Brain experimental evidence

Many brain and spinal cord neurons have the capacity to produce NO and experimental evidence indicates a role for this gas in neuronal transmission in animals. A major issue is that the effects of a gas are not limited to the release site and interpretation of the apparent neuronal actions of NO is complicated by the fact that some of the observed effects may be via changes in local blood flow. 

In regard to the experimental evidence available, a substantial number of reports on the chemical constituents of the plant are available, but much less work has been done with the pharmacological properties. Kasture et al., however, made the important observation that a triterpene isolated from R. cordifolia induces anxiety in rodents, an effect accompanied with an increase in serotonin contents in the brain (30). An interesting development from that observation would be to explore further the molecular-pharmacological pathway and the effect of this agent on the serotoninergic system because terpenes, compared with indole alkaloids, are seldom reported for serotoninergic activities. 

Another site of action for opioids is through the regulatory actions of the central nervous system (CNS) on the immune system. Substantial evidence supports the existence of a complex, bidirectional link between the CNS and the immune system (e.g., [65]). Experimental evidence indicates that morphine s immunomodulatory effects involve central opioid receptors. An initial study by Shavit and colleagues [12] found that systemic administration of morphine, but not N-methylmorphine (a form of morphine which does not readily penetrate the blood-brain barrier), produces a naltrexone-reversible suppression of splenic natural killer cell activity in the rat. That same study showed that intracerebroventricular (icv) administration of morphine dose-dependently suppresses... 

More recently, several studies in both the United States and the UK have shown that patients undergoing treatment with an SSRI will rapidly relapse when given an amino acid-containing drink that is deficient in tryptophan. The onset of the symptoms of depression is rapid (less than 24 hours) there is clinical and experimental evidence that the reduction in brain serotonin... 

Experimental evidence suggests that chronic antidepressant treatments increase the formation of transcription factors within the brain which increases neuronal plasticity and leads to recovery. 

These brain-stem regions are interrelated by diverse neuronal projections and are connected to adrenergic structures [Dampney et al. 1977 Marovitch et al. 1982], such as the locus coeruleus, which are postulated to play a role in panic attacks [Gorman et al. 1989]. Further, experimental evidence suggests that CCK interacts with these brain stem mechanisms in modulating respiratory and cardiovascular functions. Microiontophoretic application of CCK-8S to neurons of the nucleus tractus solitarius in cats decreased both neuronal firing and respiratory frequency, effects that were reversed by administration of CCK-4 [Denavit-Saubie et al. 1985]. 

The mechanisms whereby brain cells die during ischemia are not fully understood. Experimental evidence points to a complex array of parallel hemodynamic, biochemical, and electrophysiological events that combine to produce neuronal damage. In experimental cerebral ischemia, the severity of this damage can be significantly reduced by treatment with mild hypothermia (2-5°C below normal brain temperature). 

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