Vagal Nerve Stimulation - Depression

John H. johnhkm at netsprintXXXX.net.au
Wed Feb 16 08:00:00 EST 2000


If anything this argues the other way but the references may be useful.

Vagotomy Blocks the Induction of Interleukin-1 b (IL-1 b) mRNA in
the Brain of Rats in Response to Systemic IL-1 b

The Journal of Neuroscience, March 15, 1998, 18(6):2247-2253

Abstract


There is considerable interest in the mechanisms by which systemic cytokines
signal the CNS to elicit centrally controlled biological actions. This study
determined the effects of intra-peritoneal injections of interleukin-1 b
(IL-1 b) on IL-1 b mRNA and IL-1 receptor accessory protein (IL-1RAP) mRNA
produc-tion in rat liver and brain using the reverse transcription-PCR.
Saline or IL-1 b (0.5 mg/kg) was injected intraperitoneally in
subdiaphragmatically vagotomized and sham-operated (SHAM) rats. All
injections were performed at dark onset, and rats were killed 2 hr after the
injection. In SHAM rats, IL-1 b increased IL-1 b mRNA levels in the liver,
hypothalamus, hip-pocampus, and brainstem. Subdiaphragmatic vagotomy blocked
the IL-1 b-induced increase in IL-1 bmRNA in the brain-stem and hippocampus
and significantly attenuated the in- crease in the hypothalamus. Vagotomy
did not affect IL-1 b-induced IL-1 b mRNA production in the liver. IL-1RAP
mRNA was highly expressed in each region examined; however, no significant
differences in IL-1RAP mRNA production were found in any region after IL-1 b
injection. The current results indicate that the vagus nerve is involved in
transmitting cytokine signals to the brain and suggest that the induction of
brain cytokines is a critical step in the pathway by which vagal-mediated
signals result in centrally controlled symptoms of the acute phase response.


a bit ...

 In addition, vagotomy inhibits increases in ACTH se-cretion (Gaykema et
al., 1995), c-Fos expression in brain (Wan et al., 1994; Gaykema et al.,
1995), hypothalamic norepineph-rine depletion (Fleshner et al., 1995), and
elevated plasma corticosteriod levels (Fleshner et al., 1995) produced by
vari-ous peripheral immune stimuli. Finally, localized cytokine production
and interactions with receptors (e.g., on liver, tho-racic, and laryngeal
paraganglia; Goehler et al., 1997) could explain the findings that many CNS
manifestations of the acute phase response occur in the absence of
measurable circulating cytokines (Kluger, 1991). Collectively, these data
clearly sug-gest the existence of sensors for IL-1 bthat send information to
the CNS via vagal afferents. The fact that IL-1 b mRNA production in the
hypothalamus was not totally blocked by vagotomy suggests that alternative
pathways exist, in addition to the subdiaphragmatic vagus, which communicate
peripheral cytokine signals to the brain.


ULTRAMED, INC. <ultramedco at worldnet.att.net> wrote in message
news:Wdkq4.15843$LC4.290514 at bgtnsc04-news.ops.worldnet.att.net...
> Does anyone on the list know which centers
> are conducting studies on vagal nerve
> stimulation to alleviate depression?
>
> We are aware of the Cyberonics program but
> wonder if there are others.
>
> Thanks for any help.
>
> Gil Groehn
> Ultramed, Inc.
>
>






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