The following was a 10 minute presentation with slides, covering
nearly 2 years work. Rules of the BPS dictate that authors must
be specified in alphabetical order, with the senior
author/presenter asterisked. The abstract is phrased as it is as
it was for a pharmacology audience. Reference to saline, is
isotonic saline, ie the vehicle which naloxone was dissolved in.
Further studies, delivered naloxone intra-cerebro-ventricularly
to confirm that it was a CNS phenomenon. As a behavioural
experiment, the results are very clear.
In the NIMR annual report, the work was summarised as indicating
that endogenous opioid peptides are involved in the processing of
novel stimuli. Rather than regard naloxone as 'enhancing'
neophobia it is better to take the complement of that notion and
say that it retards the decline of neophobia. That decline is, I
have argued, co-extensive with 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. Opioids must be
initially OFF (theoretical elaboration on that point takes one
back to a neo-Hullian model of learning/habit formation).
I have not seen anything in the literature since this was first
reported, and by behavioural experiment standards, it is SEEMS a
dramatic effect. Has anyone the time, and resources to try to rep
licate the work? The findings stand for PVG and Sprague-Dawley
rats, male and female.
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 PHARMACOLGICAL SOCIETY (BPS)
1-3 April 1981
(Also British J Pharmacology 1981)
I am hyothesizing a critical role for the endogenous opipid
peptides in regulating what Pavlov called "Protective Inhibition"
or "transmarginal inhibition of intensity". Hull made much use of
these notions in the context of Stimulus Intensity Dynamism.
I plan to submit the work as a full paper, as it is, apart from
the above brief report, the main part of a 1980s PhD thesis.
--
David Longley
