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Hypothalamic neurons responding to hemodynamic input and to stimulation in the pons may influence adrenocorticotropin
Insights
This study identifies hypothalamic neurons sensitive to blood flow changes and electrical brainstem stimulation, suggesting a neural pathway for regulating adrenocorticotropin (ACTH) release.
Area of Science:
- Neuroscience
- Physiology
- Endocrinology
Background:
- The mediodorsal hypothalamus plays a role in regulating adrenocorticotropin (ACTH) release.
- The dorsal rostral pons is implicated in controlling ACTH release.
- Hemodynamic changes can influence neuroendocrine functions.
Purpose of the Study:
- To identify neurons in the mediodorsal hypothalamus sensitive to hemodynamic stimuli.
- To determine if these neurons also respond to electrical stimulation of the dorsal rostral pons.
- To investigate the neural pathways involved in the hemodynamic control of ACTH release.
Main Methods:
- Anesthetized cats were subjected to hemodynamic challenges (vena cava constriction, right atrial pulsation).
- Electrical stimulation was applied to the dorsal rostral pons using bipolar electrodes.
- Neuronal responses in the hypothalamus were recorded and analyzed.
Main Results:
- Some hypothalamic neurons exhibited sensitivity to hemodynamic stimuli (vena cava constriction or right atrial pulsation).
- Electrical stimulation of specific pontine sites modulated the activity of these hypothalamic neurons.
- Pontine stimulation sites influencing hemodynamically sensitive neurons were localized near areas previously linked to ACTH control.
Conclusions:
- Hypothalamic neurons involved in hemodynamic control of ACTH release receive projections from the dorsal rostral pons.
- These projections may originate from or pass through the dorsal raphe nucleus and lateral pontine nuclei (locus ceruleus, locus subceruleus).
- Some neurons may receive projections that bypass these specific pontine regions.
Abstract:
Experiments were designed to identify hemodynamically sensitive neurons in the mediodorsal hypothalamus and to determine if they were also sensitive to electrical stimulation of areas in the dorsal rostral pons that were implicated previously in the control of adrenocorticotropin (ACTH) release. Cats were anesthetized with chloralose and urethane, immobilized with gallamine, and artificially respired. Hemodynamic stimuli included constriction (CC) of the supradiaphragmatic inferior vena cava to reduce venous return and sinusoidal volume pulsation (RA) of the right atrium (1 ml peak at 1 Hz). Previously, CC was shown to facilitate and RA was shown to inhibit ACTH release. Electrical stimulation in the pons consisted of single shocks (500 microA DC, 0.05 msec, negative-to-tip) delivered on each of an array of three or four bipolar co-axial electrodes in the pons. Twenty-three neurons were tested with only RA. Of these, two were inhibited, two were facilitated, and 19 did not respond. Thirty-two neurons were tested with CC. Of these, nine were inhibited, nine were facilitated, and 14 did not respond. Seventeen neurons that responded either to RA or to CC were tested with stimulation in the pons. Of these, three were orthodromically activated and two were inhibited from a total of eight pontine sites. Six of the eight sites were within 300 microns of an area shown previously to contain neurons that responded to CC. Of 31 additional sites that were stimulated, but at which stimulation did not drive neurons that responded to hemodynamic stimuli, 26 were located more than 300 microns from this area (p less than 0.01, X2 test). The data suggest that some hypothalamic neurons involved in the hemodynamic control of ACTH release receive a projection from or through the dorsal raphe nucleus medially, and the ventral locus ceruleus, locus subceruleus, and underlying reticular formation laterally. However, other neurons may receive projections that bypass these regions.