Peter Bengtson PhD
majors: Psychology, Physiology, Anatomy. UQ, Brisbane, 1984-1988
(Honours) Thesis: Microelectrode recordings from locust auditory
receptors. UQ, Brisbane, 1989
clamp analysis of 5-HT and dopamine responses in slices of basal
forebrain. UQ, Brisbane, 1997-2001
Patch clamp and calcium
imaging of dopamine neurons in brain slices. Fondazione Santa Lucia, IRCCS, Rome,
Patch clamp and calcium
imaging of hippocampal neurons in disociated culture and organotypic
and acute brain slices. Bading group, Neurobiology division, IZN,
Heidelberg University, Heidelberg, GERMANY. September 2003-present.
Whole cell patch clamp and
fluorecent calcium imaging from live cells in brain slices and
dissociated culture preparations.
transduction of calcium signals from synapses and the nucleus. Large nuclear calcium signals are
evoked by intense synaptic input during burst activity. These nuclear
calcium signals are required to trigger the transcription necessary to
maintain late phase plasticity (>2 hours). What mediates this
calcium signalling? Is it a calcium wave travelling up the dendrite or
is it a function of voltage gated calcium entry at the soma due to the
depolarisation accompanying burst activity? What
contribution do IP3
receptors, ryanodine receptors, Store Operated Channels (SOCs) and
Voltage Operated Channels (VOCs) give in generating the
nuclear calcium signal?
The mechanism underlying increased synaptic efficacy in a
model of plasticity. A
15 minute exposure to
bicuculline triggers bursting activity (see below) which is sustained
for days in a culture preparation of hippocampal neurons. This
represents a change in efficacy of AMPA receptor-containing synapses.
Are such changes mediated by postsynaptic or presynaptic mechanisms? Is
it transcription or translation
receptors, channels and genes which
link spontaneous calcium transients to neuronal fate in neural
fate of precursor cells correlates with the presence of intermittent
transient increases in intracellular calcium concentration. What is the
link between calcium influx and the differentiation of stem cells into
channels mediate the calcium influx? What receptors or mechanisms open
these channels? What role do serotonin and growth factors such as BDNF
play in these processes? Are the same links important for the
differntiation of neural precursors from the adult brain?
The functional quantification of
NMDA receptor-mediated responses arising from synaptic Vs extrasynaptic
Synaptic NMDA receptor activation promotes
cell survival whereas extrasynaptic NMDA receptor activation promotes
necrosis. Extrasynaptic NMDA receptors are largely composed of NR2B
subunit containing receptors in mature rats. What is the relative
distribution of NMDA receptors (synaptic Vs extrasynaptic) and what
proportion of each population is blocked by the NR2B subunit selective
Postdoctoctoral position offered
|- electrophysiology and confocal microscopy
|- download details
||C. Peter Bengtson
|Im Neuenheimer Feld
|69120 Heidelberg, GERMANY
||Hippocampal culture: x20 & x80
magnification (note patch electrode)
Current clamp recordings of bicuculline induced bursting. A typical
recording for 3 minutes (top trace) from a hippocampal neuron during
exposure to bicuculline (50 µM) and an expanded traces below of
an individual burst are shown. A strong depolarizing shift accompanys
each burst of action potentials.
2. Consecutive sweeps of mEPSCs recorded from the same cell before
(pre-bicuc) and after (post-bicuc) the bicuculline protocol (15 mins
bic treatment + 30 mins washout).
3. Cumulative probability histograms generated from the cell shown in
fig 2. indicate a reduced mEPSC inter event interval but no change in
4. Shown are overlaid current responses from the same cell to bath
applied AMPA (10 µM) in the presence of tetrodotoxin (1 µM)
before and after the bicuculline protocol.
5. Histograms show the group mean ± SEM of normalized values
(posttreatment/ pretreatment) for amplitude and
interval of AMPA mediated mEPSCs recorded before and after bicuculline
(n=10) or vehicle (n=5) treatment protocols. Vehicle treatment caused a
amplitude in all cells (n=5, p<0.01 individual, p<0.05 group mean
comparison) however no
consistent change in amplitude occurred following bicuculline treatment
(increased amplitude in 4 cells, p<0.01; decreased amplitude in 2
no change in 4 cells; p=0.84 group mean comparison). No change in mean
event interval was apparent with vehicle treatment (no change in 4
p>0.05; decreased IEI in 1 cell, p<0.01; p=0.39 group mean
comparison) while bicuculline
treatment reduced the inter event interval (p<10-11
in 9 cells, no change in 1 cell;
p<0.05 group mean comparison). Also shown are the group mean
± SEM of normalized peak responses to AMPA measured in cells
before and after
the bicuculline or the vehicle treatment protocols (n=4 in each group).
The differences between
bicuculline and vehicle treatment groups were significant for mEPSC
amplitude, inter event interval and AMPA response (p<0.05).
GERACITANO, R., TOZZI, A., LONGONE, P., DIANGELANTONIO, S., BENGTSON,
C.P., BERNARDI, G. & MERCURI, N.B. (2005). Trace amines depress
GABAB responses in dopaminergic neurons by inhibiting GIRK channels. Mol Pharmacol. epub: mol104.007427v1
ARNOLD, F. J.,
HOFMANN, F., BENGTSON, C. P., WITTMANN, M., VANHOUTTE,
P. & BADING, H. (2005). Microelectrode array recordings of
cultured hippocampal networks reveal a simple model for transcription and
protein synthesis dependent plasticity. J Physiol.
*WITTMANN, M., *BENGTSON,
C. P. &
BADING, H. (2004). Extrasynaptic NMDA receptors: mediators of
excitotoxic cell death. In The Pharmacology of Cerebral Ischemia.
(Krieglstein J, Klumpp S eds.) Medpharm Scientific Publishers,
Stuttgart, pp 253-266.
BENGTSON, C. P.,
LEE, D. J. & OSBORNE, P. B. (2004). Opposing
electrophysiological actions of 5-HT on noncholinergic and cholinergic
neurons in the rat ventral pallidum in vitro. J Neurophysiol 92
BENGTSON, C. P.,
TOZZI, A., BERNARDI, G. & MERCURI, N. B. (2004).
Transient receptor potential-like channels mediate metabotropic
glutamate receptor EPSCs in rat dopamine neurones. J Physiol 555
GIORGI, M., D'ANGELO, V., MODICA, A., MARTORANA, A.,
MORELLO, M., BENGTSON, C. P. & BERNARDI, G. (2004). Down-regulation
of nitrergic transmission in the rat striatum after chronic
nigrostriatal deafferentation. Eur J
*TOZZI, A., *BENGTSON, C. P., LONGONE, P.,
CARIGNANI, C., FUSCO, F. R., BERNARDI, G. & MERCURI, N. B. (2003).
Involvement of transient receptor potential-like channels in responses
to mGluR-I activation in midbrain dopamine neurons. Eur J Neurosci 18, 2133-2145.
BENGTSON, C. P., BERNARDI, G. & MERCURI, N. B. (2004).
Voltage-gated calcium cannels mediate intracellular calcium increases
in weaver dopaminergic neurons during stimulation of D2 and gabaB
receptors. J Neurophysiol
BENGTSON, C. P., GUATTEO, E., BERNARDI, G. & MERCURI,
N. B. (2003). D-tubocurarine reduces GABA responses in rat substantia
nigra dopamine neurons. Synapse
PIERI, M., ALBO,
F., GAETTI, C., SPALLONI, A., BENGTSON, C. P.,
LONGONE, P., CAVALCANTI, S. & ZONA, C. (2003). Altered excitability
of motor neurons in a transgenic mouse model of familial amyotrophic
lateral sclerosis. Neurosci Lett
BENGTSON, C. P.
& OSBORNE, P. B. (2000). Electrophysiological
properties of cholinergic and noncholinergic neurons in the ventral
pallidal region of the nucleus basalis in rat brain slices. J Neurophysiol 83
BENGTSON, C. P.
& OSBORNE, P. B. (1999). Electrophysiological
properties of anatomically identified ventral pallidal neurons in rat
brain slices. Ann N Y Acad Sci