The long-term goal of research in this laboratory is to elucidate the role of caudal hypothalamic neurons in regulating cardiorespiratory activity.
The specific aims are to: 1) provide evidence for the physiological function of caudal hypothalamic neurons; 2) identify stimuli which alter the discharge of identified neurons; 3) determine projections of caudal hypothalamic neurons to lower brainstem and spinal cord sites; and 4) examine possible contributions of caudal hypothalamic neurons to elevated pressure present in spontaneously hypertensive rats. Both in vivo and in vitro preparations will be used to address these aims. The first set of experiments will be performed in anesthetized cats. Computer signal averaging techniques will be utilized to correlate basal discharge frequency of hypothalamic neurons with the cardiac cycle, sympathetic nerve activity and/or phrenic nerve activity. In addition, single unit responses of these neurons to various stimuli (hypoxia, hypercapnia, baroreceptor activation, pulmonary stretch receptor stimulation) will be recorded. An attempt will then be made to determine the axonal projection of all neurons studied using antidromic activation and mapping techniques. An in vitro rat brain slice preparation will be utilized to evaluate the direct effects of hypoxia and hypercapnia upon caudal hypothalamic neurons. Whole cell patch recordings will be performed in the brain slice experiments; retrograde transport of rhodamine microbeads will be used in an attempt to determine projection sites of studied neurons. In vivo experiments will also be undertaken in spontaneously hypertensive rats (SHR) to determine if neuronal activity in the caudal hypothalamus is altered relative to that of normotensive rats. Computer averaging techniques will determine the proportion of caudal hypothalamic neurons which have a cardiac and/or sympathetic discharge. Each neuron will also be tested for a response to baroreceptor stimulation. In a final set of experiments, characteristics of hypothalamic neurons from SHR rats will be compared to those of normotensive rats in a brain slice preparation. Comparisons will be made between neurons from young and mature spontaneously hypertensive rats and with normotensive controls. The results of these studies may offer insight into neurological abnormalities contributing to the origination and/or maintenance of high blood pressure and altered cardiorespiratory reflexes.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL038726-06
Application #
2219009
Study Section
Respiratory and Applied Physiology Study Section (RAP)
Project Start
1988-04-01
Project End
1995-11-30
Budget Start
1993-12-01
Budget End
1994-11-30
Support Year
6
Fiscal Year
1994
Total Cost
Indirect Cost
Name
University of Illinois Urbana-Champaign
Department
Physiology
Type
Schools of Arts and Sciences
DUNS #
041544081
City
Champaign
State
IL
Country
United States
Zip Code
61820
Ichiyama, Ronaldo M; Waldrop, Tony G; Iwamoto, Gary A (2004) Neurons in and near insular cortex are responsive to muscular contraction and have sympathetic and/or cardiac-related discharge. Brain Res 1008:273-7
Kramer, J M; Waldrop, T G (1998) Neural control of the cardiovascular system during exercise. An integrative role for the vestibular system. J Vestib Res 8:71-80
Horn, E M; Waldrop, T G (1997) Oxygen-sensing neurons in the caudal hypothalamus and their role in cardiorespiratory control. Respir Physiol 110:219-28
Nolan, P C; Waldrop, T G (1996) Ventrolateral medullary neurons show age-dependent depolarizations to hypoxia in vitro. Brain Res Dev Brain Res 91:111-20
Iwamoto, G A; Wappel, S M; Fox, G M et al. (1996) Identification of diencephalic and brainstem cardiorespiratory areas activated during exercise. Brain Res 726:109-22
Iwamoto, G A; Waldrop, T G (1996) Lateral tegmental field neurons sensitive to muscular contraction: a role in pressor reflexes? Brain Res Bull 41:111-20
Ryan, J W; Waldrop, T G (1995) Hypoxia sensitive neurons in the caudal hypothalamus project to the periaqueductal gray. Respir Physiol 100:185-94
Nolan, P C; Dillon, G H; Waldrop, T G (1995) Central hypoxic chemoreceptors in the ventrolateral medulla and caudal hypothalamus. Adv Exp Med Biol 393:261-6
Shonis, C A; Waldrop, T G (1995) In vitro effects of GABA and hypoxia on posterior hypothalamic neurons from spontaneously hypertensive and Wistar-Kyoto rats. Brain Res Bull 36:461-6
Horn, E M; Waldrop, T G (1994) Modulation of the respiratory responses to hypoxia and hypercapnia by synaptic input onto caudal hypothalamic neurons. Brain Res 664:25-33

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