R-). The lesions were drawn directly on the MRI or CT images and then transformed into stereotaxic space using MRIcroN software. Lesions were superimposed to create voxel-based lesion plots for each group. A leibemeister test was performed comparing the two groups at every brain voxel, with Bonferroni correction. Results: Twenty-one patients were included: 11 had endovascular recanalization (R+) and 10 received no or unsuccessful treatment (R-). The figure shows the lesion overlay plots and the statistical map resulting from the analysis. In total, 5,250,682 voxels were tested, yielding a Bonferroni corrected P <0.05 threshold of Z=5.6. No voxels were significantly more likely to be spared with recanalization. Mean stroke volumes were not significantly different (R-138cc, R+164 cc, P>0.1). Conclusions: Our analysis did not reveal brain regions characteristically spared with recanalization. Prior studies have shown reduced infarct volume after recanalization; ours did not, and this may be the underlying reason why no salvage pattern was observed. The effect of recanalization on stroke topography remains an important, unexplored area. We have shown that voxel-based lesion mapping has potential as a biomarker in endovascular therapy.

scholarly journals Photothrombotic Occlusion of Rat Middle Cerebral Artery: Histopathological and Hemodynamic Sequelae of Acute Recanalization

1988 ◽  
Vol 8 (3) ◽  
pp. 357-366 ◽  
Author(s):  
Hitoshi Nakayama ◽  
W. Dalton Dietrich ◽  
Brant D. Watson ◽  
Raul Busto ◽  
Myron D. Ginsberg
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cortical Neurons ◽  
Cell Damage ◽  
Thrombus Formation ◽  
Infarct Volume ◽  
Brain Regions ◽  
Mca Occlusion ◽  
Temporary Occlusion ◽  
Mixed Pattern

The histopathological and hemodynamic consequences of photochemically induced middle cerebral artery (MCA) thrombosis and recanalization were studied in the rat. Recanalization of the thrombosed MCA segment was achieved by the topical application of nimodipine at 1 h following photochemically induced occlusion. Pathological consequences of permanent and temporary occlusion were compared by morphometric procedures 7 days following thrombus formation. Rats with permanent thrombosis exhibited consistent infarction of both striatum and cortex. MCA recanalization at 1 h was associated with a significant reduction in total infarct volume. In recanalized rats, small cortical infarcts, confined to the peripheral MCA territory, were observed in only three of six rats. In contrast, a mixed pattern of infarction and ischemic cell damage was documented throughout the striatum in all rats. Local CBF (ICBF), measured autoradiographically, was significantly reduced in the MCA territory following 1 h of MCA occlusion, especially within the striatum. At 1 h after recanalization, lCBF recovered within the previously ischemic brain regions to >50% of control. Perfusion deficits were detected by carbon black infusion within focal areas of the striatum following reperfusion. Thus, cortical neurons appear to tolerate 1 h of MCA occlusion in this model. In contrast, reperfusion following 1 h of photochemically induced MCA occlusion gives rise to selective injury to the striatum.

scholarly journals Delayed (6h) Intracarotid Treatment with TNK-tPA Improves Neurological Functional Recovery after Embolic Stroke in the Unanesthetized Rat

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 352-353
Author(s):  
Ruilan Zhang ◽  
Li Zhang ◽  
Anton Goussev ◽  
Michael Chopp
Keyword(s):  
Functional Recovery ◽  
Internal Carotid ◽  
Infarct Volume ◽  
Control Group ◽  
Animal Body ◽  
Mca Occlusion ◽  
Body Weights ◽  
Before And After ◽  
Group A ◽  
Adhesive Removal

P76 We tested the hypothesis that delayed intra-arterial administration of TNK-tPA increases functional recovery in a model of focal cerebral embolic ischemia in the unanesthetized rat. Male unanesthetized Wistar rats (n=22) were subjected to middle cerebral artery (MCA) occlusion using a single fibrin rich clot. TNK-tPA (1.5 mg/kg) was administered intraarterially via an internal carotid catheter at 2 h (n=4), 4 h (n=6) or 6 h (n=6) after MCA occlusion. Non-treated ischemic rats (n=6) were used as a control group. A battery of tests (1. Rotarod test, 2. Adhesive-removal test and 3. Footfault test) was used to evaluate neurological function. Animal body weights were measured before and after MCA occlusion. All rats were sacrificed 28 days after ischemia. Infract volume and gross hemorrhage was measured. Intra-arterial treatment with TNK-tPA at 2h after ischemia significantly (p<0.01) reduced infarct volume (18.6“2.6 % of the contralateral hemisphere) and improved neurological functional recovery compared with the control rats (37.5 ”0.7%). Although infarct volumes were not significantly reduced for rats treated with intra-arterial TNK-tPA at 4h (31.2“3.1 %) and at 6h (32.9”3.1 %) after ischemia, significant (p<0.05) improvements on sensorimotor functions (adhesive removal test at 4, 14, 21, and 28 d ) and significant increases in animal body weight (7 d) were detected in rats treated with TNK-tPA at 4 h and 6h. Gross hemorrhage was 25% (2h), 33% (4h) and 33% (6h), which was not significantly different from gross hemorrhage in the control group (17 %). This study demonstrates that intra-carotid treatment with TNK-tPA even at 6h of the onset of stroke improves neurological functional recovery from brain damage without significantly increasing the incidence of intra-cerebral hemorrhage in the unanesthetized ischemic rat.

Abstract WP90: Voxel-Based Lesion Symptom Mapping (VLSM) of NIH Stroke Scale Subscore Deficits

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Margy E McCullough-Hicks ◽  
Soren Christensen ◽  
Yannan Yu ◽  
Gregory W Albers
Keyword(s):  
Infarct Volume ◽  
Reperfusion Therapy ◽  
Brain Regions ◽  
Sensory Loss ◽  
Future Research ◽  
Limb Weakness ◽  
T Score ◽  
Left Limb ◽  
Lesion Topography ◽  
Lesion Symptom Mapping

Background: Studies identifying brain regions required to preserve specific neurologic functions after stroke typically analyze infarct volume or location. Lesion topography studies have found that, independent of volume, involvement of specific regions have greater impact on clinical outcome than others, suggesting location-determined differences in eloquence. However, most anatomy-based studies define location broadly. VLSM is an imaging analysis technique that establishes a relationship between precise lesion location and clinical deficit. A group of patients with a symptom (e.g. aphasia) is analyzed; every voxel on each patient’s MRI is evaluated for lesion presence or absence. Each voxel is assigned a t-statistic, and a statistical map of all lesioned voxels is generated to pinpoint regions most strongly associated with the deficit; a high t-score indicates a lesion in that voxel has a significant effect on the specified symptom. We generated VLSM maps for 6 NIHSS subscores (aphasia, right- and left-limb weakness, and sensory loss) in a novel characterization to be used in future research. Methods: 172 acute ischemic stroke (AIS) patients with large vessel occlusions (LVOs) were analyzed. Binary masks of infarcts on D5 FLAIR sequences were created. Lesions were coregistered to standard MNI atlas space. VLSM V2.55 was used to generate statistical maps of lesion contribution to clinical deficit. Maps were thresholded to p<0.001 on basis of cluster size and permutation method. A symptom reference area was defined as a region on which voxels had a t-score >3.14. Results: VLSM maps with voxelwise thresholds of p<0.001 were generated for 6 NIHSS categories (examples in figure). Conclusions: VLSM successfully generated unique maps of 6 NIHSS subscore deficits. These maps will be used to study patients presenting with perfusion/diffusion mismatch to predict the potential for resolution of specific deficits with reperfusion therapy and aid in prognostication.

Abstract WMP41: Neuronal Sirt1 is Required for Resveratrol Preconditioning Induced Ischemic Tolerance

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Kevin B Koronowski ◽  
Isa Saul ◽  
Zachary Balmuth-Loris ◽  
Miguel Perez-Pinzon
Keyword(s):  
Knockout Mouse ◽  
Infarct Volume ◽  
Hypoxia Inducible Factor ◽  
Brain Regions ◽  
Artery Occlusion ◽  
Ischemic Tolerance ◽  
Tamoxifen Treatment ◽  
Neurological Score ◽  
Transcription Factor Activation ◽  
Cerebral Artery Occlusion

Introduction: Our previous work demonstrates that resveratrol, a naturally occurring polyphenol, protects against cerebral ischemia when administered 2 or 14 days prior to injury. Resveratrol activates Sirt1, an NAD + -dependent deacylase that regulates cellular metabolism. It has been postulated that neuronal Sirt1 directly mediates this neuroprotection but it remains to be empirically tested. Objective: The objective of this study was to generate an inducible, neuronal-specific Sirt1 knockout mouse and determine whether neuronal Sirt1 is necessary for resveratrol-induced ischemic tolerance. Methods: Twenty to twenty-five gram neuronal-specific Sirt1 knockout mice (Sirt1neu-/-) and WTs were induced with tamoxifen. Mice were randomized for 1) western blot; 2) resveratrol preconditioning (RPC; 10 mg/kg resveratrol i.p.) or vehicle (1.5% DMSO; 0.9% saline) treatment 2 days prior to 60 minute middle cerebral artery occlusion (MCAo); 3) untargeted primary metabolomics by GC-TOF-MS; or 4) transcription factor activation profiling. Twenty-four hours following MCAo, neurological score was used to assess functional outcome and infarct volume was quantified by TTC staining. Results: Tamoxifen treatment removed WT Sirt1 protein from major brain regions but not from heart (Figure 1A, n=3). In WT, RPC reduced infarct volume by 43.7% and improved neurological score by nearly 3 points, however these effects were lost in Sirt1neu-/- (Figure 1B, n=5-9). Compared to WT, metabolic profiles from Sirt1neu-/- displayed significantly altered glycolysis metabolites (Figure 1C, n=8). Activation of hypoxia inducible factor (HIF) was reduced by 48% in Sirt1neu-/- (Figure 1D, n=3). Conclusions: We generated and utilized an inducible, neuronal-specific knockout mouse to demonstrate that neuronal Sirt1 specifically is required for RPC-induced ischemic tolerance. Additionally, Sirt1 regulates glycolysis in the brain, possibly through its interaction with HIF.

Abstract P730: MCA Stroke Chronically Disrupts Hippocampal Activity and Cortico-Hippocampal Communication

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Zachary Ip ◽  
Gratianne Rabiller ◽  
Jiwei He ◽  
Shivalika Chavan ◽  
Yasuo Nishijima ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Memory Function ◽  
Brain Regions ◽  
Male Rats ◽  
Brain State ◽  
Signal Power ◽  
Hippocampal Function ◽  
Electrode Arrays ◽  
Mca Occlusion ◽  
Hippocampal Activity

Introduction: Cognition and memory deficits are common sequelae following middle cerebral artery (MCA) stroke, one of the most common strokes in humans. However MCA stroke does not compromise the structural integrity of the hippocampus, which is highly involved in memory function, because the MCA does not supply blood flow to the hippocampus. We previously reported on the acute effect of MCA stroke, where we observed increased hippocampal activity and cortico-hippocampal communication. Here we investigate chronic changes to local oscillations and cortico-hippocampal communication following MCA occlusion in rats two weeks and one month following stroke. Hypothesis: Cortical stroke affects remote brain regions, disrupting hippocampal function and cortico-hippocampal communication. Methods: We subjected male rats (n=28) to distal MCA occlusion compared to controls (n=19). We recorded local field potentials simultaneously from cortex and hippocampus two weeks and one month following stroke using 16-site linear electrode arrays under urethane anesthesia. We analyzed signal power, brain state, CFC, and sharp wave SPW-Rs to assess hippocampal function and cortico-hippocampal communication. Results: Our results show disruptions to local oscillations; lowered delta (1-3 Hz) signal power in the cortex and hippocampus, increased signal power in gamma (30-60 Hz) and high gamma (60-200 Hz) in cortex and hippocampus. Theta/delta brain state is disrupted, and SPW-Rs increase in power at two weeks, before returning to baseline levels at one month. Communication is also disrupted; Theta-gamma coupling, a measure of information being communicated between regions, breaks down after stroke. Conclusions: These results suggest that chronic stroke causes significant changes to hippocampal function, which can be characterized by these electrophysiological biomarkers, establishing putative targets for targeted stimulation therapies.

scholarly journals Cerebrovascular Hemodynamics and Ischemic Tolerance: Lipopolysaccharide-Induced Resistance to Focal Cerebral Ischemia is not Due to Changes in Severity of the Initial Ischemic Insult, but is Associated with Preservation of Microvascular Perfusion

1999 ◽  
Vol 19 (6) ◽  
pp. 616-623 ◽  
Author(s):  
Deborah A. Dawson ◽  
Kazuhide Furuya ◽  
Jun Gotoh ◽  
Yasuaki Nakao ◽  
John M. Hallenbeck
Keyword(s):  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Ischemic Injury ◽  
Ischemic Tolerance ◽  
Microvascular Perfusion ◽  
Saline Control ◽  
Ischemic Insult ◽  
Mca Occlusion ◽  
Induced Tolerance ◽  
Tissue Sparing

Lipopolysaccharide (LPS), administered 72 hours before middle cerebral artery (MCA) occlusion, confers significant protection against ischemic injury. For example, in the present study, LPS (0.9 mg/kg intravenously) induced a 31% reduction in infarct volume (compared with saline control) assessed 24 hours after permanent MCA occlusion. To determine whether LPS induces true tolerance to ischemia, or merely attenuates initial ischemic severity by augmenting collateral blood flow, local CBF was measured autoradiographically 15 minutes after MCA occlusion. Local CBF did not differ significantly between LPS- and saline-pretreated rats (e.g., 34 ± 10 and 29 ± 15 mL·100 g−1·min−1 for saline and LPS pretreatment in a representative region of ischemic cortex), indicating that the neuroprotective action of LPS is not attributable to an immediate reduction in the degree of ischemia induced by MCA occlusion, and that LPS does indeed induce a state of ischemic tolerance. In contrast to the similarity of the initial ischemic insult between tolerant (LPS-pretreated) and nontolerant (saline-pretreated) rats, microvascular perfusion assessed either 4 hours or 24 hours after MCA occlusion was preserved at significantly higher levels in the LPS-pretreated rats than in controls. Furthermore, the regions of preserved perfusion in tolerant animals were associated with regions of tissue sparing. These results suggest that LPS-induced tolerance to focal ischemia is at least partly dependent on the active maintenance of microvascular patency and hence the prevention of secondary ischemic injury.

scholarly journals Value of infarct location in the prediction of functional outcome in patients with an anterior large vessel occlusion: results from the HERMES study

2021 ◽  
Author(s):  
Manon L. Tolhuisen ◽  
Marielle Ernst ◽  
Anne M. M. Boers ◽  
Scott Brown ◽  
Ludo F. M. Beenen ◽  
...  
Keyword(s):  
Functional Outcome ◽  
Medical Management ◽  
Infarct Volume ◽  
Binary Logistic Regression ◽  
Brain Regions ◽  
Favorable Outcome ◽  
Vessel Occlusion ◽  
C Statistic ◽  
Strength Of Association

Abstract Purpose Follow-up infarct volume (FIV) is moderately associated with functional outcome. We hypothesized that accounting for infarct location would strengthen the association of FIV with functional outcome. Methods We included 252 patients from the HERMES collaboration with follow-up diffusion weighted imaging. Patients received endovascular treatment combined with best medical management (n = 52%) versus best medical management alone (n = 48%). FIV was quantified in low, moderate and high modified Rankin Scale (mRS)-relevant regions. We used binary logistic regression to study the relation between the total, high, moderate or low mRS-relevant FIVs and favorable outcome (mRS < 2) after 90 days. The strength of association was evaluated using the c-statistic. Results Small lesions only occupied high mRS-relevant brain regions. Lesions additionally occupied lower mRS-relevant brain regions if FIV expanded. Higher FIV was associated with a higher risk of unfavorable outcome, as were volumes of tissue with low, moderate and high mRS relevance. In multivariable modeling, only the volume of high mRS-relevant infarct was significantly associated with favorable outcome. The c-statistic was highest (0.76) for the models that included high mRS-relevant FIV or the combination of high, moderate and low mRS-relevant FIV but was not significantly different from the model that included only total FIV (0.75). Conclusion This study confirms the association of FIV and unfavorable functional outcome but showed no strengthened association if lesion location was taken into account.

scholarly journals ARL 17477, a Potent and Selective Neuronal NOS Inhibitor Decreases Infarct Volume after Transient Middle Cerebral Artery Occlusion in Rats

1996 ◽  
Vol 16 (4) ◽  
pp. 599-604 ◽  
Author(s):  
Zheng G. Zhang ◽  
David Reif ◽  
James Macdonald ◽  
Wen Xue Tang ◽  
Dietgard K. Kamp ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Cerebral Artery Occlusion

We tested the effects of administration of a selective neuronal nitric oxide synthase (nNOS) inhibitor, ARL 17477, on ischemic cell damage and regional cerebral blood flow (rCBF), in rats subjected to transient (2 h) middle cerebral artery (MCA) occlusion and 166 h of reperfusion (n = 48) and in rats without MCA occlusion (n = 25), respectively. Animals were administered ARL 17477 (i.v.): 10 mg/kg; 3 mg/kg; 1 mg/kg; N-nitro-L-arginine (L-NA) 10 mg/kg L-NA 1 mg/kg; and Vehicle. Administration of ARL 17477 1 mg/kg, 3 mg/kg and 10 mg/kg reduced ischemic infarct volume by 53 (p < 0.05), 23, and 6.5%, respectively. L-NA 1 mg/kg and 10 mg/kg increased infarct volume by 2 and 15%, respectively (p > 0.05). Administration of ARL 17477 (10 mg/kg) significantly (p < 0.05) decreased rCBF by 27 ± 5.3 and 24 ± 14.08% and cortical NOS activity by 86 ± 14.9 and 91 ± 8.9% at 10 min or 3 h, respectively, and did not alter mean arterial blood pressure (MABP). L-NA (10 mg/kg) significantly reduced rCBF by 23 ± 9.8% and NOS activity by 81 ± 7% and significantly (p < 0.05) increased MABP. Treatment with 3 mg/kg and 1 mg/kg ARL 17477 reduced rCBF by only 2.4 ± 4.5 and 0%, respectively, even when NOS activity was reduced by 63 ± 13.4 and 45 ± 15.7% at 3 h, respectively, (p < 0.05). The data demonstrate that ARL 17477 inhibits nNOS in the rat brain and causes a dose-dependent reduction in infarct volume after transient MCA occlusion.

Abstract W P14: Endovascular Treatment for M2 Occlusions. A Descriptive Multicenter Experience on Behalf of the Catalan Stroke Code and Reperfusion Consortium (Cat-SCR).

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Alan Flores ◽  
Alejandro Tomasello ◽  
Pere Cardona ◽  
M Anges De Miquel ◽  
Meritxell Gomis ◽  
...  
Keyword(s):  
Endovascular Treatment ◽  
Infarct Volume ◽  
Hemorrhagic Transformation ◽  
Favourable Outcome ◽  
Routine Practice ◽  
Dramatic Improvement ◽  
Good Outcome ◽  
Mca Occlusion ◽  
Mean Time

Background: Patients with M2-MCA occlusion are not always considered for endovascular treatment. We aimed to study patients with an M2 occlusion treated with endovascular procedures. Methods: We studied patients prospectively included in the SONIIA register (January 2011-December 2012), a mandatory and externally audited register that monitors quality of reperfusion therapies in Catalonia under routine practice conditions. Baseline characteristics including NIHSS and occlusion location were collected. Complete recanalization was defined as a post-procedure TICI>2a, dramatic recovery: NIHSS drop>10 points or NIHSS<2 and good outcome as mRS<3 at 3 months. 24 hours CT scan determined the presence of hemorrhagic transformation (ECASS criteria) and infarct volume. Results: Of the 571 registered patients that received endovascular treatment, 65 (11.4%) presented an M2 occlusion on initial angiogram: mean age 66±15, female 47.7% median pre-procedure NIHSS 16(IQR:6). Mean time from symptom onset to groin puncture was 289±195 minutes, 35 patients (54%) received iv tPA before the procedure. Patients were treated with mechanic thrombectomy (n=49, 75.4%), ia tPA (n=3, 4.6%), both (n=7, 10.8%) or only diagnostic angiogram (n=6, 9.2%) according to interventionalist preferences. Patients who achieved complete recanalization (78.5%) had more often dramatic improvement (48% Vs 14.8%, p=0.023) smaller infarct volumes (8 vs. 82cc, p=0.013) and better outcome (66.3% Vs 30%; p=0.032) than those who did not recanalize. Rate of SICH was 9%. Independent predictors of dramatic improvement was complete recanalization (OR: 0,169 p=0.03 CI95%: 0.034-0.838) adjusted for age and baseline NIHSS Independent predictors of good outcome at 3 months were age (OR 1.067 p=0.033 CI95%: 1.005-1132) and baseline NIHSS (OR: 1.162 p=0.007 CI95%: 1.041-1.297) Conclusion: Endovascular treatment of M2 MCA occlusion seems safe. Induced recanalization may double the chances to achieve a favourable outcome

Subacute administration of tributyltin chloride modulates neurotransmitters and their metabolites in discrete brain regions of maternal mice and their F1 offspring

2006 ◽  
Vol 22 (1) ◽  
pp. 15-25 ◽  
Author(s):  
Masashi Tsunoda ◽  
Yoshiharu Aizawa ◽  
Nobuhiro Konno ◽  
Kimiko Kimura ◽  
Yoshiko Sugita-Konishi
Keyword(s):  
Brain Regions ◽  
The Body ◽  
Developmental Neurotoxicity ◽  
Control Group ◽  
Icr Mice ◽  
Adult Mice ◽  
Tributyltin Chloride ◽  
Hydroxyindoleacetic Acid ◽  
Group A ◽  
The Central Nervous System

Tributyltin (TBT) compounds have been used as anti-fouling agents and the central nervous system is one of its target organs. TBT-induced modulations of neurotransmitters in the brains of adult mice have been reported. However, little is known about the developmental neurotoxicity of TBT. In this study, we evaluated the effects of TBT on neurotransmitters and their metabolites in discrete brain regions of female ICR mice and their offspring. Pregnant ICR mice were exposed to TBT chloride at concentrations of 0, 15 or 50 ppm in water or 125 ppm in food. Male offspring were sacrificed at one, two and three weeks after birth. The concentrations of norepinephrine, dopamine (DA), dihydoxyphenylacetic acid, homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) were determined in different brain regions by HPLC. All offspring from the 125 ppm group died immediately after birth. A significant decrease in the body weight of the TBT-treated F1 groups compared to the control group was observed in the first week. Significant increases compared to the controls were observed for the DA concentration in the striatum of the 50 ppm F1 group, and for the HVA concentration in the cerebrum and the 5-HT concentration in the medulla oblongata of the 15 and 50 ppm F1 groups in the third week. At three weeks of age, the neurotransmitters and their metabolites may be useful indexes for developmental neurotoxicity. For the dams, a significant decrease in the 5-HT concentration was observed in the cerebellum, medulla, midbrain and striatum of the 125 ppm group compared to the control group. A significant decrease in the 5-HIAA concentration was also observed in the cerebellum, midbrain and striatum of the dams in the 125 ppm group compared to the control. TBT may induce a decrease in the synthesis of 5-HT in the dams. The discrepancy between dams and offspring may be due to several factors such as age, dose, route, sex and pregnancy.

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