Posted by rakesh on February 7, 2016, at 7:37:37
In reply to Re: can anyone else think of best alt to parnate?, posted by paulb on January 31, 2016, at 14:04:33
Regulation of the synthesis and metabolism of striatal dopamine after disruption of nerve conduction
in the medial forebrain bundle.
Commissiong JW1, Slimovitch C, Toffano G.
Author information
Abstract
1. After physical (knife-cut) or chemically-mediated (tetrodotoxin 300 nM, 1.5 microliters; 1.0microliters min-1) interruption of nerve conduction in the nigrostriatal tract, there was a
marked increase in the synthesis and metabolism of dopamine in the isolated dopaminergic nerveterminals of the striatum. The effect peaked at 4 h post-transection, at which time 3,4-
dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were increased by 300% and 700%
respectively (DOPAC: 27 +/- 13 vs 80 +/- 17 nmol g-1; HVA: 6.66 +/- 3.57 vs 54 +/- 18 nmol g-1). The
increases in dopamine content and metabolism are secondary to an increase in the rate of synthesis on
the lesioned side, versus the intact, control side. 2. In both experimental situations, haloperidol (1.0
mg kg-1, i.p.)
retained its known ability to induce a significant increase in DOPAC and HVA in the striatum, despitethe interruption of nerve conduction in the nigrostriatal tract. 3. Six days after cutting the left
nigrostriatal tract, dopamine in the left striatum was reduced to less than 5% of the control value, and
DOPAC and HVA were not detectable. In the denervated, left striatum, the synthesis of dopamine
(from injected L-DOPA), and its metabolism to DOPAC and HVA, occurred to the same degree as in the
intact right side. In these DOPA-treated rats, haloperidol (1.0 mg kg-1, i.p.) caused a further increase in
DOPAC and HVA in the
intact striatum, but not in the denervated striatum. 4. Under non-stressful conditions, using acombination of anaesthetic treatments, electrical stimulation (400 muA, 0.4 ins, 15 Hz, 15 min) of the
nigrostriatal tract did not increase DOPAC or HVA in the striatum on the stimulated side. 5. It is
concluded (a) that there is a significant presynaptic, and/or local circuit mechanism capable of
activating the synthesis and metabolism of dopamine in the isolated, striatal, dopaminergic nerve
terminals. Furthermore, haloperidol can act directly on the striatal, dopaminergic nerve terminal, to
cause an increase in
the synthesis and metabolism of striatal dopamine. (b) After degeneration of the striatal dopaminergicnerves, the denervated striatum retains the ability to synthesize (from L-DOPA) and metabolize
dopamine, to the same degree as the intact, innervated, contralateral striatum. (c) When stress is
minimized, and release of dopamine is induced by electrical stimulation of the medial forebrain
bundle, the catabolism of dopamine (to DOPAC and HVA) during the release-uptake cycle may not be a
significant factor under physiological conditions. (d) When dopamine synthesis is increased in the
striatum, the
normal blood concentration of tyrosine is adequate to sustain the increased synthesis, and precursoravailability is not a limiting factor. (e) These results suggest that some of the basic concepts about the
neurochemical/neurophysiological regulation of monoaminergic neurones may require further
reevaluation.
I read this article by author toffano g.i feel me not having normal and complete sensation.lack of
dopamine and this article are related.
I tried to contact the author but failed.please if someone can help .
Furthermore can someone professional Interpret it and cure mei have a few days after which my dadwill retire and I m unable to do job because of my health conditions.someone please help me or guide
me.i dont know what to do.
poster:rakesh
thread:1085648
URL: http://www.dr-bob.org/babble/20160131/msgs/1086016.html