Neural tuning for sound duration: role of inhibitory mechanisms in the inferior colliculus

Science ◽  
1994 ◽  
Vol 264 (5160) ◽  
pp. 847-850 ◽  
Author(s):  
J. Casseday ◽  
D Ehrlich ◽  
E Covey
1994 ◽  
Vol 266 (2) ◽  
pp. R496-R502 ◽  
Author(s):  
A. S. Haibara ◽  
W. A. Saad ◽  
J. V. Menani ◽  
L. A. Camargo ◽  
A. Renzi

In this study we investigated the influence of electrolytic lesion or of opioid agonist injections into the lateral hypothalamus (LH) on the dipsogenic, natriuretic, kaliuretic, antidiuretic, pressor, and bradycardiac effects of cholinergic stimulation of the medial septal area (MSA) in rats. Sham- and LH-lesioned male Holtzman rats received a stainless steel cannula implanted into the LH. Other groups of rats had cannulas implanted simultaneously into the MSA and LH. Carbachol (2 nmol) injection into the MSA induced water intake, pressor, and bradycardic responses. LH lesion reduced all of these effects (1-3 and 15-18 days). Previous injection of synthetic opiate agonist, FK-33824 (100 ng), into the LH reduced the water intake, natriuresis, kaliuresis, and pressor responses induced by carbachol injected into the MSA. These data show that both electrolytic lesion or injection of an opiate agonist in the LH reduces the fluid-electrolyte and cardiovascular responses to cholinergic activation of the MSA. The involvement of LH with central excitatory and inhibitory mechanisms related to fluid-electrolytic and cardiovascular control is suggested.


1992 ◽  
Vol 263 (3) ◽  
pp. G419-G425 ◽  
Author(s):  
A. M. Salapatek ◽  
T. Hynna-Liepert ◽  
N. E. Diamant

In five cats we examined 1) the role of a cholinergic mechanism in cholecystokinin octapeptide (CCK-OP) excitation of the lower esophageal sphincter (LES) and 2) the interaction between CCK-OP-induced excitation and inhibition of the LES. Under ketamine anesthesia, LES pressure was monitored with a sleeve catheter. With CCK-OP, LES excitation was seen in four of five cats, and inhibition was seen in three of five cats. (4-Hydroxy-2-butynyl)trimethylammonium chloride (McNeil-A343) produced similar responses in the same cats but was less potent than CCK-OP. Atropine and/or hexamethonium reduced the response to CCK-OP. Pirenzepine had no effect on any CCK-OP response but reduced relaxation and enhanced excitation produced by McNeil-A343. Phentolamine increased CCK-OP-induced relaxation. In conclusion, CCK-OP can produce LES contraction through a preganglionic cholinergic mechanism involving a nicotinic synapse; however, induction of relaxation occurs predominantly at a postganglionic site involving adrenergic modulation. There is animal-to-animal variability in the balance of excitatory and inhibitory mechanisms to the LES, which determines the effect of a drug capable of activating both mechanisms.


2013 ◽  
Vol 256 ◽  
pp. 82-94 ◽  
Author(s):  
Guillermo Cabrera ◽  
Matías Cavelli ◽  
Carolina Lopez ◽  
Zulma Rodriguez-Servetti ◽  
Giancarlo Vanini ◽  
...  
Keyword(s):  

2005 ◽  
Vol 93 (6) ◽  
pp. 3390-3400 ◽  
Author(s):  
W. R. D’Angelo ◽  
S. J. Sterbing ◽  
E.-M. Ostapoff ◽  
S. Kuwada

A major cue for the localization of sound in space is the interaural time difference (ITD). We examined the role of inhibition in the shaping of ITD responses in the inferior colliculus (IC) by iontophoretically ejecting γ-aminobutyric acid (GABA) antagonists and GABA itself using a multibarrel pipette. The GABA antagonists block inhibition, whereas the applied GABA provides a constant level of inhibition. The effects on ITD responses were evaluated before, during and after the application of the drugs. If GABA-mediated inhibition is involved in shaping ITD tuning in IC neurons, then applying additional amounts of this inhibitory transmitter should alter ITD tuning. Indeed, for almost all neurons tested, applying GABA reduced the firing rate and consequently sharpened ITD tuning. Conversely, blocking GABA-mediated inhibition increased the activity of IC neurons, often reduced the signal-to-noise ratio and often broadened ITD tuning. Blocking GABA could also alter the shape of the ITD function and shift its peak suggesting that the role of inhibition is multifaceted. These effects indicate that GABAergic inhibition at the level of the IC is important for ITD coding.


1997 ◽  
Vol 273 (5) ◽  
pp. R1786-R1792 ◽  
Author(s):  
Joel M. Kaplan ◽  
William H. Siemers ◽  
Ulrika Smedh ◽  
Gary J. Schwartz ◽  
Harvey J. Grill

The effect of gastric branch vagotomy (GVX) on the gastric emptying of glucose was evaluated during two phases of emptying control: as the stomach fills and in the postload period. GVX and control rats received a series of intragastric glucose infusions (1.0 ml/min) through indwelling gastric fistulas. In experiment 1, gastric samples were withdrawn either immediately after the offset of 9- or 18-min infusions of 12.5% glucose or at various times up to 36 min postinfusion. In experiment 2, samples were withdrawn either immediately or 30 min after termination of 12-min infusions of 12.5 or 25% glucose. After gastric fill, glucose solute emptying rate was stable over time, not influenced by concentration doubling, and, surprisingly, not affected by GVX. During gastric fill, solute emptying rate doubled with concentration in both GVX and control rats. For each concentration, however, glucose emptied during fill at almost twice the rate in GVX compared with control rats. This accelerated emptying of glucose during fill in GVX rats is consistent with a gastric vagal contribution to inhibitory mechanisms (e.g., receptive relaxation) that operate as the stomach fills under normal conditions. The absence of a GVX effect on emptying after fill suggests either that gastric branch vagal efferents play little role in feedback inhibitory control of glucose emptying under normal conditions or that other systems compensate for the function previously served by vagal gastric branch efferents. Further work is required to address the possible role of the gastric vagus in feedback control of gastric emptying when nutritive fluids other than glucose are delivered.


2014 ◽  
Vol 1543 ◽  
pp. 209-222
Author(s):  
Ningqian Wang ◽  
Xiao Wang ◽  
Xiaoli Yang ◽  
Jie Tang ◽  
Zhongju Xiao

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