[Neuroscience] Re: A hypothesis (Re: Can a single neuron release multiple neurotransmitters?)

[John H.]

Entertained by my own EIMC wrote:
> Hi  John,
>
> 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
> so! ;-)
>
> 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
> some
> 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*
> activity.

One of the intriguing things I've come across lately is that in many
neuropathological states there is a massive change in receptor levels.
This is a big chicken and egg question for me because I'm trying to
understand the processes involved in slow, subtle cellular degeneration
that precedes cell death events. Sustained major depression is a good
model but the data is confounded because depression comes in many forms
and it is difficult to differentiate the forms in individuals.
Nonetheless there is cell loss in the temporal lobe, loss of
neurogenesis, and loss of BDNF, a critical growth factor. There is a
complex interplay of various agents but I can see how the balance can
slowly shift to a state where things start going bad. In one set of
comparison studies it was found that when effective in treating
depression CBT induced the same changes as measured by MRI as did
antidepressants. There is more than one way to skin a cat. We have
geneally opted for the pharmacological route because it is quick and
reasonably effective but the data suggest that in treating depression
there is a very wide range of non pharmacological treatments that can
be very beneficial not only in treating depression but in promoting
health in general.


> 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".)
> ------------------------

If I'm reading you correctly the above touches on something I've been
thinking a lot about lately. There is evidence to run the argument that
specific events in a person's life can so fundamentally alter their
physiological balance as to have profound implications for their future
prospects and there is also evidence that various interventions, at
either the acute or latter periods, can help restore the person's
physiological balance towards a more functional state. One example writ
large, in our backyard as it were, is the current health and
environmental situation for many aboriginal children. The research
makes it abundantly clear that particularly prior to 3 years of age,
maturational processes can be skewed to less desirables outcomes.
Malnutrition prenatally and in early childhood, when combined with a
stressful environment, is a recipe for dysfunctional human beings. We
may not be able to save most of the adults  but if we allow this to
happen to their children we're just creating clones. It is now an
intractable problem. One of the great challenges for psychology will be
to find ways to help these people become happier and more functonal in
their lives. One of the great promises of recent research is that we
may be able to create strategies to kickstart neurogenesis and shift
the endocrinological and immunological functions towards more
favourable outcomes. But we need to be able to attack the problem at
both biological and environmental levels.



>
> 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!
>
> Peter
>
> "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
> > looked
> >
> > Extract
> >
> > 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,
> >
> >
> > John.
> >
> >
> >
> > 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
> >> 'the
> >> first').
> >>
> >> Please confirm or debunk as appropriate!
> >>
> >> P
> >