Capturing Sandhill Cranes with Alpha-Chloralose

1973 ◽  
Vol 37 (1) ◽  
pp. 94 ◽  
Author(s):  
Lovett E. Williams ◽  
Robert W. Phillips
Keyword(s):  
Sandhill Cranes ◽  
Alpha Chloralose

Capture of Sandhill Cranes Using Alpha-chloralose: A 10-Year Follow-up

2014 ◽  
Vol 50 (1) ◽  
pp. 143-145 ◽  
Author(s):  
Barry K. Hartup ◽  
Lauren Schneider ◽  
J. Michael Engels ◽  
Matthew A. Hayes ◽  
Jeb A. Barzen
Keyword(s):  
Sandhill Cranes ◽  
Alpha Chloralose

scholarly journals CAPTURE OF SANDHILL CRANES USING ALPHA-CHLORALOSE

2003 ◽  
Vol 39 (4) ◽  
pp. 859-868 ◽  
Author(s):  
Matthew A. Hayes ◽  
Barry K. Hartup ◽  
Jeanne M. Pittman ◽  
Jeb A. Barzen
Keyword(s):  
Sandhill Cranes ◽  
Alpha Chloralose

Feeding Ecology of Sandhill Cranes during Spring Migration in Nebraska

1986 ◽  
Vol 50 (1) ◽  
pp. 71 ◽  
Author(s):  
Kenneth J. Reinecke ◽  
Gary L. Krapu
Keyword(s):  
Feeding Ecology ◽  
Spring Migration ◽  
Sandhill Cranes

scholarly journals ALPHA-CHLORALOSE IMMOBILIZATION OF ROCK DOVES IN OHIO

1999 ◽  
Vol 35 (2) ◽  
pp. 239-242 ◽  
Author(s):  
Jerrold L. Belant ◽  
Thomas W. Seamans
Keyword(s):  
Alpha Chloralose

Age of Sexual Maturity of Sandhill Cranes from Mid-Continental North America

1989 ◽  
Vol 53 (1) ◽  
pp. 43 ◽  
Author(s):  
Thomas C. Tacha ◽  
Donald E. Haley ◽  
Paul A. Vohs
Keyword(s):  
North America ◽  
Sexual Maturity ◽  
Sandhill Cranes

T2-T5 spinothalamic neurons projecting to medial thalamus with viscerosomatic input

1985 ◽  
Vol 54 (1) ◽  
pp. 73-89 ◽  
Author(s):  
W. S. Ammons ◽  
M. N. Girardot ◽  
R. D. Foreman
Keyword(s):  
Receptive Fields ◽  
Cell Group ◽  
Spinothalamic Tract ◽  
Medial Thalamus ◽  
Dorsal Nucleus ◽  
Afferent Fibers ◽  
C Fiber ◽  
Antidromic Responses ◽  
Alpha Chloralose ◽  
Stimulation Of

Spinothalamic tract neurons projecting to medial thalamus (M-STT cells), ventral posterior lateral nucleus (VPL) of the thalamus (L-STT cells), or both thalamic regions (LM-STT cells) were studied in 19 monkeys anesthetized with alpha-chloralose. Twenty-seven M-STT cells were antidromically activated from nucleus centralis lateralis, nucleus centrum medianum, or the medial dorsal nucleus. Stimulation of VPL elicited antidromic responses from 22 cells and 13 cells were activated from both VPL and medial thalamus. Antidromic conduction velocities of M-STT cells were significantly slower than those of L-STT or LM-STT cells. M-STT cells were located in laminae I, IV, V, and VII with greater numbers found in the deepest laminae. L-STT cells were located mostly in lamina IV, whereas most LM-STT cells were found in lamina V. Twenty-four of 27 M-STT cells, all L-STT cells, and all LM-STT cells received input from both cardiopulmonary sympathetic and somatic afferent fibers. WDR cells were most common among the L-STT and LM-STT groups, whereas HT cells were the most common class in the M-STT cell group. Excitatory receptive fields of M-STT cells were large, and often bilateral. Receptive fields of L-STT cells were simple and never bilateral. Receptive fields of LM-STT cells could be similar to M-STT or L-STT cells. Thirty-three percent of the M-STT cells, 37% of the L-STT cells, and 62% of the LM-STT cells had inhibitory receptive fields. Inhibition was elicited most often by a noxious pinch of the hindlimbs. Sixteen of 23 (70%) M-STT cells received C-fiber cardiopulmonary sympathetic input in addition to A-delta-fiber input. The other 7 cells received only A-delta-fiber input. Only 45% of the L-STT cells and 38% of the LM-STT cells received both A-delta- and C-fiber inputs. The maximum number of spikes elicited by A-delta-input was related to segmental locations for L-STT cells with greatest responses in T2 and lesser responses in more caudal segments; however, no such trend was apparent for M-STT cells or for responses to C-fiber input for either group. Electrical stimulation of the left thoracic vagus nerve inhibited 7 of 18 M-STT cells, 10 of 16 L-STT cells, and 6 of 12 LM-STT cells. These results are the first description of visceral input to cells projecting to medial thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

Role of paraventricular and supraoptic nuclei in central cardiovascular regulation in the cat

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
Inhibitory Influence ◽  
Sympathetic Nervous Systems ◽  
Aortic Depressor Nerve ◽  
Bilateral Lesions ◽  
Alpha Chloralose ◽  
Supraoptic Nuclei ◽  
Stimulation Of

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.

Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats

1995 ◽  
Vol 269 (3) ◽  
pp. R662-R668 ◽  
Author(s):  
T. Ando ◽  
T. Ichijo ◽  
T. Katafuchi ◽  
T. Hori
Keyword(s):  
Prostaglandin E2 ◽  
Sympathetic Nerve ◽  
Time Course ◽  
Sympathetic Nerve Activity ◽  
Dependent Manner ◽  
Central Administration ◽  
Nerve Activity ◽  
High Doses ◽  
Alpha Chloralose ◽  
Dose Dependent

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.

Nucleus tractus solitarius and control of blood pressure in chronic sinoaortic denervated rats

1992 ◽  
Vol 263 (2) ◽  
pp. R258-R266 ◽  
Author(s):  
A. M. Schreihofer ◽  
A. F. Sved
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Nucleus Tractus Solitarius ◽  
Inhibitory Influence ◽  
Baroreceptor Reflexes ◽  
Alpha Chloralose ◽  
And Control ◽  
Bilateral Destruction ◽  
Conscious Control

To determine the role of the nucleus tractus solitarius (NTS) in the tonic maintenance of arterial pressure (AP) following chronic baroreceptor denervation, the present study examined the effect of inhibition of the NTS on AP in chronic sinoaortic denervated (SAD) and control rats. One to two weeks after complete SAD (no residual arterial baroreceptor reflexes) mean AP was not significantly different from that of control rats. Bilateral microinjections of muscimol and lidocaine into the NTS markedly increased AP in alpha-chloralose-anesthetized control rats. However, microinjections of these neuroinhibitory drugs had no effect on AP in SAD rats. Similarly, 1 h after bilateral destruction of the NTS conscious control rats were hypertensive, while AP in SAD rats was not changed. Plasma levels of vasopressin (VP), which were also elevated in control rats 1 h after NTS lesions, were not significantly altered in SAD rats. These results demonstrate that inhibition of the NTS has no effect on AP or plasma levels of VP in chronic SAD rats. This suggests neither the NTS nor afferents to the NTS supply a tonic inhibitory influence on AP after chronic baroreceptor denervation.

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