Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons

Guanethidine-induced destruction of sympathetic postganglionic neurons in neonatal rats leads to transneuronal degeneration of the sympathetic preganglionic neurons. Using this model, we have been able to show a approximately 35% decrease in [3H]substance P ([3H]SP) binding in the intermediolateral cell column--suggesting that sympathetic preganglionic neurons possess substance P receptors. Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons.

Brain Res. 1985 Apr 29;193-6. pii:0006-8993(85)90146-5.
Reduction of [3H]substance P binding in the intermediolateral cell column after sympathectomy. Takano Y,Loewy AD
https://www.gcbi.com.cn/gclib/html/pubmed/detail/2581658

https://archive.is/bfPLv

Substance P is an important element in pain perception. The sensory function of substance P is thought to be related to the transmission of pain information into the central nervous system. Substance P coexists with the excitatory neurotransmitter glutamate in primary afferents that respond to painful stimulation.[16] Substance P has been associated with the regulation of mood disorders, anxiety, stress,[17] reinforcement,[18] neurogenesis,[19] respiratory rhythm,[20] neurotoxicity, nausea and emesis,[21] pain, and nociception.[22] Substance P and other sensory neuropeptides can be released from the peripheral terminals of sensory nerve fibers in the skin, muscle, and joints. It is proposed that this release is involved in neurogenic inflammation, which is a local inflammatory response to certain types of infection or injury.[23] The regulatory function of SP also involves the regulation of its high-affinity receptor, NK-1. Substance P receptor antagonists may have important therapeutic applications in the treatment of a variety of stress-related illnesses, in addition to their potential as analgesics.

https://en.wikipedia.org/wiki/Substance_P

sympathectomized subjects act but do not feel emotional

in the absence of autonomic arousal, behavior that appears emotional will not be experienced as emotional

"In the presence of a barking dog, for example, the sympathectomized cats manifested almost all of the signs of feline rage. Finally, Cannon notes the report of Dana (1921) that a patient with a spinal-cord lesion and almost totally without visceral sensation still manifested emotionality.
For either the Jamesian or the present formulation such data are crucial, since both views demand visceral arousal as a necessary condition for emotional arousal. When faced with this evidence, James's defenders (e.g., Wenger, 1950; Mandler, 1962) have consistently made the point that the apparently emotional behavior manifested by sympathectomizied animals and men is well-learned behavior, acquired long before sympathectomy. There is a dual implication in this position: first, that sympathetic arousal facilitates the acquisition of emotional behavior, and second, that sympathectomized subjects act but do not feel emotional. There is a small but growing evidence supporting these contentions. Wynne and Solomon (1955) have demonstrated that sympathectomized dogs acquire an avoidance response considerably more slowly than control dogs. Further, on extinction trials most of their 13 sympathectomized animals extinguished quickly, whereas not a single one of the 30 control dogs gave any indication of extinction over 200 trials. Of particular interest are two dogs who were sympathectomized after they had acquired the avoidance response. On extinction trials these two animals behaved precisely like the control dogs - giving no indication of extinction. Thus, when deprived of visceral innervation, animals are quite slow in acquiring emotionally-linked avoidance responses and in general, quick to extinguish such responses." (p. 163)

"A line of thought stimulated by the Wynne and Solomon (1955) and the Hohmann (1962) studies may indeed be the answer to Cannon's observations that there can be emotional behavior without visceral activity. From the evidence of these studies, it would appear, first, that autonomic arousal greatly facilitates the acquisition of emotional behavior but it is not necessary for its maintenance if the behavior is acquired prior to sympathectomy; and second, that in the absence of autonomic arousal, behavior that appears emotional will not be experienced as emotional." (p. 167)

Acta Physiol Scand. 2000 Sep;170(1):33-8.

Middle cerebral artery blood velocity during exercise with beta-1 adrenergic and unilateral stellate ganglion blockade in humans.

Ide K1, Boushel R, Sørensen HM, Fernandes A, Cai Y, Pott F, Secher NH.

Author information

Abstract

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.

Sympathectomy at the level of the T2 ganglion leads to decreased negative feedback to the hypothalamus

Compensatory sweating was originally thought to be a mechanism of excessive sweating (in an anatomical region with an intact sympathetic nervous system) to maintain a constant rate of total sweat secretion.90 However, this theory was not confirmed by other studies, demonstrating that compensatory sweating represented a reflex action by an altered feedback mechanism at the level of the hypothalamus which is dependent on the level at which sympathetic denervation occurs. Sympathectomy at the level of the T2 ganglion leads to decreased negative feedback to the hypothalamus. When performing a sympathectomy at a lower level, the negative feedback to the hypothalamus is less inhibited, leading to a decrease in compensatory sweating. Chou et al.91 have proposed the term ‘reflex sweating’ to replace compensatory sweating. Other side effects described in a review article by Dumont89 are gustatory sweating, cardiac effects, phantom sweating, lung function changes, dry hands and altered taste. Besides these side effects there are significant risks of complications during and after surgery (arterial or venous vascular injury, pneumothorax, infection, Horner syndrome etc.).

JEADV 2012, 26, 1–8 Journal of the European Academy of Dermatology and Venereology

Sympathectomy and parasympathectomy leads to the hyperfunction of the serotoninergic system and pathology

We studied the balance of activity of sympathetic, parasympathetic, and serotoninergic divisions of the autonomic nervous system in the regulation of the heart function in rabbits. High activities of the sympathetic and parasympathetic system are associated with antagonistic interactions between them. Moderation of activity of these systems could be accompanied by activation of the serotoninergic system. Physiological sympathectomy and parasympathectomy lead to hyperfunction of the serotoninergic system and pathology.

Bulletin of Experimental Biology and Medicine, Vol. 140, No. 5, 2005 PHYSIOLOGY

Disturbances in brain serotonergic systems result in a range of phenotypes such as depression, suicide and anxiety disorders.
http://www.biomedcentral.com/1471-2202/10/50

Changes in cerebral capillary bed following cervical sympathectomy

Changes in the cerebral capillary bed following cervical sympathectomy,' Arch. Neurol. and Psychiat., 1929, 21, 1102.Tracy J. Putnam
The Cerebral Circulation: Some New Points in its Anatomy, Physiology and Pathology
J Neurol Psychopathol, Jan 1937; s1-17: 193 - 212.

High plasma norepinephrine and depression

High plasma norepinephrine and depression

Copyright © 1999 Society of Biological Psychiatry. Published by Elsevier Science Inc.

Plasma norepinephrine and prediction of outcome in major depressive disorder

Timothy G. Johnston^a, Christopher B. Kelly^, a, Michael R. Stevenson^b and Stephen J. Cooper^a 
a Department of Mental Health, Whitla Medical Building, The Queen’s University of Belfast, Belfast, UK (TGJ, CBK, SJC)
^b Department of Medical Statistics, Mulhouse Building, The Queen’s Unversity of Belfast, Belfast, UK (MRS)
Received 1 February 1999; revised 17 May 1999; accepted 21 May 1999. Available online 30 November 1999.

Background: Several epidemiologic and clinical factors have been shown to predict long term outcome in major depressive disorder (MDD). The value of biological predictors has not been extensively studied. This study examined whether plasma norepinephrine may be useful in predicting outcome in MDD.
Methods: Forty patients were followed up 8 years after an index major depressive episode. Three outcome variables were assessed: time to first recurrence (the primary outcome measure), the Lee and Murray criteria and the Depression Outcome Scale (DOS). The results were examined against plasma norepinephrine value, at the index episode, using survival analysis and linear regression.
Results: High plasma norepinephrine at the index episode was positively and significantly associated with time to first recurrence for patients with nonpsychotic MDD (n = 31, χ² = 8.38, on 1 df, p < .01). Similarly, plasma norepinephrine was significantly associated with good global outcome, both using Lee and Murray criteria (n = 34, adjusted R² = .24, p < .01) and DOS criteria (n = 31, adjusted R² = .17, p < .01) for this group of patients. In contrast, plasma norepinephrine was not significantly related to outcome for MDD with psychotic features.
Conclusions: Plasma norepinephrine at index episode seems to be a predictor of outcome in MDD.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T4S-3Y0RJKC-F&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a88b42c007e4dcb51054a00cf6662e2d

cervical sympathectomy works systemically through hypothalamus endocrine system

Background: To investigate the general action of stellate ganglion block (SGB), we examined the effects of heat stimulation and cold stress on the behavior and stress hormone of the bilateral cervical sympathectomy rats as a long-term and repeated SGB model. Methods: Wistar's male rats were divided into three groups: control (C), sham operation (S) and sympathectomy (Sx) groups. After 2 weeks, two experiments were done. One was measurement of escape response time from the heat stimulus and the other was hormone measurement. Serum adreno-corticotropic hormone (ACTH), .ALPHA.-melanocyte stimulating hormone (.ALPHA.-MSH) and .BETA.-endorphine (.BETA.-END) levels were measured assigning 3 groups to 2 subgroups with and without cold stress. Results: Escape response time was significantly extended in the Sx group. ACTH in the Sx group was significantly higher than in other groups, but changes of ACTH by cold stress were similar in 3 groups. In the Sx group .ALPHA.-MSH was hardly changed by cold stress while .ALPHA.-MSH was significantly decreased in the S group. Changes of .BETA.-END by cold stress were similar in the S and Sx groups. Conclusions: These results suggest that SGB works systemically through hypothalamus endocrine system and affects stress hormone differently. (author abst.)

http://sciencelinks.jp/j-east/article/200402/000020040204A0020288.php

Limbic-cortical dysregulation: a proposed model of depression

cognition and reward processing

Recent functional magnetic resonance imaging (fMRI) investigations of the interaction between cognition and reward processing have found that the lateral prefrontal cortex (PFC) areas are preferentially activated to both increasing cognitive demand and reward level. Conversely, ventromedial PFC (VMPFC) areas show decreased activation to the same conditions, indicating a possible reciprocal relationship between cognitive and emotional processing regions. We report an fMRI study of a rewarded working memory task, in which we further explore how the relationship between reward and cognitive processing is mediated. We not only assess the integrity of reciprocal neural connections between the lateral PFC and VMPFC brain regions in different experimental contexts but also test whether additional cortical and subcortical regions influence this relationship. Psychophysiological interaction analyses were used as a measure of functional connectivity in order to characterize the influence of both cognitive and motivational variables on connectivity between the lateral PFC and the VMPFC.

These findings provide evidence for a dynamic interplay between lateral PFC and VMPFC regions and are consistent with an emotional gating role for the VMPFC during cognitively demanding tasks. Our findings also support neuropsychological theories of mood disorders, which have long emphasized a dysfunctional relationship between emotion/motivational and cognitive processes in depression.
http://dl.acm.org/citation.cfm?id=1480468

Sympathectomy reduces emotional, stress-induced sweating indicating that it affects the stress-response

"...for reasons that are not obvious, many patients with facial hyperhidrosis and hyperhidrosis of the feet will benefit from upper thoracic sympathectomy. " 

(The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 261-264)

"Bilateral upper thoracic sympathicolysis is followed by redistribution of body perspiration, with a clear decrease in the zones regulated by mental or emotional stimuli, and an increase in the areas regulated by environmental stimuli, though we are unable to establish the etiology of this redistribution." 

(Surg Endosc. 2007 Nov;21(11):2030-3. Epub 2007 Mar 13.) 


"Palmar hyperhidrosis of clinical severity is a hallmark physical sign of many anxiety disorders, including generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and especially social phobia.4 These are increasingly well understood and highly treatable neurobiological conditions. They are mod- erately heritable hard-wired fear responses,5 and are linked to amygdalar and locus coeruleus hyper-reactivity during psycho- social stress.6,7 Anxiety disorders are known to be much more common among women. This is consistent with the finding of Krogstad et al. that among controls sweating was reported more often by men, while among the hyperhidrosis group sweating was reported more often among women."

"A surgical treatment for anxiety-triggered palmar hyperhidrosis is not unlike treating tearfulness in major depression by severing the nerves to the lacrimal glands. We have recently made a similar argument advocating a psychopharmacological, rather then a surgi- cal, first-line treatment for blushing.9" 
(Journal Compilation - 2006 British Association of Dermatologists - British Journal of Dermatology 2006, DOI: 10.1111/j.1365-2133.2006.07547.x)

"Surgical treatment of facial blushing requires careful patient selection. The effect is a normalization of the threshold to trigger facial blushing especially in social situations."

Clin Auton Res (2003) 13 [Suppl 1] : I/26 – I/30 

"So when the sympathetic nervous system is activated,

it alerts the hypothalamus, which alerts the pituitary gland, which tells the adrenal gland (atop your kidney) to make stress chemicals. Those chemicals travel through the bloodstream and affect your whole body. In your brain, they inflame the amygdala (increasing the intensity of sadness, fear, and anger) and block the hippocampus from laying down memory tracks.

If these chemicals continue for any length of time, the hippocampus shrinks and the amygdala enlarges. You can see these changes on an MRI brain scan. Parts of the cortex (the gray area on the outside that does most of your thinking) are also affected, including the VMPF (ventral medial prefrontal cortex), which controls emotions by calming the amygdala. Other areas in our cortex that help us speak and think coherently also can decrease in size.

THE LONGER THE SYMPATHETIC NERVOUS SYSTEM STAYS ON, THE MORE DAMAGE IT CAN DO TO YOUR BRAIN."

http://www.ptsdupdate.com/treatment-hyper-arousal-symptoms/

Sympathetic system modulation to treat post-traumatic stress disorder (PTSD): A review of clinical evidence and neurobiology

Journal of Affective Disorders 142 (2012) 1–5
http://axon.psyc.memphis.edu/~charlesblaha/7705/papers_S14/Woodward_Matt_PTSD_Neurobiology.pdf