T. S. Kuhn's "Paradigm Shift" - why it's 'difficult'

David Longley David at longley.demon.co.uk
Tue Sep 9 06:36:47 EST 2003


In article
<yQY6b.130812$0v4.9535784 at bgtnsc04-news.ops.worldnet.att.net>, KP_PC
<k.p.collins at worldnet.att.net> writes
>"Bill Pascoe" <Bill.Pascoe at newcastle.edu.au> wrote in message
>news:3F568339.1060609 at newcastle.edu.au...
>| What is the AoK reference?
>| [...]
>
>"AoK" is an acronym for ""On the Automation
>of Knowing within Central Nervous Systems:
>A Brief Introduction to Neuroscientific Duality
>Theory", which is a manuscript that describes
>a unified theory of central nervous system
>function, cognition, affect and behavior, giving
>concrete biological mechanisms for the
>phenema of creativity, curiosity, volition, and
>a lot more, all of which reduces directly to the
>proven Neuroscience experimental results.
>
>It was written long ago and remains not formally
>published.
>
>I send it out in the form of an old MSDOS (c)
>hypertext doc to anyone who wants to give it
>a read.
>
>Please msg back if you want a copy. [If so,
>please be a bit patient. I'm online only spor-
>adically these days.]
>
>Cheers, Bill, ken
>
>
Of course you could just conjecture that neophobia is perhaps a
behavioural antecedent to the plasticity which has in the past been
referred to as "learning" or "habit formation". There are opioid peptide
receptors in all of the primary sensory nuclei. To a very large extent,
(more than one might like to think) we tend to do our best not to have
to learn or change.

In the NIMR annual report at the time, summarised as the work below
(which I did between 79 and 81 and presented in 81) as indicating  that
endogenous opioid peptides are involved in the processing of  novel
stimuli.  However, more precisely it would be better to regard  naloxone
not as  'enhancing' neophobia but to take the complement of that notion
and say that it retards the decline of neophobia. That decline is,  I
argued, is co-extensive with what we refer to as "learning", or "habit
formation". The pre-requisite  to learning, or if you prefer, the
constraint  on learning, is a variant of the UCR of neophobia. This
would indicate that endogenous opioids systems would must be inhibited
during the processing of noxious stimulation and come back on after
mitigation of such stimulation.

J.F.W. DEAKIN & D.C. LONGLEY*
(*introduced by T.J. Crow)

National Institute for Medical Research,
Mill Hill, London, NW7 1AA

Several   studies  report  that  naloxone,  an  opiate   receptor
antagonist,  reduces  deprivation induced  eating  and  drinking.
However,  in  the present study, naloxone (5mg/kg,i.p.)  did  not
reduce food intake of rats maintained on a 22 h deprivation - 2 h
feeding   schedule.   In  contrast,   naloxone   (5   mg/kg,i.p.)
progressively reduced water intake in deprived animals to 46%  of
saline  treated controls. No effects of naloxone (1, 5 mg/kg)  on
established  bar  pressing for food or water were  observed  with
either  continuous  or fixed ratio  schedules  of  reinforcement.
However,  naloxone (5mg/kg) accelerated extinction of  responding
when food and water were no longer available.

Animals  treated  with naloxone (5mg/kg) during training  of  the
bar-pressing  ate  only  26% of  the  pellets  delivered  whereas
controls  ate  all pellets delivered. Since the animals  had  not
previously experienced the pellets or the operant apparatus,  the
possibilities  arose that naloxone effects were due  to  enhanced
neophobic  effects of the novel food pellets or  novel  apparatus
cues, or were due to conditioned taste aversion. Therefore,  food
novelty,   apparatus  novelty  and  timing  of  injections   were
independently  varied  in different groups of 8-10  rats  treated
with saline or naloxone. Rats were maintained at 85% body  weight
with 12g lab chow per day. On experimental days 46 small  pellets
(Cambden  instruments) were placed on a small petri dish  in  the
home  cage of some groups or released from a pellet dispenser  in
an  operant box for other groups. The dependent variable was  the
number of pellets eaten over 15 minutes.

Naloxone (1,5 mg/kg i.p.) injected 5 or 20 min before test almost
completely  suppressed pellet eating if the animals had not  been
previously  exposed  to the pellets (p<0.01 't'  test  vs  saline
groups).  This  occurred  independently  of  whether  tests  were
carried  out  in  the home cage or novel  operant  box.  Naloxone
induced  suppression  of  pellet  eating  was  almost  completely
abolished  in either environment if animals had been  exposed  to
the pellets for the five preceding days in the same or  different
environment.  Naloxone  (5mg/kg, i.p.)  administered  immediately
after  pellet eating tests failed to suppress  subsequent  pellet
eating.

Thus, naloxone suppressed pellet eating if the pellets were novel
and if naloxone was administered before eating tests. The results
suggest  naloxone enhances neophobic effects of novel  foods  and
that  suppression of novel pellet eating is not due  to  enhanced
effects  of  novelty of apparatus cues or  to  conditioned  taste
aversion.

Reference

FRENK, H & ROGERS G.H. (1979) The suppressant effects of naloxone
                              on food and water intake in the rat.
                              Behav. Neural. Biol, 26, 23-40.

PROCEEDINGS OF THE BRITISH PHARMACOLOGICAL SOCIETY (BPS)
1-3 April 1981
(Also British J Pharmacology 1981)


PS: A better way of understanding the Kuhnian "paradigm" notion and all
that he says about it is to read Quine's "Two Dogmas of Empiricism"
(1951;1961), particularly with respect to the second dogma. The
relationship is no coincidence I'm sure ;-)
-- 
David Longley



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