Brain monkey

Parylene s use in the medical field is linked to electronics. Certain pacemaker manufacturers use it as a protective conformal coating on pacemaker circuitry (69). The coated circuitry is sealed in a metal can, so that the parylene coating serves only as a backup should the primary barrier leak. There is also interest in its use as an electrode insulation in the fabrication of miniature electrodes for long-term implantation to record or to stimulate neurons in the central or peripheral nervous system, as the "front end" of experimental neural prostheses (70). One report describes the 3-yr survival of functioning parylene-coated electrodes in the brain of a monkey (71). 

Numerous experiments on rodents, as well as dogs and monkeys, with dosage levels up to 43 g of MSG per kilogram of body weight have failed to show any link between dietary use of MSG and brain damage. In the case of dogs and monkeys, even experiments involving injection of MSG have not shown any effects on the brain. 

Dopaminergic neurotoxin that causes parkinsonism via lesion of nigrostriatal dopamine neurons in rat, mice, monkeys. Unlike the dopaminergic neurotoxin MPTP (N-methy 1-4-phenyl-1,2,3,6-tetrahydropyridine) it does not cross the blood-brain barrier. 

Yanagita T, Takahashi S, Ishida K, et al Voluntary inhalation of volatile anesthetics and organic solvents by monkeys. Jpn J Clin Pharmacol 1 13—16, 1970 Yavich L, Zvartau E A comparison of the effects of individual organic solvents and their mixture on brain stimulation reward. Pharmacol Biochem Behav 48 661— 664, 1994... 

Dobrenis K, Makman MH, Stefano GB (1995) Occurrence of the opiate alkaloid-selective p. receptor in mammahan microglia, astrocytes and Kupffer cells. Brain Res 686 239-248 Donahoe RM (2004) Multiple ways that drug abuse might influence AIDS progression clues from a monkey model. J Neuroimmunol 147 28-32... 

There has been great concern over the large-scale outbreak of BSE that occurred in the UK from 1988 as a result of feeding cattle with supplements prepared fiom sheep and cattle offal. Brain extracts firm BSE cattle have transmitted the disease to mice, sheep, cattle, pigs and monkeys. Studies of 12 recent cases of atypical CJD in the UK have provided evidence that the bovine prions have infected humans through the consumption of contaminated beef... 

Viral vaccines present problems of safety testing far more complex than those experienced with bacterial vaccines. With killed viral vaccines the potential hazards are those due to incomplete virus inactivation and the consequent presence of residual live virus in the preparation. The tests used to detect such live virus consist of the inoculation of susceptible tissue cultures and of susceptible animals. The cultures are examined for cytopathic effects and the animals for symptoms of disease and histological evidence of infection at autopsy. This test is of particular importance in inactivated poliomyelitis vaccine, the vaccine being injected intraspinally into monkeys. At autopsy, sections of brain and spinal cord are examined microscopically for the histological lesions indicative of proliferating poliovirus. 

The dendrites of neurons adjacent to those which degenerate also show extensive growth and sprouting which could facilitate abnormal and disorganised synaptic transmission and cause hyperactivity. It is also known that the dendrites of cells around an alumina focus in monkeys, as well as in human epileptic brain, lose their spinous processes, which might contribute to the paroxysmal discharge by facilitating the spread of depolarisation to the neuron soma. Certainly an increase in the number of Na+ channels on the dendrites of spinal motoneurons, which would facilitate the occurrence of reactive dendritic Na+ spikes, has been seen after axotomy. 

Seiden et al. (1975-76) reported that, in monkeys administered amphetamine for several months and saerifieed 3 to 6 months after the last injection, the levels of DA in the brain were redueed. This long-term reduction in brain DA suggested but did not prove that METH was toxie to DA cells. 

Seiden, L.S. Fischman, M.W. and Schuster, C.R. Long-term methamphetamine induced changes in brain catecholamine in tolerant rhesus monkeys. Drug Alcohol Depend 1 215-219, 1975-76. 

Johannessen, J.N. Insel, T.R. Battaglia, G. Kuhar, M.J. and De Souza, E.B. MDMA selectively destroys brain serotonin terminals in rhesus monkeys. Abstr Soc Neurosci 14 557, 1988. 

Langston, J.W. Fomo, L.S. Rebert, C.S. and Irwin, I. Selective nigral toxicity after systemic administration of 1-methy 1-4-phenyl-1,2,5,6-tetra-hydropyrine (MFTP) in the squirrel monkey. Brain Res 292 390-394, 1984. 

MDMA produced a dose-related depletion of serotonin without altering the eoncentration of either dopamine or norepinephrine in the monkey brain (table 1). Even the lowest dose of MDMA produced a substantial depletion... 

TABLE 2. Decreased concentration of 5-HIAA in the monkey brain 2 weeks... 

Effects in Laboratory Animals. As highlighted in other chapters, the central toxicities during and after repeated stimulant bingeing may be related to neuronal or terminal destruction and/or depletion of neurotransmitter in the brain. In monkeys and cats, the report by Duarte-Escalante and Ellinwood (1970) of neuronal chromatolysis associated with decreased catecholamine histofluorescence following chronic METH intoxication has been followed by extensive neurochemical demonstrations of damage to the monoamine pathways by chronic stimulants (Seiden and Ricaurte 1987). 

Another characteristic of PCP which has been studied with great interest over the last 5 years, is the ability of PCP to produce a discriminative stimulus in monkeys, rats, and pigeons. As discussed elsewhere in this volume, by Browne, the discriminative stimulus properties of PCP are shared not only by other members of the arylcycloalkylamine class, but by psychotomimetic benzo-morphans and substituted dioxolanes. The structure-activity relationships (SAR) within and between these classes are virtually identical to those found when studying the displacement of 3H-PCP from its binding site in rat brain membranes. This correlation... 

Lilienthal H, Winneke G. 1996. Lead effects on the brain stem auditory evoked potentials in monkeys during and after the treatment phase. Neurotoxicol Teratol 18 17-32. 

Logdberg B, Berlin M, Schutz A. 1987. Effects of lead exposure on pregnancy outcome and the fetal brain of squirrel monkeys. Scand J Work Environ Health 13 135-145. 

Lopez-Gimenez, J. F., Vilaro, M. T., Palacios, J. M. Mengod, G. (2001). Mapping of 5-HT2a receptors and their mRNA in monkey brain [3H]MDL100,907 autoradiography and in situ hybridization studies. J. Comp. Neurol. 429, 571-89. 

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