Posted on 11/12/2003 8:37:51 AM PST by A. Pole
Edited on 04/13/2004 2:11:01 AM PDT by Jim Robinson. [history]
In the field of catecholamine transmitters, dopamine (DA) pathways have then been recognized to play a critical role in cognition and emotion, and the last decade has seen a large increase in the experimental evidence for a role of DA in both synaptic plasticity and memory processes.
Since the discovery of LTP in the hippocampus ([Bliss and Lomo, 1973]), synapses that undergo plastic changes have been described in various parts of the brain and particularly in brain regions that receive DA innervations. It is now well established that the strength of synaptic transmission can be modified on a long-term basis by specific patterns of activation such as high frequency trains that produce LTP, and also by the action of endogenous modulators such as DA.
Different approaches from unit recording to lesion and pharmacological studies have demonstrated that DA plays a critical role in the modulation of neuronal activities that are related to different forms of learning and memory.
Converging evidence indicates that DA innervation of the prefrontal cortex plays a major role in working memory, a form of memory that allows to maintain and manipulate active representations of information that are held temporarily in mind. DA loss in the prefrontal cortex can lead to a great deficit in the performance of a working memory task in monkeys ([Brozoski et al]) as does lesion of the VTA in the rat ( [Simon et al]).
Synaptic plasticity induced in the different regions examined (hippocampus, striatum and prefrontal cortex) does not appear to recruit the DA systems in similar manners. It is conceivable that a local regulation of these plastic events is specific to the region where the synapses are activated. Although a comparable DA modulation appears to be present in the hippocampus and the prefrontal cortex, only the consolidation of LTP in the hippocampus is dependent on D1 receptors whereas a potential permissive and facilitatory effect of DA and D1 agonists is observed at an early stage of LTP and required for the initiation of this plastic event in the prefrontal cortex.
On top of a different subcellular DA innervation and spatial distribution of D1 and D5 receptors in the two regions that could explain these discrepancies, a distinct temporal combination between the glutamate and the modulatory DA pathways might also be at the origin, for functional purposes, of the immediate versus delayed recruitment of DA systems. Indeed, DA neurons are differentially activated depending on cognitive demands. Thus, the heterosynaptic influence of the DA signal could gain its selectivity from the activity patterns that are initiated in the VTA during changes in behavioral states and that are present in the DA inputs to the post-synaptic sites in the hippocampus or the prefrontal cortex. Whether the mesohippocampal or mesocortical DA systems are involved in different memory processes would differentially alter the relative strength of the synapses in the two regions. This mode of synaptic plasticity and modulation by a DA tone demonstrates a dynamic and specific regulation of synapses that may be important for memory.
The future will define more precisely at the cellular level which specific target cells of DA terminals and which receptors influence intrinsic and extrinsic circuits and at the molecular level which proteins are specifically involved in these DA/glutamate interactions relevant to plasticity and memory processes. Increased understanding of these mechanisms may also be relevant to the pathophysiology of DA-related psychiatric disorders.
Do some research to get a good pipe. Some examples.
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And just how old would this hypothetical child have to be to be in danger?
If true, do you have a problem with self medication?
Except for the adrenalin rush from pissing off smokers ?
Nicotine is a toxic alkaloid found in a range of plants, most notably tobacco. Nicotine is also used as a pesticide. Nicotine stimulates nicotinic acetylcholine receptors throughout the central and autonomic nervous systems. In severe poisoning confusion and convulsions are accompanied by arrhythmias and parasympathetic over stimulation (see organophosphate poisoning).
Children most frequently encounter nicotine in the form of cigarette or cigarette butt ingestion. Vomiting is the commonest symptom following cigarette ingestion and tends to limit toxicity. Asymptomatic children who have ingested less than one cigarette or two cigarette butts should be observed for two hours. No specific treatment is required. Children who have consumed more than this amount, should receive activated charcoal.
--Poisoning in children 5: Rare and dangerous poisons Archives of Disease in Childhood 2002;87:407-410
Management of children who have ingested ß blockers, digoxin, oral hypoglycaemics, organophosphates, carbon monoxide, cyanide, isopropanol, ethylene glycol, methanol, Ecstasy, LSD, cocaine, nicotine, and isoniazid
M Riordan1, G Rylance2 and K Berry3
1 Department of Pediatrics, Yale University Medical School, USA
2 Department of General Paediatrics, Royal Victoria Infirmary, Newcastle upon Tyne, UK
3 Accident and Emergency Department, Birmingham Children’s Hospital, Birmingham, UK
When you smoke almost most of nicotine (and other alkaloids) get destroyed by the fire. Very small part gets absorbed. Straight tobacco is too toxic.
So that's your self medication, huh?
I feel sorry for anyone that has to piss off someone else for the rush of adrenaline.
You must be what I've heard reffered to as an "adrenaline junkie". Addicted yet?
Tit for tat. ;^)
Use an emoticon to disable confusion.
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