Brain catecholaminergic systems

Clear similarities exist between the effects of LSD and those of other hallucinogens on catecholaminergic systems. Anden et al. (5) noted that psilocybin and DMT accelerate NE turnover in the rat brain. Hallucinogens of other chemical series, notably methoxyamphetamines (e.g., DOM) (68) and THC (13), also increase the rate of synthesis and utilization of NE in brain. The increase due to THC probably involves a direct action of the drug, since an enhanced conversion of 3H-tyrosine into 3H-NE was found in synaptosomes incubated in the presence of 3 to 10 fiM THC (13). 

The results shown in Table 3.7 are especially apt in support of this conclusion. There are innate differences in the efficiency of the mesencephalic catecholaminergic system. For the brain of animals (nos.) 1, 2, 4, 5, and 6 the hot plate heated to 50 °C was already an adequate stimulus to enhance the excitability of the cortical neurons for escape and to survive the tribulation without perceivable consequences. Animals 3 and 7 escaped, but fell ill thereafter. Animals 8, 9, and 10 were unable to cope with the situation and died. 

Kinetic studies of the catecholamine levels in the spinal fluid would be the most direct means for exploring the function of the catecholaminergic system in the brain. However, it would be difficult in such studies to obtain repeated samples at small enough intervals of time to permit proper evaluation of the catecholaminergic system and its homeostasis. 

Because the various transmitter systems in the brain are directly and indirectly linked together, purely catecholaminergic or purely serotoninergic depressions are unlikely. Furthermore, the majority of antidepressants known today have multiple effects, especially after repeated administration, and thus affect a number of transmitter systems. This fact is taken into account by more recent hypotheses of depression in that a balance between several transmitter systems is postulated as a prerequisite for mental health, whereas affective psychoses are believed to be a reflection of an imbalance. 

J.M. Bell, W.L. Whitmore, T. Cowdery and T.A. Slotkin, Perinatal dietary supplementation with a soy lecithin preparation Effects on development of central catecholaminergic neurotransmitter systems, Brain Res. Bull. 17(2) (1986) 189-195. 

Figure 10.19. False transmitters that are used for antihypertensive treatment, a a-Methyldopa passes the blood brain barrier and is decarboxylated to a-methyldopamine, which upon synaptic release stimulates presynaptic 02-receptors. b Guanethidine acts on catecholaminergic synapses in the peripheral autonomous nervous system.

The A-methyl-4-phenyl-pyridinium ion (MPF ), the degradation product of MPDP, is an effective substrate for the catecholaminergic synaptosomal uptake system (Javitch et al., 1985 Chiba et al., 1985). Active uptake of MPP was also observed in synaptosomes prepared from ex-trastriatal brain regions (e.g. hypothalamus, hippocampus, cerebellum) (Chiba et al., 1985). At least two possible pathways exist by which MPP has been postulated to be toxic ... 

Min N, Joh TH, Jkim KS, Peng C, Son JH. 5 upstream DNA sequence of the rat tyrosine hydroxylase gene directs high-level and tissue specific expression to catecholaminergic neurons in the central nervous system of transgenic mice. Mol Brain Res 1994 27 281-289. 

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