[Neuroscience] Re: A hypothesis (Re: Can a single neuron release
Entertained by my own EIMC
(by write_eimc At ozemail.com.au)
Wed Jan 10 02:51:38 EST 2007
Thanks for all the (confirmatory) information!
I had hardly a clue about - and about what science knew about - how brains
work when I started to find out anything relevant to Primal Theory/Therapy.
Eventually I came to see that all relevant and reasonably rigorous
scientific facts or findings stack up to support the observation and
conclusion that Janov's interpretation of folks' psychophysiology (and
implicitly of fauna's) is the best and most balanced possible.
That Janov also inspires too high hopes (or unrealistic expectations) in
some people is a separate issue - and he most certainly is not alone doing
I feel that I have produced a personally satisfying philosophical complement
to 'the primal theoretical position'.
It is a "complement" which I could described something like this:
A, from closely to peripherally relevant, philosophical overview or outlook
based on corroborated results of detail-oriented research and as thorough
and as rational as (for me) possible conceptualized associations (or
percEPTively spotted correlations) between aspects of What Is going on that
range from what is readily observed to what is knowable (observable and
detectable) within realistic bounds only thanks to sophisticated scientific
means and methods.
A more specific comment apropos primal theoretical/therapeutic promises:
There is plenty of indirect evidence that neural motivational vectors can in
cases become rerouted *not* into new AEVASIVE directions but into a fairly
fundamentally 'opposite' direction. In other words, such "vectors" can be
nudged (relatively rarely spontaneously so but far more reliably and
regularly given conducive lifetime settings, an appropriately prepared
rational-philosophical attitude, and an appropriate kind of help) to the
effect of a removal of "synaptic hibernation" at specific synaptic sites -
i.e. synaptic sites of distress-gating/filtering/delaying/precluding LTD and
more or less chronic GABArgic/opioidergic/dopaminergic *inhibitory*
Such a reconnection of specific neural information (in a sense also a way to
release the pressure from, or a radically different less repercussive way of
storing the conditioned permanent residues of, "specific/synaptic
hibernation imploring/inducing type" predicaments) can free-up
neural/behavioral resources that would otherwise have kept on working in the
insidious service of repressive/defensive (however possibly also more or
less "ambiadvantageous") handling of CURSES.
(CURSES ~= "Pain"/"primal pain", or "engrams".)
I (also) have enough selective synaptic hibernation/freezing of
mirror-neurons that monitor the mood of cricket-winging poms to never having
sung one single lament for them. ;->
But I cheered plenty for us aussies!
Apropos which I hope you had a chance to watch the World Cup in soccer -
i.e. proper football ;-) Can't wait till next time!
Cheers, and all the best!
"John H." <j_hasenkam At yahoo.com.au> wrote in message
news:1167832816.678362.224090 At i12g2000cwa.googlegroups.com...
> Very vaguely Peter, my memory on this is not clear, but I think there
> were some news reports a few years indicating that neurons can "switch
> careers"; though this was only during embryonic development. so I
> Other examples of two fast neurotransmitters released from the same
> neuron include GABA and glycine in interneurons of the spinal cord (5)
> and glutamate and dopamine in ventral midbrain dopamine neurons (6). Of
> all CNS neurons, the granule cells of the dentate gyrus appear to be
> the champions of neurotransmitter colocalization: glutamate,
> enkephalin, dynorphin, zinc, and finally GABA (2)(
> Trick was to search for "single neuron" AND neurotransmitter. Stop
> making me think dude, it's been a long day and I'm tired.
> Shall we sing a lament for the poms?. They are not taking those Ashes
> back dude. I'll brain the bastards if they do!!!
> Be well,
> Epilepsy Curr. 2002 Sep;2(5):143-145. Related Articles, Links
> The GAD-given Right of Dentate Gyrus Granule Cells to Become GABAergic.
> Mody I.
> Departments of Neurology and Physiology, The David Geffen School of
> Medicine, UCLA, Los Angeles, California.
> JANUS, THE ANCIENT ROMAN GOD OF GATES AND DOORS HAD TWO FACES: one
> looked into the past, and the other, into the future. Do neurons
> possess a Janus face when it comes to neurotransmitters, or a given
> neuron is to be forever solely gamma-aminobutyric acid (GABA) ergic,
> glutamatergic, dopaminergic, peptidergic, or
> YOURPREFERREDTRANSMITTERergic? The answer is that the terminals of many
> neurons are homes to even more than two neurotransmitters. All this in
> spite of the "one neuron-one transmitter" usual misinterpretation of
> Sir Henry Hallett Dale's postulate, originally meant to indicate that a
> metabolic process taking place in the cell body can influence all
> processes of the same neuron. A large variety of neurons in the CNS,
> many of them GABAergic, produce and release chemicals that satisfy some
> of the criteria used to define neurotransmitters. The usual scenario
> for a dual-transmitter terminal is that the fast-acting transmitter
> such as GABA or glutamate is stored in regular synaptic vesicles,
> whereas a neuropeptide is stored in dense core vesicles (1). The
> vesicular zinc found in many glutamatergic terminals also may be
> considered to be a second neurotransmitter, based on its vesicular
> packaging with the aid of a specific vesicular transporter, and its
> postsynaptic actions through high-affinity binding sites and permeation
> through certain channels (2). Whenever a "fast" and a "slow"
> neurotransmitter are present in the same presynaptic terminal, it is
> customary to assume that their release can be differentially regulated
> (1). There is little convincing experimental support for this
> phenomenon in the mammalian CNS. The coexistence of two "fast"
> neurotransmitters in the same terminal is less frequent, but not
> unheard of. In neonatal sympathetic neurons cocultured with cardiac
> myocytes, norepinephrine and acetylcholine coexist and have opposite
> actions on the cardiac muscle cells (3). Very recently we learned that
> brain-derived neurotrophic factor acting at the low-affinity
> neurotrophin receptor p75(NTR), perhaps as part of a programmed
> developmental switch, can convert the phenotype of the sympathetic
> neuron from noradrenergic to cholinergic (4). Other examples of two
> fast neurotransmitters released from the same neuron include GABA and
> glycine in interneurons of the spinal cord (5) and glutamate and
> dopamine in ventral midbrain dopamine neurons (6). Of all CNS neurons,
> the granule cells of the dentate gyrus appear to be the champions of
> neurotransmitter colocalization: glutamate, enkephalin, dynorphin,
> zinc, and finally GABA (2)(7)(8)(9). With this many transmitters in a
> single neuron, there are probably different ways in which they can be
> released. Dynorphin and other opioid peptides can be released directly
> from the dendrites to inhibit excitatory transmission (8). A similar
> mechanism may take place for GABA, as described in cortical GABAergic
> neurons (10).
> PMID: 15309121 [PubMed - as supplied by publisher]
> Entertained by my own EIMC wrote:
>> I *hypothesize* (or speculate) the existence (or is it already known?) of
>> neurons that release one type of transmitter when firing for a relatively
>> short time but a different transmitter after a while when firing
>> persistently for a relatively long time (or perhaps that after a while of
>> persistent firing release 'the last' transmitter at a higher ration to
>> Please confirm or debunk as appropriate!
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