The general context of this study is the exploration of the central pathways responsible for the autonomic responses to nociception. The proposed work specifically focuses on how the trigeminal nucleus might control adrenal catecholamine secretion in the anesthetized cat. The work is divided into three parts.
The first aim i s to identify the putative trigeminal transmitters involved in controlling the secretion of ACTH and adrenal catecholamines. This will be achieved in part by measuring the rate of secretion of adrenal catecholamines, blood ACTH levels, and the hemodynamic effects produced by the microinjection into the trigeminal nucleus of agonists and antagonists to selected neurotransmitter receptors. A selection of receptor antagonists will then be injected into the trigeminal nucleus to determine if one type of chemical can successfully block the release of adrenal catecholamine evoked by orofacial nociceptive stimulation. Finally the hypothesis that nociceptive stimulation releases excitatory amino acids in the trigeminal nucleus will be directly tested by attempting to collect an overflow of one of these substances by the push-pull cannula method. The second part of the project is designed to identify potential relay nuclei interposed between the trigeminal nucleus and spinal preganglionic neurons which control the adrenal medulla. Each putative relay will be incapacitated in a reversible manner by microinjection of a local anesthetic until a significant attenuation of the adrenal response to nociceptive stimulation of the orofacial sphere is achieved.
The third aim explores the potentiative interactions between orofacial nociceptive stimulation and peripheral chemoreceptor activation on the release of ACTH and adrenal catecholamines. Finally, a series of neurophysiological unit recording experiments will test whether some integration between orofacial somatic nociceptive inputs and certain visceral inputs such as peripheral chemoreceptors occurs within the trigeminal complex perhaps on neurons which project directly to lower brainstem autonomic relays such as the parabrachial complex.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS026137-05
Application #
3411803
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1988-04-01
Project End
1995-03-31
Budget Start
1992-04-01
Budget End
1993-03-31
Support Year
5
Fiscal Year
1992
Total Cost
Indirect Cost
Name
Rhode Island Hospital (Providence, RI)
Department
Type
DUNS #
161202122
City
Providence
State
RI
Country
United States
Zip Code
02903
Tashiro, A; Okamoto, K; Chang, Z et al. (2010) Behavioral and neurophysiological correlates of nociception in an animal model of photokeratitis. Neuroscience 169:455-62
Chang, Z; Okamoto, K; Tashiro, A et al. (2010) Ultraviolet irradiation of the eye and Fos-positive neurons induced in trigeminal brainstem after intravitreal or ocular surface transient receptor potential vanilloid 1 activation. Neuroscience 170:678-85
Okamoto, Keiichiro; Tashiro, Akimasa; Chang, Zheng et al. (2010) Bright light activates a trigeminal nociceptive pathway. Pain 149:235-42
Okamoto, K; Bereiter, D F; Tashiro, A et al. (2009) Ocular surface-evoked Fos-like immunoreactivity is enhanced in trigeminal subnucleus caudalis by prior exposure to endotoxin. Neuroscience 159:787-94
Okamoto, K; Thompson, R; Tashiro, A et al. (2009) Bright light produces Fos-positive neurons in caudal trigeminal brainstem. Neuroscience 160:858-64
Bereiter, David A; Okamoto, Keiichiro; Tashiro, Akimasa et al. (2005) Endotoxin-induced uveitis causes long-term changes in trigeminal subnucleus caudalis neurons. J Neurophysiol 94:3815-25
Hirata, Harumitsu; Okamoto, Keiichiro; Tashiro, Akimasa et al. (2004) A novel class of neurons at the trigeminal subnucleus interpolaris/caudalis transition region monitors ocular surface fluid status and modulates tear production. J Neurosci 24:4224-32
Hirata, Harumitsu; Okamoto, Keiichiro; Bereiter, David A (2003) GABA(A) receptor activation modulates corneal unit activity in rostral and caudal portions of trigeminal subnucleus caudalis. J Neurophysiol 90:2837-49
Bereiter, D A; Bereiter, D F; Hirata, H (2002) Topical cannabinoid agonist, WIN55,212-2, reduces cornea-evoked trigeminal brainstem activity in the rat. Pain 99:547-56
Hirata, H; Takeshita, S; Hu, J W et al. (2000) Cornea-responsive medullary dorsal horn neurons: modulation by local opioids and projections to thalamus and brain stem. J Neurophysiol 84:1050-61

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