THE ROLE OF THE MEDIAL FOREBRAIN BUNDLE IN MEDIATING ADRENOCORTICAL RESPONSES TO NEUROGENIC STIMULI

1971 ◽  
Vol 51 (4) ◽  
pp. 745-749 ◽  
Author(s):  
S. FELDMAN ◽  
N. CONFORTI ◽  
I. CHOWERS
Keyword(s):  
Medial Forebrain Bundle ◽  
Acoustic Stimulation ◽  
Plasma Corticosterone ◽  
Neural Pathways ◽  
Afferent Pathway ◽  
Lower Plasma ◽  
Bilateral Lesions ◽  
Adrenocortical Responses ◽  
Intact Rats

SUMMARY The effects of ether stress and of photic and acoustic stimulation on adrenocortical responses were studied in normal rats and in rats with bilateral lesions in the medial forebrain bundle (MFB). While the response to ether stress was slightly reduced, the neurogenic stimuli produced much lower plasma corticosterone levels in the lesioned animals compared with intact rats. The neural pathways and the role of the MFB in mediating adrenocortical responses to neurogenic stimuli are discussed. The present results demonstrate that the MFB is the main final afferent pathway through which neural impulses to the hypothalamus are propagated, thus activating the secretion of adrenocorticotrophin.

COMPLETE INHIBITION OF ADRENOCORTICAL RESPONSES FOLLOWING SCIATIC NERVE STIMULATION IN RATS WITH HYPOTHALAMIC ISLANDS

1975 ◽  
Vol 78 (3) ◽  
pp. 539-544 ◽  
Author(s):  
Shaul Feldman ◽  
Nisim Conforti ◽  
Israel Chowers
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Acoustic Stimulation ◽  
Plasma Corticosterone ◽  
Neural Pathways ◽  
Implanted Electrodes ◽  
Sciatic Nerve Stimulation ◽  
Adrenocortical Responses ◽  
Pentobarbital Anaesthesia ◽  
Intact Rats

ABSTRACT Previous studies from this laboratory have demonstrated that in rats with hypothalamic islands the adrenocortical response to photic and acoustic stimulation was partially inhibited indicating that they were at least to a certain degree neurally mediated, though ether stress produced normal adrenocortical responses. With the purpose of determining to what extent afferent somatosensory connections to the hypothalamus participate in the activation of adrenocortical responses following sciatic nerve stimulation, the effects of this stimulus applied through chronically implanted electrodes were studied on the plasma corticosterone levels in pentobarbital anaesthetized intact animals and in rats with hypothalamic islands. Ether stress or sciatic nerve stimulation for 2 min in intact rats produced a rise of plasma corticosterone to 32.1 ± 1.2 and 32.1 ± 1.8 μg/100 ml, respectively. However, in animals with hypothalamic islands the corresponding values were 29.2 ± 1.8 and 12.4 ± 0.8 μg/100 ml, respectively. The latter value was not significantly different from the basal corticosterone levels (13.0 ± 1.2 μg/100 ml) found in rats 15 min after pentobarbital anaesthesia, the time when the sciatic stimulus was applied. The present data indicate that the adrenocortical discharge following sciatic nerve stimulation is completely inhibited by hypothalamic deafferentation and therefore depends entirely on the activation of the afferent neural pathways to the hypothalamus.

EFFECTS OF PARTIAL HYPOTHALAMIC DEAFFERENTATIONS ON ADRENOCORTICAL RESPONSES

1972 ◽  
Vol 69 (3) ◽  
pp. 526-530 ◽  
Author(s):  
S. Feldman ◽  
N. Conforti ◽  
I. Chowers
Keyword(s):  
Medial Forebrain Bundle ◽  
Acoustic Stimulation ◽  
Sensory Inputs ◽  
Adrenocortical Responses ◽  
Intact Rats

ABSTRACT The effects of ether stress and photic and acoustic stimulation on adrenocortical responses were studied in normal rats and in three groups of animals with partial hypothalamic anterior, anterolateral and posterolateral deafferentations, respectively. Animals with anterior deafferentation only, show the same responses as the intact rats, while in the two other groups the response to ether was normal, but that to photic and acoustic stimulation was significantly inhibited. These data would indicate that the transmission of impulses in the medial forebrain bundle and possibly posterior sensory inputs to the hypothalamus play an important role in the adrenocortical responses following neurogenic stimulation.

INHIBITION AND FACILITATION OF FEEDBACK INFLUENCES OF DEXAMETHASONE ON ADRENOCORTICAL RESPONSES TO ETHER STRESS IN RATS WITH HYPOTHALAMIC DEAFFERENTATIONS AND BRAIN LESIONS

1976 ◽  
Vol 82 (4) ◽  
pp. 785-791 ◽  
Author(s):  
Shaul Feldman ◽  
Nissim Conforti
Keyword(s):  
Negative Feedback ◽  
Medial Forebrain Bundle ◽  
Inhibitory Effect ◽  
Brain Lesions ◽  
The Difference ◽  
Sites Of Action ◽  
Bilateral Lesions ◽  
Adrenocortical Responses ◽  
The Brain ◽  
Intact Rats

ABSTRACT In order to elucidate the mechanisms and the sites of action of the negative feedback of corticoids in the regulation of ACTH secretion, the effects of systemically administered dexamethasone on adrenocortical responses to ether stress were studied in intact rats and in 11 experimental groups. These included animals with partial anterior, anterolateral, posterolateral, posterior and small posterior deafferentations as well as bilateral lesions in the medial forebrain bundle (MFB), fasciculus longitudinalis dorsalis (FLD), medial and lateral midbrain reticular formation (MRF) and in the ventrolateral pons. In rats with posterior hypothalamic deafferentation the degree of the inhibitory effect of dexamethasone was much smaller than that in intact animals. In animals with lesions in the FLD and MRF, dexamethasone also produced a reduction in the suppression of the response, though the difference was not significant. Bilateral lesions in the MFB and MP have on the other hand very significantly enhanced the effect of the negative feedback of dexamethasone when compared to intact rats. These data would indicate that hypothalamic deafferentations and brain lesions may change the sensitivity of the hypothalamus for the feedback control of corticoids and that there exist two antagonistic systems, an inhibitory and a facilitatory, in the brain which mediate this effect.

Role of monkey precentral cortex in control of voluntary jaw movements

1975 ◽  
Vol 38 (1) ◽  
pp. 146-157 ◽  
Author(s):  
E. S. Luschei ◽  
G. M. Goodwin
Keyword(s):  
Electrical Stimulation ◽  
Visual Stimulus ◽  
Neural Pathways ◽  
Unilateral Lesion ◽  
Jaw Movements ◽  
Face Area ◽  
The Face ◽  
Bilateral Lesions

Monkeys were trained to produce a low, steady biting force for 0.5-2.5 s, and then a rapid forceful bite in response to a visual stimulus. After large bilateral lesions of the precentral face area, monkeys emitted repetitive forceful bites on the apparatus, but could not perform the force-holding task. They eventually relearned the task, but the force exerted was never as steady as it was prelesion, and often oscillated at about 2 and/or 5-6 Hz. After retraining, two animals with large bilateral lesions of the face area produced median RT responses equal to or only slightly longer than their prelesion performance, indicating that neural pathways not involving the precentral cortex can mediate quick visual RT responses. The variability of RTs was permanently increased, probably as a result of the persistent unsteadiness of the force-holding response. Incomplete bilateral lesions of the precentral face area, a complete unilateral lesion of that area, and bilateral lesions adjacent regions of cortex produced either mild, transient difficulties with the biting taks, or no problems at all. The results indicate that the precentral cortex has a role in the control of voluntary jaw movements. Lesions caused difficulty in controlling, but not producing, closing jaw movements, thereby suggesting that this role is predominantly to inhibit jaw-closing motoneurons or the systems that excite them. Electrical stimulation studies of the face area of the precentral cortex of the unanesthetized monkey point to the same conclusion.

Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity

2018 ◽  
Vol 107 (2) ◽  
pp. 147-157 ◽  
Author(s):  
Sheng-Feng Tsai ◽  
Hung-Tsung Wu ◽  
Pei-Chun Chen ◽  
Yun-Wen Chen ◽  
Megan Yu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Tissue Expansion ◽  
Plasma Corticosterone ◽  
High Fat ◽  
Obesity In Mice ◽  
Bilateral Lesions

Background: The notion that exposure to chronic stress predisposes individuals to developing type 2 diabetes (T2D) has gained much attention in recent decades. Long-term stress induces neuroadaptation in the amygdala and increases corticosterone levels. Corticosterone, the major stress hormone in rodents, induces insulin resistance and obesity in mice. However, little is known about whether the stress-induced amygdalar neuroadaptation could promote the risk of T2D. Methods: We used an 11-week high-fat diet (HFD) feeding paradigm to induce insulin dysfunction in mice, followed by implementation of a 10-day social defeat (SD) stress protocol. Results: Mice receiving SD at the beginning of the HFD feeding aggravated HFD-induced insulin resistance and white adipose tissue expansion. HFD mice had higher levels of plasma corticosterone, which was not affected by the SD. The SD stress upregulated the expression of TrkB and synaptotagmin-4 in the amygdala of HFD mice. Bilateral lesions of the central amygdalae before SD stress inhibited the stress-induced aggravating effect without affecting the HFD-induced elevation of plasma corticosterone. Conclusions: Stress aggravates HFD-induced insulin resistance and neuroadaptation in the amygdala. The HFD-induced insulin resistance is amygdala-dependent. Understanding the role of stress-induced amygdalar adaptation in the development of T2D could inform therapies aimed at reducing chronic stressors to decrease the risk for T2D.

Stress- and cold-induced adrenocortical responses in repetitively immobilized or cold-acclimated rats

1987 ◽  
Vol 65 (7) ◽  
pp. 1448-1451 ◽  
Author(s):  
Takehiro Yahata ◽  
Kazuhiko Murazumi ◽  
Akihiro Kuroshima
Keyword(s):  
Cold Acclimation ◽  
Cold Exposure ◽  
Immobilization Stress ◽  
Acute Stress ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Nonshivering Thermogenesis ◽  
Adrenocortical Hormone ◽  
Adrenocortical Responses

To evaluate the role of adrenocortical hormones in stress- or cold-induced nonshivering thermogenesis, plasma corticosterone (CS) and deoxycorticosterone (DOCS) were measured with the aid of HPLC under various conditions. Repetitive immobilization stress (3 h/day, for 1 or 4 weeks) elevated the resting level (24 h after the last immobilization) of CS, but not DOCS. Acute stress (immobilization for 30 min) or cold exposure (−5 °C for 15 min) caused marked increases of CS and DOCS in both nonstressed naive controls and repetitively stressed rats. Four weeks, but not 1 week, of repetitive immobilization stress potentiated the responsiveness of CS to both acute stress and cold, and that of DOCS to acute stress, but not to cold. Cold acclimation (5 °C, 4 weeks) significantly elevated both corticosteroids but did not affect the resting levels (18 h after being transferred to 25 °C) or the responsiveness of both CS and DOCS to either acute stress or cold. These results suggest that repetitive immobilization stress, but not cold acclimation, could enhance nonshivering thermogenesis, at least in part, through an improvement in the responsiveness of adrenocortical hormone secretion to acute stress or cold.

ADRENOCORTICAL RESPONSES FOLLOWING SCIATIC NERVE STIMULATION IN RATS WITH PARTIAL HYPOTHALAMIC DEAFFERENTATIONS

1975 ◽  
Vol 80 (4) ◽  
pp. 625-629 ◽  
Author(s):  
Shaul Feldman ◽  
Nissim Conforti ◽  
Israel Chowers
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Neural Pathways ◽  
Mediobasal Hypothalamus ◽  
Adrenocortical Response ◽  
Sciatic Nerve Stimulation ◽  
Adrenocortical Responses ◽  
Intact Rats

ABSTRACT Studies from this laboratory have demonstrated that the adrenocortical response following sciatic nerve stimulation is completely inhibited in rats with hypothalamic islands, indicating that this response depends entirely on the activation of afferent neural pathways to the hypothalamus. With the purpose of identifying the site of entry of these neural pathways into the mediobasal hypothalamus the effects of partial hypothalamic deafferentations were studied. It was found that in rats with posterior or posterolateral deafferentation the adrenocortical responses were similar to those obtained in intact rats, while anterior and anterolateral deafferentation resulted in a reduction of 62.3 and 53.3 %, respectively. These results would indicate that the sciatic impulses which activate the adrenocortical response involve neural afferents which enter the mediobasal hypothalamus by an anterior pathway.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

scholarly journals Anatomy and Neural Pathways Modulating Distinct Locomotor Behaviors in Drosophila Larva

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 90
Author(s):  
Swetha B. M. Gowda ◽  
Safa Salim ◽  
Farhan Mohammad
Keyword(s):  
Motor Neurons ◽  
Model Systems ◽  
Neural Pathways ◽  
Animal Movements ◽  
Drosophila Larvae ◽  
The Central Nervous System ◽  
Drosophila Larva ◽  
Locomotor Behaviors ◽  
Basic Level

The control of movements is a fundamental feature shared by all animals. At the most basic level, simple movements are generated by coordinated neural activity and muscle contraction patterns that are controlled by the central nervous system. How behavioral responses to various sensory inputs are processed and integrated by the downstream neural network to produce flexible and adaptive behaviors remains an intense area of investigation in many laboratories. Due to recent advances in experimental techniques, many fundamental neural pathways underlying animal movements have now been elucidated. For example, while the role of motor neurons in locomotion has been studied in great detail, the roles of interneurons in animal movements in both basic and noxious environments have only recently been realized. However, the genetic and transmitter identities of many of these interneurons remains unclear. In this review, we provide an overview of the underlying circuitry and neural pathways required by Drosophila larvae to produce successful movements. By improving our understanding of locomotor circuitry in model systems such as Drosophila, we will have a better understanding of how neural circuits in organisms with different bodies and brains lead to distinct locomotion types at the organism level. The understanding of genetic and physiological components of these movements types also provides directions to understand movements in higher organisms.

scholarly journals DNA Methyltransferase 3A Is Involved in the Sustained Effects of Chronic Stress on Synaptic Functions and Behaviors

2020 ◽  
Author(s):  
Jing Wei ◽  
Jia Cheng ◽  
Nicholas J Waddell ◽  
Zi-Jun Wang ◽  
Xiaodong Pang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dna Methyltransferase ◽  
Epigenetic Modification ◽  
Substantial Reduction ◽  
Dna Methyltransferases ◽  
Male Rats ◽  
Neural Pathways ◽  
Dnmt Inhibitors ◽  
Synaptic Functions

Abstract Emerging evidence suggests that epigenetic mechanisms regulate aberrant gene transcription in stress-associated mental disorders. However, it remains to be elucidated about the role of DNA methylation and its catalyzing enzymes, DNA methyltransferases (DNMTs), in this process. Here, we found that male rats exposed to chronic (2-week) unpredictable stress exhibited a substantial reduction of Dnmt3a after stress cessation in the prefrontal cortex (PFC), a key target region of stress. Treatment of unstressed control rats with DNMT inhibitors recapitulated the effect of chronic unpredictable stress on decreased AMPAR expression and function in PFC. In contrast, overexpression of Dnmt3a in PFC of stressed animals prevented the loss of glutamatergic responses. Moreover, the stress-induced behavioral abnormalities, including the impaired recognition memory, heightened aggression, and hyperlocomotion, were partially attenuated by Dnmt3a expression in PFC of stressed animals. Finally, we found that there were genome-wide DNA methylation changes and transcriptome alterations in PFC of stressed rats, both of which were enriched at several neural pathways, including glutamatergic synapse and microtubule-associated protein kinase signaling. These results have therefore recognized the potential role of DNA epigenetic modification in stress-induced disturbance of synaptic functions and cognitive and emotional processes.

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