Book of abstracts - British Neuroscience Association

40.07
Neurotransmitter interaction and the adaptive response to the
absence of food in the pharynx of C. elegans
Luedtke S, Walker R, Hopper N, O`Connor V, Holden-Dye L
University of Southampton; School of Biological Sciences, Bassett
Crescent East,, Southampton,, SO16 7PX
We are interested in peptidergic and classical neurotransmitter
interaction and how these modulate behaviour as a response to
internal and external signals. As a model behaviour we are using the
pharyngeal pumping in the nematode C. elegans. The pharyngeal
nervous system regulates feeding behaviour in C. elegans. This neural
network regulates muscle pumping via a number of different classical
transmitters and neuropeptides. We are trying to delineate a
mechanism that controls pharyngeal pumping in the intact worm under
differing environmental conditions (on food and increasing time off
food). Placing worms off food identified 3 distinct behavioural phases
of pharyngeal pumping with increasing time. Subsequent analyses of
several mutants have shown modified responses to the absence of
food. In particular a number of mutants in classical and peptidergic
inhibitors support the notion that pharynx is under negative regulation
that is lessened with increasing time of food. We are currently trying to
correlate the distinct phases of pharyngeal behaviour with the
metabolic status of the worm (measuring fat storage) and switches in
the locomotory behaviours worms use when foraging for food. In doing
so we hope to develop an integrated view of cellular and behavioural
adaptive responses underlying feeding behaviour.
Funded by the Gerald Kerkut Charitable Trust. We are grateful to the
C. elegans Genetics Centre for providing strains.
40.08
Distinguishing between error detection and error awareness:
implications for clinical research
O’Connell R G, Dockree P M, Bellgrove M A, Lau A, Fitzgerald M, Foxe J J,
Robertson I H
School of Psychology and Trinity College Institute of Neuroscience, Trinity
College Dublin
In everyday life our ability to detect errors is critical for smooth and dynamic
interaction with our environment, providing us with the opportunity to realign
our behaviour with prevailing goals and to learn the consequences of
different behaviours. Error processing is reliant, in part, on communication
between anterior cingulate and lateral prefrontal cortices and is impaired in
a number of putatively frontal conditions including schizophrenia, ADHD
and OCD. A common limitation of error processing studies, and particularly
those involving clinical groups, has been a failure to distinguish between
error detection and conscious error awareness. Damage to the frontal lobes
has been associated with decreased awareness of one’s deficits including
a tendency to ‘miss’ errors during neuropsychological tasks. The present
study constitutes a systematic electrophysiological investigation of error
processing networks in a group of adults diagnosed with ADHD. Eighteen
patients and 21 matched controls performed a Go/No-go response
inhibition paradigm that was specially designed to ascertain levels of error
awareness. This experiment reveals that adults with ADHD are significantly
less likely to consciously detect their errors and identifies a number of ERP
abnormalities relating to aspects of performance monitoring and conscious
error processing. The Error Positivity (Pe) is identified as a key marker of
conscious error processing and is found to be attenuated in the patient
group even following consciously detected errors. In addition, the results of
source analysis indicate de-activation of midline frontal regions during
conscious error processing in the ADHD group.
40.09
Effects of early life deprivation and fluoxetine treatment on
central dopamine D2 receptors in adult Wistar rats
Leventopoulos M (1), Lukito S (1),, Russig H (2), Feldon J (2), Pryce C
R (2), Opacka–Juffry J. (1)
(1)Roehampton University, London, UK., (2)Behavioural Neurobiology
Laboratory, Swiss Federal Institute of Technology, Zurich,
Switzerland.,
Studies on animal models of depression have shown that early life
stress affects monoamine status in adult rats. The present study on
adult Wistar rats exposed to early life deprivation (ED) assessed the
level of postsynaptic dopamine D2 receptor binding in the subregions
of cortex, striatum and nucleus accumbens (NAc).
Male Wistar rat P1–14 pups were isolated for 4h/day (ED) or were
handled for 1 minute (CON). They were weaned at P21 and left
undisturbed until 4-6 months old. The ED and CON groups were
halved to receive either vehicle or fluoxetine (FLX, 10 mg/kg, 31 days).
Thus gave four treatment groups: CON-VEH, CON-FLX, ED-VEH and
ED-FLX, n=8 each. ED-VEH rats showed significantly reduced
motivation to obtain sucrose in a progressive ratio schedule (vs CON-
VEH); FLX reversed this deficit.
Quantitative receptor autoradiography was used to determine D2
receptor binding with [3H]raclopride. D2 binding in dorsolateral
striatum and NAc, both core and shell, was significantly reduced (by
16-20%) in ED vs CON. Although fluoxetine treatment did not
significantly affect these changes, it caused a significant reduction in
D2 binding in the prelimbic cortex, dorsolateral and ventromedial
striatum and NAc core and shell in CON-FLX vs CON-VEH.
Correlation analysis of D2 binding between NAc core and shell in each
of the treatment groups indicated a different response to fluoxetine
between NAc core and NAc shell in ED rats when compared with
CON. This is of interest, considering the putative differential
involvement of NAc core versus shell in reward-related behaviour
40.10
Changes in 5HT1A and 5HT2C receptor binding in response to early
life deprivation and fluoxetine treatment in adult Wistar rats
Leventopoulos M (1), Opacka–Juffry J (1), Russig H (2), Feldon J (2), Pryce
C R (2)
(1)Roehampton University, London, UK., (2)Behavioural Neurobiology
Laboratory, Swiss Federal Institute of Technology, Zurich, Switzerland.,
Early life deprivation (ED) can act as a risk factor in aetiology of
depression; in rats, it leads to depression-like behaviour in adulthood. The
central serotonergic system is a putative player in such long-term
responses. The present study hypothesised that ED would reduce
postsynaptic 5HT receptor binding in the brain regions that regulate
depression-like behaviour, and that the antidepressant fluoxetine would
correct receptor responses in adult rats.
Male Wistar rat P1–14 pups were isolated for 4h/day (ED) or were handled
for 1 minute (CON). They were weaned at P21 and left undisturbed until 4-
6 months old. The ED and CON groups were halved to receive either
vehicle or fluoxetine (FLX, 10 mg/kg, 31 days). Thus, four treatment groups
were studied: CON-VEH, CON-FLX, ED-VEH and ED-FLX, n=8 each. ED-
VEH rats showed significantly reduced motivation to obtain sucrose in a
progressive ratio schedule (vs CON-VEH); FLX reversed this deficit.
Quantitative receptor autoradiography was used to determine 5HT1A and
5HT2C receptor binding with [3H]WAY100635 and [3H]mesulergine (added
spiperone and 8-OH-DPAT), respectively. 5HT1A binding was significantly
reduced in anterior cingulate, premotor cortex and ventral hippocampal
CA1 in ED-VEH vs CON-VEH specifically. Same regions and, additionally,
prelimbic and frontal cortices, and accumbens had significantly reduced
5HT2C binding. Whilst fluoxetine reversed the ED-dependent changes in
5HT1A binding in cortices, it did not correct those of 5HT2C.
These results indicate that the depression-like behavioural phenotype
studied here implicates abnormal serotonergic regulation. 5HT1A receptor
acts as a selective therapeutic target for behavioural improvement achieved
with antidepressant treatment.
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