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
