Electrical stimulation of the ventral noradrenergic bundle (VNAB) results in norepinephrine (NE) release in the paraventricular nucleus of the hypothalamus (PVN) in a frequency-dependent manner. Blockade of the NE transporter, but not the dopamine transporter, caused prolonged electrically-evoked NE release in the PVN, confirming the signal as NE. This study provides the first real-time evidence of NE release in the PVN in response to VNAB stimulation and establishes fast-scan cyclic voltammetry as an effective method for measuring catecholamine release in this region.

1. ELECTRICAL STIMULATION OF THE VENTRAL NORADRENERGIC BUNDLE RESULTS IN
NOREPINEPHRINE RELEASE IN THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS
A.I. Gerth and M.F. Roitman
Department of Psychology, University of Illinois at Chicago, Chicago, IL
INTRODUCTION
METHODS CONCLUSIONS
RESULTS
Fast-Scan Cyclic Voltammetry
Electrical stimulation of the VNAB results in
frequency-dependent NE release in the PVN.
NET, but not DAT blockade, causes prolonged electrically-evoked
release in the PVN – confirming the evoked signal as NE
In vivo recordings, compared to those made in vitro, support
the identification of the evoked signal as NE
• Electrical stimulation of the VNAB causes a phasic increase in
PVN NE.
• Strong correlation between background subtracted cyclic
voltammograms obtained in vivo and in vitro
• NET, but not DAT inhibition, results in prolonged
stimulated NE release
• Electrical stimulation of the VNAB results NE release in the PVN
at stimulation frequencies that are similar to those that evoke
NE in the bed nucleus of the stria terminalis as well as DA
release in the striatum.
• These data are the first to show real-time NE release in the PVN
– a key regulator of the autonomic response to stress.
• Future work will aim focus on visceral stressors known to
activate brainstem NE neurons that project to the PVN.
• Anesthetized rats were implanted with:
• Guide cannula aimed at the medial
parvocellular region of the PVN,
• Chlorinated silver wire reference electrode
• Stimulating electrode targeting the VNAB
• A carbon-fiber recording electrode was
lowered into the PVN and the VNAB was
stimulated(200 μA, 60 pulses, 60 Hz) once
every 5 min
• After evoking a signal, a stable baseline was
acquired (defined as 3 consecutive
recordings where peak signal differed no
more than 10%), rats were injected with
either:
• Desipramine: (10 mg/kg; n = 3)
NE Transporter (NET) Blocker
• GBR 12909: (10 mg/kg; n = 4)
DA Transporter (DAT) Blocker
• Stimulations continued for 1 hour post-
treatment
• To determine frequency-dependency, a
stable signal was acquired with 60 Hz
stimulation. Data were then acquired with
60, 30, and 10 Hz stimulations (pulse
number and current remained constant). This work was supported by the National
Institutes of Drug Addiction grant DA025634
5 secs 5 secs
A.
B.
• The paraventricular nucleus of the hypothalamus (PVN)
receives significant norepinephrine (NE) input from the
ventral noradrenergic bundle (VNAB).
• NE input is targeted to a region in the PVN responsible
for hormonal regulation of the stress response.
• The real-time release and regulation of extracellular NE
in the PVN remains unknown.
• Fast-scan cyclic voltammetry (FSCV) has been used to
capture real-time fluctuations in catecholamines
including NE. However, it has not been extensively used
in the PVN.
• An understanding of the signaling dynamics of NE in the
PVN will yield further insight into autonomic function.
Poster: BBB26
Averager2
In Vitro (1 µM NE)
In Vivo
In Vitro (1 µM NE)
In Vivo
r2 = .91