Participation of the hippocampus in the facilitatory effect of an exteroceptive stimulus on milk ejection

1984 ◽  
Vol 55 (1) ◽  
Author(s):  
R.P. Deis ◽  
J. Prilusky
Keyword(s):  
Facilitatory Effect ◽  
Exteroceptive Stimulus ◽  
Milk Ejection

Role of the paraventricular nucleus in controlling the frequency of milk ejection and the facilitatory effect of centrally administered oxytocin in the suckled rat

1990 ◽  
Vol 125 (3) ◽  
pp. 467-NP ◽  
Author(s):  
J. B. Wakerley ◽  
T. S. Juss ◽  
R. Farrington ◽  
C. D. Ingram
Keyword(s):  
Paraventricular Nucleus ◽  
Medial Septum ◽  
Facilitatory Effect ◽  
Milk Ejection ◽  
Before And After ◽  
Radiofrequency Lesions ◽  
Group 3 ◽  
Series Of Experiments ◽  
Milk Ejection Reflex ◽  
Facilitatory Action

ABSTRACT The milk-ejection reflex was studied in anaesthetized, lactating Wistar rats in order to evaluate the contribution of the paraventricular nucleus (PVN) to the patterning of milk ejection and the facilitatory action of centrally administered oxytocin. In the first series of experiments, radiofrequency lesions were performed and centred: (1) antero-dorsal to the PVN, damaging parts of the medial septum and anterior hypothalamus; (2) in the PVN, such that much of the parvocellular division was destroyed, but parts of the magnocellular division remained intact; or (3) in the PVN, destroying both parvocellular and magnocellular divisions. Suckling tests performed before and after lesioning showed that the milk-ejection interval was significantly increased (decreased frequency) after lesioning in groups 2 and 3, but that milk-ejection amplitude was significantly decreased only in group 3. These results suggest that damage to the parvocellular division of the PVN affects milk-ejection frequency, but that damage to the magnocellular PVN only affects amplitude. Subsequent tests on rats injected into the PVN with the neurotoxin N-methyl-d,l-aspartate revealed a fall in the amplitude and frequency of milk ejection, similar to that after complete radiofrequency lesions of the PVN. In the second series of experiments, the facilitatory action of centrally administered oxytocin (1 mU, 2.2 ng) was examined in animals bearing either sham or complete PVN lesions. In both groups, intracerebroventricular injection of oxytocin was able to increase the frequency of milk ejections, although the incidence of milk ejection was lower in the pre- and post-injection period in the PVN-lesioned animals. In conclusion, the parvocellular component of the PVN may be an important site for regulating milk-ejection frequency, possibly mediated by its centrally projecting oxytocin neurones. However, the PVN does not appear to be the principle target site by which central oxytocin exerts its facilitatory effect on the frequency of milk ejection. Journal of Endocrinology (1990) 125, 467–475

Facilitatory effect of hypothalamo-neurophypophysial tract stimulation on milk ejection frequency in the lactating rat

1990 ◽  
Vol 118 (1) ◽  
pp. 67-70 ◽  
Author(s):  
C.D. Ingram ◽  
I. Davison ◽  
J.B. Wakerley
Keyword(s):  
Facilitatory Effect ◽  
Milk Ejection

scholarly journals The effect of an exteroceptive stimulus on milk ejection in lactating rats

1968 ◽  
Vol 197 (1) ◽  
pp. 37-46 ◽  
Author(s):  
R. P. Deis
Keyword(s):  
Exteroceptive Stimulus ◽  
Milk Ejection

Facilitatory effect of antidromic stimulation on milk ejection-related activation of oxytocin neurons during suckling in the rat

1985 ◽  
Vol 59 (1) ◽  
pp. 21-25 ◽  
Author(s):  
Hideo Negoro ◽  
Kiyoshi Uchide ◽  
Kazumasa Honda ◽  
Takashi Higuchi
Keyword(s):  
Facilitatory Effect ◽  
Milk Ejection ◽  
Antidromic Stimulation

Rationalization and internalization

2001 ◽  
Vol 60 (4) ◽  
pp. 215-230 ◽  
Author(s):  
Jean-Léon Beauvois
Keyword(s):  
Phase 1 ◽  
Facilitatory Effect ◽  
Phase 2 ◽  
Causal Explanations ◽  
Reduction Effect ◽  
Dissonance Reduction

After having been told they were free to accept or refuse, pupils aged 6–7 and 10–11 (tested individually) were led to agree to taste a soup that looked disgusting (phase 1: initial counter-motivational obligation). Before tasting the soup, they had to state what they thought about it. A week later, they were asked whether they wanted to try out some new needles that had supposedly been invented to make vaccinations less painful. Agreement or refusal to try was noted, along with the size of the needle chosen in case of agreement (phase 2: act generalization). The main findings included (1) a strong dissonance reduction effect in phase 1, especially for the younger children (rationalization), (2) a generalization effect in phase 2 (foot-in-the-door effect), and (3) a facilitatory effect on generalization of internal causal explanations about the initial agreement. The results are discussed in relation to the distinction between rationalization and internalization.

EFFECT OF LOCALLY IMPLANTED OESTROGEN ON THE RESPONSE OF THE RAT'S LACTATING MAMMARY GLAND TO OXYTOCIN

1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Recording System ◽  
Saline Infusion ◽  
High Dose ◽  
Low Doses ◽  
Milk Ejection ◽  
Lactating Mammary Gland ◽  
Small Rise

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.

CATECHOLAMINE ANTAGONISM TO OXYTOCIN-INDUCED MILK-EJECTION

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr
Keyword(s):  
Receptor Blockade ◽  
Milk Ejection ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Alpha Receptors ◽  
Adrenergic Blockers ◽  
Beta Receptor Blockade ◽  
Second Pain ◽  
Stimulation Of

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.

Applying indices of udder blood supply to estimate milk ejection inhibition in cows

2017 ◽  
pp. 79-89
Author(s):  
V.P. Meshcheryakov ◽  
◽  
Ye.G. Cheremukha
Keyword(s):  
Blood Supply ◽  
Milk Ejection

Aluminum Suppresses Effect of Nicotine on Gamma Oscillations (20-40 Hz) in Mouse Hippocampal Slices

2018 ◽  
Vol 17 (6) ◽  
pp. 404-411 ◽  
Author(s):  
Syeda Mehpara Farhat ◽  
Touqeer Ahmed
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Cholinergic System ◽  
Acetylcholine Receptors ◽  
Peak Power ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Gamma Oscillation ◽  
Facilitatory Effect

Background: Aluminum (Al) causes neurodegeneration and its toxic effects on cholinergic system in the brain is well documented. However, it is unknown whether and how Al changes oscillation patterns, driven by the cholinergic system, in the hippocampus. Objective: We studied acute effects of Al on nicotinic acetylcholine receptors (nAChRs)-mediated modulation of persistent gamma oscillations in the hippocampus. Method: The field potential recording was done in CA3 area of acute hippocampal slices. Results: Carbachol-induced gamma oscillation peak power increased (1.32±0.09mV2/Hz, P<0.01) in control conditions (without Al) by application of 10µM nicotine as compared to baseline value normalized to 1. This nicotine-induced facilitation of gamma oscillation peak power was found to depend on non-α7 nAChRs. In slices with Al pre-incubation for three to four hours, gamma oscillation peak power was reduced (5.4±1.8mV2/Hz, P<0.05) and facilitatory effect of nicotine on gamma oscillation peak power was blocked as compared to the control (18.06±2.1mV2/Hz) or one hour Al pre-incubated slices (11.3±2.5mV2/Hz). Intriguingly wash-out, after three to four hours of Al incubation, failed to restore baseline oscillation power and its facilitation by nicotine as no difference was observed in gamma oscillation peak power between Al wash-out slices (3.4±1.1mV2/Hz) and slices without washout (3.6±0.9mV2/Hz). Conclusion: This study shows that at cellular level, exposure of hippocampal tissue to Al compromised nAChR-mediated facilitation of cholinergic hippocampal gamma oscillations. Longer in vitro Al exposure caused permanent changes in hippocampal oscillogenic circuitry and changed its sensitivity to nAChR-modulation. This study will help to understand the possible mechanism of cognitive decline induced by Al.

scholarly journals Subcortical circuits mediate communication between primary sensory cortical areas in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Lohse ◽  
Johannes C. Dahmen ◽  
Victoria M. Bajo ◽  
Andrew J. King
Keyword(s):  
Cortical Neurons ◽  
Common Property ◽  
Primary Auditory Cortex ◽  
Facilitatory Effect ◽  
Thalamic Nuclei ◽  
Auditory Midbrain ◽  
Cortical Areas ◽  
Auditory Responses ◽  
Evoked Activity

AbstractIntegration of information across the senses is critical for perception and is a common property of neurons in the cerebral cortex, where it is thought to arise primarily from corticocortical connections. Much less is known about the role of subcortical circuits in shaping the multisensory properties of cortical neurons. We show that stimulation of the whiskers causes widespread suppression of sound-evoked activity in mouse primary auditory cortex (A1). This suppression depends on the primary somatosensory cortex (S1), and is implemented through a descending circuit that links S1, via the auditory midbrain, with thalamic neurons that project to A1. Furthermore, a direct pathway from S1 has a facilitatory effect on auditory responses in higher-order thalamic nuclei that project to other brain areas. Crossmodal corticofugal projections to the auditory midbrain and thalamus therefore play a pivotal role in integrating multisensory signals and in enabling communication between different sensory cortical areas.

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