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Journal articles on the topic 'Monkey; Brain; Neurology'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Nakai, Mitsukazu, Toru Itakura, Ichiro Kamei, Kunio Nakai, Yutaka Naka, Harumichi Imai, and Norihiko Komai. "Autologous transplantation of the superior cervical ganglion into the brain of parkinsonian monkeys." Journal of Neurosurgery 72, no. 1 (January 1990): 91–95. http://dx.doi.org/10.3171/jns.1990.72.1.0091.

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✓ The effect of autologous transplantation of the superior cervical ganglion (SCG) into the brain of parkinsonian monkeys was studied through quantitative measurement of animal behavior. The motor activity of the monkey was measured with a telemetry system during the experiment. After experimental parkinsonism was induced by repeated intravenous injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), three monkeys were treated with autologous transplantation of the SCG into both caudate nuclei. One monkey served as a control without SCG transplantation after MPTP treatment. Three SCG-transplanted monkeys showed biphasic (acute and chronic) behavioral amelioration of parkinsonism after transplantation. In the acute stage, the animals showed transient hyperkinesia with aggressive behavior and loss of circadian rhythm. In the chronic stage following acute hyperkinesia, the animals regained normal behavior and circadian rhythm without aggressiveness. In contrast with the transplanted monkeys, the control monkey failed to show recovery of the bradykinesia and muscle rigidity.

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2

Fleischer, Jerry E., William L. Lanier, James H. Milde, and John D. Michenfelder. "Lidoflazine Does Not Improve Neurologic Outcome When Administered after Complete Cerebral Ischemia in Primates." Journal of Cerebral Blood Flow & Metabolism 7, no. 3 (June 1987): 366–71. http://dx.doi.org/10.1038/jcbfm.1987.74.

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In order to investigate the effects of the calcium entry blocker lidoflazine on neurologic outcome in primates following an episode of global brain ischemia. 12 pigtail monkeys ( Macaca nemestrina) were subjected to 17 min of complete cerebral ischemia, followed by 48 h of intensive care treatment and daily neurologic evaluations for 96 h. The monkeys were randomly assigned to receive, in a blind fashion, either lidoflazine 1.0 mg/kg (n = 6) or inactive lidoflazine solvent (n = 6) at 5 min, 8 h, and 16 h postischemia. One monkey in the lidoflazine group did not meet preestablished protocol criteria and was excluded from data analysis. The remaining monkeys were well matched for age, sex, and other physiologic variables. Neurologic outcome was not significantly different between the lidoflazine- and placebo-treated groups (p > 0.5). No monkey in either group achieved a normal neurologic exam by 96 h postischemia. Three lidoflazine-treated monkeys and two placebo-treated monkeys died prior to the 96-h neurologic evaluation. These deaths were judged to be neurologic in origin. The authors conclude that lidoflazine does not improve neurologic outcome in primates when administered after 17 min of complete cerebral ischemia.

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3

Tabuchi, Kazuo, Akira Nishimoto, Kengo Matsumoto, Toru Satoh, Susumu Nakasone, Takashi Fujiwara, and Hajime Ogura. "Establishment of a brain-tumor model in adult monkeys." Journal of Neurosurgery 63, no. 6 (December 1985): 912–16. http://dx.doi.org/10.3171/jns.1985.63.6.0912.

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✓ A brain-tumor model in adult monkeys may be significant because of the biological similarity to humans as well as the feasibility for surgical manipulation and for sequential computerized tomography (CT) scanning. In the present study, brain tumors were successfully produced in Japanese monkeys (Macaca fuscata), each weighing 2 to 10.8 kg, with an average age of 5.1 years old. Tumor cells were implanted by intracerebral inoculation of 4 × 107 chick embryo fibroblasts infected with the Schmidt-Ruppin strain of Rous sarcoma virus (RSV). With a 15- to 67-day latency, brain tumors were induced in 11 (73.3%) of 15 RSV-inoculated monkeys. Contrast-enhanced CT scans delineated all solitary intracerebral tumors greater than 4 to 6 mm in diameter. The CT images were proved at autopsy to be accurate within 2 mm in determining the size of tumor. Five of the 11 monkeys with intracerebral tumors died, with an average survival time of 26.6 days after RSV inoculation. The induced tumors were classified as either glioma or sarcoma by the presence or absence of glial fibrillary acidic protein (GFAP) and S-100 protein. A chromosome analysis of cultured tumor cells showed a diploid number of 42, indicating monkey origin. It is concluded that the reproducible brain tumor in the adult Japanese monkey inoculated with RSV can serve as a good experimental brain-tumor model for the further study of human malignant brain tumors.

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4

Obayashi, Shigeru, Tetsuya Suhara, Koichi Kawabe, Takashi Okauchi, Jun Maeda, Yoshihide Akine, Hirotaka Onoe, and Atsushi Iriki. "Functional Brain Mapping of Monkey Tool Use." NeuroImage 14, no. 4 (October 2001): 853–61. http://dx.doi.org/10.1006/nimg.2001.0878.

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5

Hossmann, K. A., and B. Grosse Ophoff. "Recovery of Monkey Brain after Prolonged Ischemia. I. Electrophysiology and Brain Electrolytes." Journal of Cerebral Blood Flow & Metabolism 6, no. 1 (February 1986): 15–21. http://dx.doi.org/10.1038/jcbfm.1986.3.

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Adult normothermic monkeys were submitted to 1 h of total cerebral ischemia, followed by blood recirculation for 1.5–24 h. During ischemia EEG and evoked potentials were suppressed within 12 s and 3 min, respectively. Upon recirculation, high-voltage EEG bursts began to reappear after 82–125 min, followed by gradual return of continuous background activity and near normalization of EEG frequency pattern within 24 h. Somatically evoked potentials, in contrast, exhibited only partial recovery, and consciousness did not return during the observation period. At the end of the experiments, tissue contents of sodium, potassium, calcium, and magnesium were measured in the gray and white matter of parietal lobe by atomic absorption spectros-copy. Gray matter sodium content gradually increased by ∼50% from 41.0 to 59.8 μmol/g wet wt during 24 h of recirculation. The other electrolytes including calcium did not change during the observation period. Postisch-emic recovery reported in this and the accompanying article is attributed to careful control of postischemic general physiological state and prevention or treatment of postischemic complicating side effects such as postischemic brain edema, hypotension, acidosis, pulmonary distress, and anuria. No specific drug treatment such as application of calcium antagonists or metabolic inhibitors was necessary to achieve this effect.

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6

MATSUMI, Nobuhiko, Kengo MATSUMOTO, Nobuya MISHIMA, Eiji MORIYAMA, Tomohisa FURUTA, Akira NISHIMOTO, and Kohji TAGUCHI. "Thermal Damage Threshold of Brain Tissue —Histological Study of Heated Normal Monkey Brains—." Neurologia medico-chirurgica 34, no. 4 (1994): 209–15. http://dx.doi.org/10.2176/nmc.34.209.

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7

NAKAGAWA, Minoru, Kengo MATSUMOTO, Hisato HIGASHI, Tomohisa FURUTA, and Takashi OHMOTO. "Acute Effects of Interstitial Hyperthermia on Normal Monkey Brain." Neurologia medico-chirurgica 34, no. 10 (1994): 668–75. http://dx.doi.org/10.2176/nmc.34.668.

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8

Wagner, Kenneth R., and Ronald E. Myers. "Topography of brain metabolites: Rhesus monkey, goat, and cat." Experimental Neurology 89, no. 1 (July 1985): 146–58. http://dx.doi.org/10.1016/0014-4886(85)90272-9.

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9

GHILARDI, M. FELICE, IVAN BODIS-WOLLNER, MARCO C. ONOFRJ, MARCIA S. MARX, and ANDREW A. GLOVER. "SPATIAL FREQUENCY-DEPENDENT ABNORMALITIES OF THE PATTERN ELECTRORETINOGRAM AND VISUAL EVOKED POTENTIALS IN A PARKINSONIAN MONKEY MODEL." Brain 111, no. 1 (1988): 131–49. http://dx.doi.org/10.1093/brain/111.1.131.

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10

KANAZAWA, ICHIRO, MINORU KIMURA, MIHO MURATA, YOSHIHARU TANAKA, and FUMIAKI CHO. "CHOREIC MOVEMENTS IN THE MACAQUE MONKEY INDUCED BY KAINIC ACID LESIONS OF THE STRIATUM COMBINED WITH L-DOPA." Brain 113, no. 2 (1990): 509–35. http://dx.doi.org/10.1093/brain/113.2.509.

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11

Kilbourn, Michael R., B. Hockley, L. Lee, and R. A. Koeppe. "Successful [18F]FEOBV imaging of the VAChT in monkey brain." NeuroImage 41 (January 2008): T93. http://dx.doi.org/10.1016/j.neuroimage.2008.04.062.

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12

Hashimoto, Nobuo, Choegon Kim, Haruhiko Kikuchi, Masayuki Kojima, Yoo Kang, and Fumitada Hazama. "Experimental induction of cerebral aneurysms in monkeys." Journal of Neurosurgery 67, no. 6 (December 1987): 903–5. http://dx.doi.org/10.3171/jns.1987.67.6.0903.

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✓ Saccular cerebral aneurysms were successfully induced in two monkeys treated with ligation of the common carotid artery, experimental hypertension, and β-aminopropionitrile feeding. The cerebral aneurysms developed on the large arteries at the base of the brain, such as the anterior communicating artery and the internal carotid artery at the origin of the posterior communicating artery. Because of the similarity of the monkey to man as a species, the present results strongly suggest the significance of postnatal aggravating factors in the development of cerebral aneurysms in man.

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13

HOCHERMAN, SHRAGA, and RAZ YIRMIYA. "NEURONAL ACTIVITY IN THE MEDIAL GENICULATE NUCLEUS AND IN THE AUDITORY CORTEX OF THE RHESUS MONKEY REFLECTS SIGNAL ANTICIPATION." Brain 113, no. 6 (1990): 1707–20. http://dx.doi.org/10.1093/brain/113.6.1707.

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14

Stone, James L., Ramsis F. Ghaly, Kodanallur S. Subramanian, Peter Roccaforte, and James Kane. "Transtentorial Brain Herniation in the Monkey: Analysis of Brain Stem Auditory and Somatosensory Evoked Potentials." Neurosurgery 26, no. 1 (January 1990): 26–31. http://dx.doi.org/10.1227/00006123-199001000-00003.

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15

Pineda, J. A., T. C. Holmes, D. Swick, and S. L. Foote. "Brain-stem auditory evoked potentials in squirrel monkey (Saimiri sciureus)." Electroencephalography and Clinical Neurophysiology 73, no. 6 (December 1989): 532–43. http://dx.doi.org/10.1016/0013-4694(89)90262-9.

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16

Zhou, Xiaoyun, Bin Ji, Chie Seki, Yuji Nagai, Takafumi Minamimoto, Masayuki Fujinaga, Ming-Rong Zhang, et al. "PET imaging of colony-stimulating factor 1 receptor: A head-to-head comparison of a novel radioligand, 11C-GW2580, and 11C-CPPC, in mouse models of acute and chronic neuroinflammation and a rhesus monkey." Journal of Cerebral Blood Flow & Metabolism 41, no. 9 (March 24, 2021): 2410–22. http://dx.doi.org/10.1177/0271678x211004146.

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Colony-stimulating factor 1 receptor (CSF1R) is a specific biomarker for microglia. In this study, we developed a novel PET radioligand for CSF1R, 11C-GW2580, and compared it to a reported CSF1R tracer, 11C-CPPC, in mouse models of acute and chronic neuroinflammation and a rhesus monkey. Dynamic 11C-GW2580- and 11C-CPPC-PET images were quantified by reference tissue-based models and standardized uptake value ratio. Both tracers exhibited increased uptake in the lesioned striata of lipopolysaccharide-injected mice and in the forebrains of AppNL-G-F/NL-G-F-knock-in mice, spatially in agreement with an increased 18-kDa translocator protein radioligand retention. Moreover, 11C-GW2580 captured changes in CSF1R availability more sensitively than 11C-CPPC, with a larger dynamic range and a smaller inter-individual variability, in these model animals. PET imaging of CSF1R in a rhesus monkey displayed moderate-to-high tracer retention in the brain at baseline. Homologous blocker (i. e. unlabeled tracer) treatment reduced the uptake of 11C-GW2580 by ∼30% in all examined brain regions except for centrum semi-ovale white matter, but did not affect the retention of 11C-CPPC. In summary, our results demonstrated that 11C-GW2580-PET captured inflammatory microgliosis in the mouse brain with higher sensitivity than a reported radioligand, and displayed saturable binding in the monkey brain, potentially providing an imaging-based quantitative biomarker for reactive microgliosis.

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17

Boraud, Thomas, Erwan Bezard, Bernard Bioulac, and Christian E. Gross. "Dopamine agonist-induced dyskinesias are correlated to both firing pattern and frequency alterations of pallidal neurones in the MPTP-treated monkey." Brain 124, no. 3 (March 2001): 546–57. http://dx.doi.org/10.1093/brain/124.3.546.

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18

Escola, L., Th Michelet, F. Macia, D. Guehl, B. Bioulac, and P. Burbaud. "Disruption of information processing in the supplementary motor area of the MPTP-treated monkey: A clue to the pathophysiology of akinesia?" Brain 126, no. 1 (January 1, 2003): 95–114. http://dx.doi.org/10.1093/brain/awg004.

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19

King, Christopher, Timothy Robinson, C. Edward Dixon, Gutti R. Rao, Donald Larnard, and C. Edwin M. Nemoto. "Brain Temperature Profiles during Epidural Cooling with the ChillerPad in a Monkey Model of Traumatic Brain Injury." Journal of Neurotrauma 27, no. 10 (October 2010): 1895–903. http://dx.doi.org/10.1089/neu.2009.1178.

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20

Kawamoto, Yasuhiro, Shinichi Nakamura, Toshio Kawamata, Ichiro Akiguchi, and Jun Kimura. "Cellular localization of brain-derived neurotrophic factor-like immunoreactivity in adult monkey brain." Brain Research 821, no. 2 (March 1999): 341–49. http://dx.doi.org/10.1016/s0006-8993(99)01082-3.

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21

Ohba, Hiroyuki, Norihiro Harada, Shingo Nishiyama, Takeharu Kakiuchi, Yuichi Kimura, and Hideo Tsukada. "Feedback-Controlled Bolus plus Infusion (FC-B/I) Method for Quantitative Drug Assessment in Living Brain with PET." Journal of Cerebral Blood Flow & Metabolism 33, no. 1 (September 12, 2012): 85–90. http://dx.doi.org/10.1038/jcbfm.2012.134.

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We have developed a feedback-controlled bolus plus infusion (FC-B/I) method for monitoring the interaction between positron emission tomography (PET) ligands and their specific target molecules with PET. The usefulness of the FC-B/I method was evaluated by the direct interaction between [11C]raclopride, a dopamine D2 receptor (D2R) ligand, and cold raclopride (10 and 100 μg/kg) in the brains of conscious monkeys. The present results demonstrated that the FC-B/I method could achieve the equilibrium state of [11C]raclopride in the striatum of monkey brain, and also that the cold raclopride-induced reduction of [11C]raclopride binding to D2R was observed in a dose-dependent manner. Good correlations of distribution volume ratio of the striatum to cerebellum between the conventional bolus plus infusion (B/I) method and the FC-B/I method as well as between the conventional bolus injection method and the FC-B/I method were observed. These results indicated that the system could be a useful tool for the evaluation of interaction between drug candidates and their target molecules like enzymes, receptors, and transporters by using of their specific PET ligands.

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22

Gregoriou, Georgia G., and Helen E. Savaki. "When vision guides movement: a functional imaging study of the monkey brain." NeuroImage 19, no. 3 (July 2003): 959–67. http://dx.doi.org/10.1016/s1053-8119(03)00176-9.

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23

Yasuno, Fumihiko, S. Zoghbi, Mc Julie, M. Ichise, R. Gladding, A. Brown, J. Bacher, V. Pike, and R. Innis. "Quantification of serotonin 5-HT1A receptors in monkey brain with [11C](−)-RWAY." NeuroImage 31 (January 2006): T98. http://dx.doi.org/10.1016/j.neuroimage.2006.04.085.

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24

Nagasaka, Kazuaki, Ichiro Takashima, Keiji Matsuda, and Noriyuki Higo. "Brain activity changes in a monkey model of central post-stroke pain." Experimental Neurology 323 (January 2020): 113096. http://dx.doi.org/10.1016/j.expneurol.2019.113096.

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25

Alekseichuk, I., K. Mantell, S. Shirinpour, and A. Opitz. "Translational non-invasive brain stimulation from mouse to monkey to human." Brain Stimulation 12, no. 2 (March 2019): 476. http://dx.doi.org/10.1016/j.brs.2018.12.552.

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26

Bodsch, W., A. Barbier, M. Oehmichen, B. Grosse Ophoff, and K. A. Hossmann. "Recovery of Monkey Brain after Prolonged Ischemia. II. Protein Synthesis and Morphological Alterations." Journal of Cerebral Blood Flow & Metabolism 6, no. 1 (February 1986): 22–33. http://dx.doi.org/10.1038/jcbfm.1986.4.

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Recovery of protein synthesis following 1 h of complete ischemia of the monkey brain was assessed by 3H-labeled amino acid incorporation in vivo at various postischemic periods between 1.5 and 24 h. The regional autoradiographic patterns obtained were compared on the basis of precursor-product relationships determined biochemically at the end of the tracer incorporation studies. Shortly after ischemia, protein synthesis was severely inhibited, but it gradually recovered with increasing recirculation times. In the cerebellum it returned to almost normal levels within 3 h and in the cortex within 24 h. Hippocampal and thalamic regions, however, did not recover control levels of protein synthesis at 24 h. His-toautoradiographic evaluation of amino acid incorporation in individual neurons revealed recovery of pyramidal neurons in the CA1 and CA3 sectors of the hippocampus within 6 h of recirculation, which, however, was followed by secondary inhibition after longer recirculation. Neurons in cortical layer 5 steadily recovered to near control within 24 h, with the exception of those located in arterial border zones, which returned to only 50% of control at 24 h. Incomplete recovery was also observed in thalamic neurons and Purkinje cells. The regional and histoauto-radiographic pattern of protein synthesis correlated with the morphological appearance of cells. Ischemic cell changes (mainly of the dark type with microvacuolization and perineuronal glial swelling) were marked after short recirculation times but gradually disappeared in parallel with the return of protein synthesis in most regions of the brain. Only in pyramidal cells of the hippocampus, thalamic neurons, and Purkinje cells were changes not reversed during the observation period. The results obtained corroborate the electrophysiological observations reported in the first part of this investigation and support the notion that the majority of the neurons of monkey brain survive complete cerebrocirculatory arrest of 1 h for at least 1 day.

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27

Mercer, L. D., P. M. Beart, M. K. Horne, D. I. Finkelstein, P. Carrive, and G. Paxinos. "On the distribution of cholecystokinin B receptors in monkey brain." Brain Research 738, no. 2 (November 1996): 313–18. http://dx.doi.org/10.1016/s0006-8993(96)00477-5.

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28

Doudet, Doris J., Catherine A. McLellan, Richard Carson, H. Richard Adams, Hitoshi Miyake, Thomas G. Aigner, Ronald T. Finn, and Robert M. Cohen. "Distribution and Kinetics of 3-O-Methyl-6-[18F]fluoro-L-DOPA in the Rhesus Monkey Brain." Journal of Cerebral Blood Flow & Metabolism 11, no. 5 (September 1991): 726–34. http://dx.doi.org/10.1038/jcbfm.1991.129.

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Most attempts to model accurately [18F]-DOPA imaging of the dopamine system are based on the assumptions that its main peripheral metabolite, 3-O-methyl-6-[18F]fluoro-L-DOPA ([18F]3-OM-DOPA), crosses the blood-brain barrier but is present as a homogenous distribution throughout the brain, in part because it is not converted into [18F]DOPA in significant quantities. These assumptions were based mainly on data in rodents. Little information is available in the primate. To verify the accuracy of the above assumptions, we administered 18F-labeled 3-OM-DOPA to normal rhesus monkeys and animals with lesions of the DA nigrostriatal system. No selective 18F regional accumulation in brain was apparent in normal or lesioned animals. The plasma metabolite analysis revealed that only the negatively charged metabolites (e.g., sulfated conjugates) that do not cross the blood-brain barrier were found in significant quantities in the plasma. A one-compartment, three-parameter model was adequate to describe the kinetics of [18F]3-OM-DOPA. In conclusion, assumptions concerning [18F]3-OM-DOPA's behavior in brain appear acceptable for [18F]DOPA modeling purposes.

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29

Wang, Xingxing, Tianna Zhou, George D. Maynard, Pramod S. Terse, William B. Cafferty, Jeffery D. Kocsis, and Stephen M. Strittmatter. "Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury." Brain 143, no. 6 (May 6, 2020): 1697–713. http://dx.doi.org/10.1093/brain/awaa116.

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Abstract After CNS trauma such as spinal cord injury, the ability of surviving neural elements to sprout axons, reorganize neural networks and support recovery of function is severely restricted, contributing to chronic neurological deficits. Among limitations on neural recovery are myelin-associated inhibitors functioning as ligands for neuronal Nogo receptor 1 (NgR1). A soluble decoy (NgR1-Fc, AXER-204) blocks these ligands and provides a means to promote recovery of function in multiple preclinical rodent models of spinal cord injury. However, the safety and efficacy of this reagent in non-human primate spinal cord injury and its toxicological profile have not been described. Here, we provide evidence that chronic intrathecal and intravenous administration of NgR1-Fc to cynomolgus monkey and to rat are without evident toxicity at doses of 20 mg and greater every other day (≥2.0 mg/kg/day), and far greater than the projected human dose. Adult female African green monkeys underwent right C5/6 lateral hemisection with evidence of persistent disuse of the right forelimb during feeding and right hindlimb during locomotion. At 1 month post-injury, the animals were randomized to treatment with vehicle (n = 6) or 0.10–0.17 mg/kg/day of NgR1-Fc (n = 8) delivered via intrathecal lumbar catheter and osmotic minipump for 4 months. One animal was removed from the study because of surgical complications of the catheter, but no treatment-related adverse events were noted in either group. Animal behaviour was evaluated at 6–7 months post-injury, i.e. 1–2 months after treatment cessation. The use of the impaired forelimb during spontaneous feeding and the impaired hindlimb during locomotion were both significantly greater in the treatment group. Tissue collected at 7–12 months post-injury showed no significant differences in lesion size, fibrotic scar, gliosis or neuroinflammation between groups. Serotoninergic raphespinal fibres below the lesion showed no deficit, with equal density on the lesioned and intact side below the level of the injury in both groups. Corticospinal axons traced from biotin-dextran-amine injections in the left motor cortex were equally labelled across groups and reduced caudal to the injury. The NgR1-Fc group tissue exhibited a significant 2–3-fold increased corticospinal axon density in the cervical cord below the level of the injury relative to the vehicle group. The data show that NgR1-Fc does not have preclinical toxicological issues in healthy animals or safety concerns in spinal cord injury animals. Thus, it presents as a potential therapeutic for spinal cord injury with evidence for behavioural improvement and growth of injured pathways in non-human primate spinal cord injury.

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30

Brem, Henry, Rafael J. Tamargo, Alessandro Olivi, Michael Pinn, Jon D. Weingart, Moody Wharam, and Jonathan I. Epstein. "Biodegradable polymers for controlled delivery of chemotherapy with and without radiation therapy in the monkey brain." Journal of Neurosurgery 80, no. 2 (February 1994): 283–90. http://dx.doi.org/10.3171/jns.1994.80.2.0283.

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✓ Sustained drug delivery by biodegradable polymer devices can increase the therapeutic efficacy of drugs by producing high local tissue concentrations over extended periods of time. It has been shown previously that implantation of controlled-release polymers impregnated with the nitrosourea carmustine (BCNU) extended the period of survival in rats bearing the 9L glioma compared with similar rats treated with systemically administered BCNU. This study evaluated the effect on the monkey brain of interstitial delivery of BCNU by the biodegradable polyanhydride copolymer poly[bis(p-carboxyphenoxy)propane]anhydride (PCPP) and sebacic acid (SA) in a 20:80 formulation (PCPP:SA). The effect of combining interstitial BCNU with radiation therapy was also evaluated. Eighteen male cynomologus monkeys were randomly assigned to one of four groups: a control group; a group with implantation of empty polymer; a group with implantation of BCNU-loaded polymer; and a group with implantation of empty polymer in the right hemisphere and BCNU-loaded polymer in the left hemisphere, followed by irradiation. The effects were evaluated radiologically and histologically at specified times. A local reaction by the brain to the polymer was found, which was greater when the polymer contained BCNU. Local cerebral edema was observed radiographically on postoperative Day 14 and had resolved by Day 72. Histologically, a subacute cellular inflammatory response was seen on postoperative Day 16, which had changed to a chronic inflammatory response by Day 72. In the group with radiation therapy administered to the hemisphere bearing BCNU-loaded polymer, only localized pathological changes were detected. In all animals, brain distant from the polymer implantation site was normal. No neurological or general deleterious effects were seen in any of the animals. It is concluded that the interstitial delivery of BCNU by the polyanhydride polymer PCPP:SA is safe in the primate brain and that concomitant radiation therapy did not lead to any adverse effects. These experimental findings are important to an understanding of the clinical effects of PCPP:SA implants in treating brain diseases.

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31

Kawamura, Kazunori, Yuichi Kimura, Hideo Tsukada, Tadayuki Kobayashi, Shingo Nishiyama, Takeharu Kakiuchi, Hiroyuki Ohba, et al. "An increase of sigma1 receptors in the aged monkey brain." Neurobiology of Aging 24, no. 5 (September 2003): 745–52. http://dx.doi.org/10.1016/s0197-4580(02)00152-5.

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32

Koehler, Raymond C., Zeng-Jin Yang, Jennifer K. Lee, and Lee J. Martin. "Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy." Journal of Cerebral Blood Flow & Metabolism 38, no. 12 (August 28, 2018): 2092–111. http://dx.doi.org/10.1177/0271678x18797328.

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Perinatal hypoxia-ischemia resulting in death or lifelong disabilities remains a major clinical disorder. Neonatal models of hypoxia-ischemia in rodents have enhanced our understanding of cellular mechanisms of neural injury in developing brain, but have limitations in simulating the range, accuracy, and physiology of clinical hypoxia-ischemia and the relevant systems neuropathology that contribute to the human brain injury pattern. Large animal models of perinatal hypoxia-ischemia, such as partial or complete asphyxia at the time of delivery of fetal monkeys, umbilical cord occlusion and cerebral hypoperfusion at different stages of gestation in fetal sheep, and severe hypoxia and hypoperfusion in newborn piglets, have largely overcome these limitations. In monkey, complete asphyxia produces preferential injury to cerebellum and primary sensory nuclei in brainstem and thalamus, whereas partial asphyxia produces preferential injury to somatosensory and motor cortex, basal ganglia, and thalamus. Mid-gestational fetal sheep provide a valuable model for studying vulnerability of progenitor oligodendrocytes. Hypoxia followed by asphyxia in newborn piglets replicates the systems injury seen in term newborns. Efficacy of post-insult hypothermia in animal models led to the success of clinical trials in term human neonates. Large animal models are now being used to explore adjunct therapy to augment hypothermic neuroprotection.

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33

Beal, M. Flint, Michael F. Mazurek, and Joseph B. Martin. "A comparison of somatostatin and neuropeptide Y distribution in monkey brain." Brain Research 405, no. 2 (March 1987): 213–19. http://dx.doi.org/10.1016/0006-8993(87)90290-3.

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34

Letourneau, R., J. J. Rozniecki, V. Dimitriadou, and T. C. Theoharides. "Ultrastructural evidence of brain mast cell activation without degranulation in monkey experimental allergic encephalomyelitis." Journal of Neuroimmunology 145, no. 1-2 (December 2003): 18–26. http://dx.doi.org/10.1016/j.jneuroim.2003.09.004.

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35

Tsukada, Hideo, Hiroyuki Ohba, Shingo Nishiyama, Masakatsu Kanazawa, Takeharu Kakiuchi, and Norihiro Harada. "PET Imaging of Ischemia-Induced Impairment of Mitochondrial Complex I Function in Monkey Brain." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (January 22, 2014): 708–14. http://dx.doi.org/10.1038/jcbfm.2014.5.

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To assess the capability of 18F-2-tert-butyl-4-chloro-5-{6-[2-(2-fluoroethoxy)-ethoxy]-pyridin-3-ylmethoxy}-2H-pyridazin-3-one (18F-BCPP-EF), a novel positron emission tomography (PET) probe for mitochondrial complex I (MC-I) activity, as a specific marker of ischemia-induced neuronal death without being disturbed by inflammation, translational research was conducted using an animal PET in ischemic brains of Cynomolgus monkeys ( Macaca fascicularis). Focal ischemia was induced by the right middle cerebral artery occlusion for 3 hours, then PET scans were conducted at Day-7 with 15O-gases for regional cerebral blood flow (rCBF) and regional cerebral metabolism of oxygen (rCMRO2), and 18F-BCPP-EF for MC-I with arterial blood sampling. On Day-8, the additional PET scans conducted with 11C-flumazenil (11C-FMZ) for central-type benzodiazepine receptors, 11C-PBR28 for translocator protein, and 18F-fluoro-2-deoxy-D-glucose (18F-FDG) for regional cerebral metabolic rate of glucose (rCMRglc). The total distribution volume ( VT) values of 18F-BCPP-EF showed the significant reduction in MC-I activity in the damaged area at Day-7. When correlated with rCBF and rCMRO2, the VT values of 18F-BCPP-EF provided better correlation with rCMRO2 than with rCBF. In the inflammatory regions (region of interest, ROIPBR) of the ischemic hemisphere detected with 11C-PBR28, higher 18F-FDG uptake and lower VT of 18F-BCPP-EF, 11C-FMZ, and rCMRO2 than those in normal contralateral hemisphere were observed. These results strongly suggested that 18F-BCPP-EF could discriminate the neuronal damaged areas with neuroinflammation, where 18F-FDG could not owing to its high uptake into the activated microglia.

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Branston, N. M., P. Bentivoglio, F. Momma, and L. Symon. "Changes in pyramidal tract conduction with experimental brain-stem ischaemia in the monkey." Electroencephalography and Clinical Neurophysiology 69, no. 5 (May 1988): 469–75. http://dx.doi.org/10.1016/0013-4694(88)90069-7.

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Hahn, Gerald, Gorka Zamora-López, Lynn Uhrig, Enzo Tagliazucchi, Helmut Laufs, Dante Mantini, Morten L. Kringelbach, Bechir Jarraya, and Gustavo Deco. "Signature of consciousness in brain-wide synchronization patterns of monkey and human fMRI signals." NeuroImage 226 (February 2021): 117470. http://dx.doi.org/10.1016/j.neuroimage.2020.117470.

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Kamasak, Mustafa, E. Morris, C. Bouman, and B. Christian. "Direct reconstruction of sinograms to parametric images of 18F-fallypride binding in monkey brain." NeuroImage 31 (January 2006): T92. http://dx.doi.org/10.1016/j.neuroimage.2006.04.079.

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Cui, Ding, and Koen Nelissen. "Examining cross-modal fMRI adaptation for observed and executed actions in the monkey brain." NeuroImage 233 (June 2021): 117988. http://dx.doi.org/10.1016/j.neuroimage.2021.117988.

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MITCHELL, I. J., M. A. SAMBROOK, and A. R. CROSSMAN. "SUBCORTICAL CHANGES IN THE REGIONAL UPTAKE OF [3H]-2-DEOXYGLUCOSE IN THE BRAIN OF THE MONKEY DURING EXPERIMENTAL CHOREIFORM DYSKINESIA ELICITED BY INJECTION OF A GAMMA-AMINOBUTYRIC ACID ANTAGONIST INTO THE SUBTHALAMIC NUCLEUS." Brain 108, no. 2 (1985): 405–22. http://dx.doi.org/10.1093/brain/108.2.405.

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41

Wenk, Gary L., Donna J. Pierce, Robert G. Struble, Donald L. Price, and Linda C. Cork. "Age-related changes in multiple neurotransmitter systems in the monkey brain." Neurobiology of Aging 10, no. 1 (January 1989): 11–19. http://dx.doi.org/10.1016/s0197-4580(89)80005-3.

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42

Starr, Philip A., Thyagarajan Subramanian, Roy A. E. Bakay, and Thomas Wichmann. "Electrophysiological localization of the substantia nigra in the parkinsonian nonhuman primate." Journal of Neurosurgery 93, no. 4 (October 2000): 704–10. http://dx.doi.org/10.3171/jns.2000.93.4.0704.

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✓ During ablative surgery and implantation of deep-brain stimulators for the treatment of movement disorders, electrophysiological techniques are often used for localization of subcortical targets. New restorative therapies for Parkinson disease, aimed at delivering drugs or cells to the substantia nigra (SN), are becoming available. Therefore, precise surgical approaches to the dopaminergic cell—containing region of the SN are required to avoid damage to nearby structures such as the corticospinal tract and subthalamic nucleus. In a study conducted in nonhuman primates, the authors evaluated the utility and accuracy of electrophysiological techniques in localizing the SN.Three adult rhesus monkeys were used as hosts for intranigral cell transplants. The monkeys were rendered hemiparkinsonian by intracarotid injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. With the aid of stereotactic guidance, chronic recording chambers were placed on the skull of each monkey and directed at the SN. In each monkey, 20 to 40 trajectories were explored with a microelectrode. Spontaneous and movement-related single-unit activities were recorded in the SN, pars reticulata, subthalamic nucleus, globus pallidus, striatum, thalamus, and red nucleus. Motor and ocular responses to microstimulation in the subthalamic area were noted. Using the electrophysiological and stereotactic information that was obtained, three-dimensional maps of the nigral complex were constructed to infer the location of the SN pars compacta. The maps were subsequently used to guide intranigral placement of fetal dopaminergic cells. Accurate delivery was verified by histological analysis.Based on the characteristic electrophysiological properties of the SN and surrounding structures in the parkinsonian state, microelectrode recording techniques may be used to ensure accurate placement of cell transplantation in the intranigral region.

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Takeda, Y., M. Kobayashi, H. Taninishi, T. Sasaki, M. Arai, and K. Morita. "Pharyngeal cooling decreases brain temperature and intracranial pressure during resuscitation in monkey." Journal of Neurosurgical Anesthesiology 18, no. 4 (October 2006): 326. http://dx.doi.org/10.1097/00008506-200610000-00124.

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Farde, L., B. Andrée, N. Ginovart, C. Halldin, and S. O. Thorberg. "PET determination of robalzotan occupancy of 5-HT1A receptors in the monkey brain." European Neuropsychopharmacology 8 (November 1998): S168. http://dx.doi.org/10.1016/s0924-977x(98)80214-9.

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Kaufman, Marc C., and Bertha K. Madras. "[3H]CFT ([3H]win 35,428) accumulation in dopamine regions of monkey brain: comparison of a mature and an aged monkey." Brain Research 611, no. 2 (May 1993): 322–25. http://dx.doi.org/10.1016/0006-8993(93)90519-s.

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Tsubokura, Shogo, Yasuyoshi Watanabe, Hiroaki Ehara, Kazuvuki Imamura, Osamu Sugimoto, Hirovuki Kagamiyama, Shozo Yamamoto, and Osamu Hayaishi. "Localization of prostaglandin endoperoxide synthase in neurons and glia in monkey brain." Brain Research 543, no. 1 (March 1991): 15–24. http://dx.doi.org/10.1016/0006-8993(91)91043-z.

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Laćan, Goran, Antonio A. F. De Salles, Alessandra A. Gorgulho, Scott E. Krahl, Leonardo Frighetto, Eric J. Behnke, and William P. Melega. "Modulation of food intake following deep brain stimulation of the ventromedial hypothalamus in the vervet monkey." Journal of Neurosurgery 108, no. 2 (February 2008): 336–42. http://dx.doi.org/10.3171/jns/2008/108/2/0336.

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Object Deep brain stimulation (DBS) has become an effective therapy for an increasing number of brain disorders. Recently demonstrated DBS of the posterior hypothalamus as a safe treatment for chronic intractable cluster headaches has drawn attention to this target, which is involved in the regulation of diverse autonomic functions and feeding behavior through complex integrative mechanisms. In this study, the authors assessed the feasibility of ventromedial hypothalamus (VMH) DBS in freely moving vervet monkeys to modulate food intake as a model for the potential treatment of eating disorders. Methods Deep brain stimulation electrodes were bilaterally implanted into the VMH of 2 adult male vervet monkeys by using the stereotactic techniques utilized in DBS in humans. Stimulators were implanted subcutaneously on the upper back, allowing ready access to program stimulation parameters while the animal remained conscious and freely moving. In anesthetized animals, intraoperatively and 6–10 weeks postsurgery, VMH DBS parameters were selected according to minimal cardiovascular and autonomic nervous system responses. Thereafter, conscious animals were subjected to 2 cycles of VMH DBS for periods of 8 and 3 days, and food intake and behavior were monitored. Animals were then killed for histological verification of probe placement. Results During VMH DBS, total food consumption increased. The 3-month bilateral implant of electrodes and subsequent periods of high-frequency VMH stimulation did not result in significant adverse behavioral effects. Conclusions This is the first study in which techniques of hypothalamic DBS in humans have been applied in freely moving nonhuman primates. Future studies can now be conducted to determine whether VMH DBS can change hypothalamic responsivity to endocrine signals associated with adiposity for long-term modulation of food intake.

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HIGASHI, Hisato, Kengo MATSUMOTO, Minoru NAKAGAWA, Tomohisa FURUTA, and Takashi OHMOTO. "192Ir Induced Radiation Damage in Monkey Brain Assessed with Magnetic Resonance Imaging and Histological Examination." Neurologia medico-chirurgica 35, no. 9 (1995): 639–47. http://dx.doi.org/10.2176/nmc.35.639.

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Gao, Yang, Azma Mareyam, Yi Sun, Thomas Witzel, Nicolas Arango, Irene Kuang, Jacob White, et al. "A 16-channel AC/DC array coil for anesthetized monkey whole-brain imaging at 7T." NeuroImage 207 (February 2020): 116396. http://dx.doi.org/10.1016/j.neuroimage.2019.116396.

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Chefer, Svetlana, B. Le Foll, A. Kimes, D. Shumway, V. Kurian, S. R. Goldberg, E. Stein, and A. Mukhin. "Quantification of α4β2* nicotinic acetylcholine receptors (nAChRs) in squirrel monkey brain using PET and 2FA." NeuroImage 31 (January 2006): T138. http://dx.doi.org/10.1016/j.neuroimage.2006.04.122.

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