Neuron monoaminergic

TABLE 1. Effects of amphetamine-related compounds on monoaminergic neurons... 

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... 

TABLE 2. Nature of neurotoxic damage to brain monoaminergic neurons... 

Drug Brain Monoaminergic Neurons Showing Neurotoxic Damage Neurotoxicity Occurring in Humans... 

GABAergic neurons responsible for the inactivation of monoaminergic neurons during PS... 

Although there has been a substantial body of pharmacological evidence in support of the monoamine theory of depression, clinical biochemical data have been less convincing (Luchins, 1976) this is where differences in the concentrations of NA and 5-HT and their metabolites or hormones, which are ultimately under the control of brain monoaminergic neurons (neuroendocrine markers), have been compared between depressed patients and normal controls. However, by the early 1970s a major difficulty with the theory was becoming apparent this was the time lag between the immediate... 

Median forebrain bundle A bundle of monoaminergic neuronal axons travelling from the brainstem through the diencephalon to various limbic structures. 

The serotonergic system is not the only monoaminergic neuronal population affected by LSD numerous reports also mention that the turnover of catecholamines is significantly altered in LSD-treated rats. Thus a decrease in cerebral norepinephrine (NE) levels was first reported by Freedman (35) in rats treated acutely with LSD. Tolerance to this action develops rapidly, since LSD no longer... 

The possible effects of hallucinogens on central monoaminergic neurons were first explored by Freedman (34), who discovered that a single injection of LSD increases 5-HT levels in the rat brain, whereas its inactive congener BOL fails to affect brain 5-HT. Since this change is associated with a decrease in the concentration of the main metabolite of 5-HT, 5-hydroxyindole acetic acid (5-HIAA) (Fig. 1), Rosecrans et al. (98) postulated that LSD administration in... 

Lewy bodies (LB) are neuronal inclusions, composed of abnormal neurofilament and synaptic proteins, thought to be surrogate markers for neuronal dysfunction and eventual cell death. They are found in diverse locations including cholinergic and monoaminergic neurons of the brainstem, diencephalon. 

A fourth modification of the classical model involves nitric oxide (NO), a new form of nonsynaptic interneuronal communication, or volume transmission. Nitric Oxide inhibits the uptake of dopamine, norepinephrine (Lonart and Johnson, 1994), and serotonin (Asano et ah, 1997) into neurons and is closely linked to glutamate-mediated neurotransmission. Nitric Oxide synthase is switched on only by glutamatergic receptors and appears to enhance the strength of glutamatergic input to monoaminergic neurons without requiring direct synaptic contact (Kiss and Vizi, 2001). 

Neuropeptide Y [NPY] is a 36-amino acid peptide. The function of NPY, one of the most abundant peptide transmitters of the mammalian brain, remains unclear because of a lack of specific receptor antagonists. NPY meets many of the criteria of a neurotransmitter itself. NPY is costored and interacts with several monoaminergic neurons within the CNS [Lundberg et al. 1982], for example, noradrenergic afferents from the nucleus solitary tract to the amygdala. Both somatostatin and NPY colocalize at GABA interneurons within the amygdala, neocortex, and striatum. NPY also selectively modulates N-methyl-D-aspartate-induced hippocampal activation (pyramidal neurons] via oreceptors [Debonnel et al. 1994]. 

FIGURE 5—13. This figure represents the normal state of a monoaminergic neuron. This particular neuron is releasing the neurotransmitter norepinephrine (NE) at the normal rate. All the regulatory elements of the neuron are also normal, including the functioning of the enzyme monoamine oxidase (MAO), which destroys NE, the NE reuptake pump which terminates the action of NE, and the NE receptors which react to the release of NE. 

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