Activation of postganglionic neurones via non-nicotinic synaptic mechanisms by stimulation of thin preganglionic axons

1984 ◽  
Vol 401 (3) ◽  
pp. 318-320 ◽  
Author(s):  
W. Jänig ◽  
R. Krauspe ◽  
G. Wiedersatz
Keyword(s):  
Synaptic Mechanisms ◽  
Stimulation Of ◽  
Postganglionic Neurones

Properties and synaptic mechanisms of bicuculline-induced epileptiform bursts in neocortical slices from children with intractable epilepsy

1993 ◽  
Vol 70 (5) ◽  
pp. 1759-1766 ◽  
Author(s):  
Y. I. Kim ◽  
W. J. Peacock ◽  
F. E. Dudek
Keyword(s):  
Nmda Receptors ◽  
Stimulus Intensity ◽  
Gray Matter ◽  
Intracellular Recording ◽  
Intractable Epilepsy ◽  
Onset Latency ◽  
Distant Site ◽  
Neurosurgical Treatment ◽  
Synaptic Mechanisms ◽  
Stimulation Of

1. Bicuculline-induced epileptiform bursts in slices of neocortical tissue resected from children (3 mo to 14 yr) undergoing neurosurgical treatment for intractable epilepsy were studied with conventional intracellular recording techniques. The purposes of this study were to characterize the bursts evoked in immature human neocortical slices, to gain further insight to how N-methyl-D-aspartate (NMDA) and non-NMDA receptors contribute to the genesis of the bursts, and to determine whether the characteristics of the bursts were related to patient age or clinically defined abnormality of the tissue. 2. Epileptiform bursts evoked by focal stimulation of the underlying white or gray matter in bicuculline (10 microM) were all-or-none events. Once evoked, the bursts in a given neuron appeared very similar to one another, regardless of stimulus intensity. Stronger stimuli only decreased the onset latency of the bursts. The bursts evoked with relatively weak stimuli (< 2-3 times the threshold), particularly those from stimulation of a distant site (4-5 mm), were variable in onset latency. The bursts from stimulation of a close site (0.5-2 mm) with stronger stimuli (> 3 times the threshold) were invariable in onset latency. 3. Across different cells, particularly across the cells in different slices, the bursts were quite variable in terms of their morphology and duration. When measured at one-half of the amplitude of the underlying depolarization (approximately 20-50 mV), the duration of the bursts ranged from 20 to 775 ms (n = 80 cells). In 23% of the cases (18 of 80 cells), afterdischarges lasting for tens of milliseconds to a few seconds followed the bursts.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac effects of electrically induced intrathoracic autonomic reflexes

1988 ◽  
Vol 66 (6) ◽  
pp. 714-720 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Anatomical Variation ◽  
Electrical Excitation ◽  
Neural Structure ◽  
Cardiac Responses ◽  
Neuronal Mechanisms ◽  
Autonomic Reflexes ◽  
Left Recurrent Laryngeal Nerve ◽  
The Right ◽  
Synaptic Mechanisms ◽  
Stimulation Of

Electrical stimulation of the afferent components in one cardiopulmonary nerve (the left vagosympathetic complex at a level immediately caudal to the origin of the left recurrent laryngeal nerve) in acutely decentralized thoracic autonomic ganglionic preparations altered cardiac chronotropism and inotropism in 17 of 44 dogs. Since these neural preparations were acutely decentralized, the effects were mediated presumably via intrathoracic autonomic reflexes. The lack of consistency of these reflexly generated cardiac responses presumably were due in part to anatomical variation of afferent axons in the afferent nerve stimulated. As stimulation of the afferent components in the same neural structure caudal to the heart (where cardiopulmonary afferent axons are not present) failed to elicit cardiac responses in any dog, it is presumed that when cardiac responses were elicited by the more cranially located stimulations, these were due to activation of afferent axons arising from the heart and (or) lungs. When cardiac responses were elicited, intramyocardial pressures in the right ventricular conus as well as the ventral and lateral walls of the left ventricle were augmented. Either bradycardia or tachycardia was elicited. Following hexamethonium administration no responses were produced, demonstrating that nicotonic cholinergic synaptic mechanisms were involved in these intrathoracic cardiopulmonary–cardiac reflexes. In six of the animals, when atropine was administered before hexamethonium, reflexly generated responses were attenuated. The same thing occurred when morphine was administered in four animals. In contrast, in four animals following administration of phentolamine, the reflexly generated changes were enhanced. As electrical excitation of afferent axons in one cardiopulmonary nerve of an acutely decentralized preparation can alter cardiac chronotropism and (or) inotropism, it is concluded that intrathoracic autonomic neuronal mechanisms exist which can modify heart rate and contractility in the absence of influences from central nervous system neurons. Furthermore, it appears that intrathoracic cardiopulmonary–cardiac reflexes capable of modifying the heart utilize a number of different synaptic mechanisms.

The Ferrier Lecture: The nature of central inhibition

1961 ◽  
Vol 153 (953) ◽  
pp. 445-476 ◽  
Keyword(s):  
Scientific Paper ◽  
Nobel Lecture ◽  
Central Inhibition ◽  
The Central Nervous System ◽  
Theoretical Paper ◽  
The Subject ◽  
The Brain ◽  
Synaptic Mechanisms ◽  
Scientific Life ◽  
Stimulation Of

I feel greatly honoured by the invitation to give the Ferrier Lecture. I attended the first Ferrier Lecture, given by Sherrington in 1929, and I learned from Sherrington to value and admire the pioneer contributions of David Ferrier to neurology. In choosing the subject of inhibition for my lecture I was prompted by the peculiar challenge that inhibition has presented to physiologists ever since it was first demonstrated by the Weber brothers in 1846 that stimulation of the vagus nerve could stop the heart and by Setchenov in 1863 that stimulation of areas in the brain could slow or prevent reflex responses of frog limbs. It was Sherrington who greatly extended and organized knowledge of inhibition in the central nervous system; first, by a series of remarkable investigations, and finally by a theoretical paper published by the Royal Society in 1925, in which excitation and inhibition were given equivalent status in the synaptic mechanisms controlling neuronal discharge. His interest in central inhibition continued to the end of his scientific life, and was the subject of his Nobel Lecture in 1932. I might mention that both my first scientific paper and my D.Phil. thesis were concerned with inhibition, and that I have continued to be more interested in the problem of synaptic inhibition than in any other aspect of neurophysiology. In recent years progress has been so rapid that our understanding of the nature of central inhibition is in several respects more complete than that of central excitation. This illumination has followed rather rapidly upon a long period of ingenious theorizing which is now only of historical interest

scholarly journals Synaptic mechanisms underlying modulation of locomotor-related motoneuron output by premotor cholinergic interneurons

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Filipe Nascimento ◽  
Matthew James Broadhead ◽  
Efstathia Tetringa ◽  
Eirini Tsape ◽  
Laskaro Zagoraiou ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Motor Output ◽  
Fictive Locomotion ◽  
Common Pathway ◽  
Spinal Interneurons ◽  
Genetic Ablation ◽  
Cholinergic Interneurons ◽  
Spinal Motor ◽  
Synaptic Mechanisms ◽  
Stimulation Of

Spinal motor networks are formed by diverse populations of interneurons that set the strength and rhythmicity of behaviors such as locomotion. A small cluster of cholinergic interneurons, expressing the transcription factor Pitx2, modulates the intensity of muscle activation via ‘C-bouton’ inputs to motoneurons. However, the synaptic mechanisms underlying this neuromodulation remain unclear. Here, we confirm in mice that Pitx2+ interneurons are active during fictive locomotion and that their chemogenetic inhibition reduces the amplitude of motor output. Furthermore, after genetic ablation of cholinergic Pitx2+ interneurons, M2 receptor-dependent regulation of the intensity of locomotor output is lost. Conversely, chemogenetic stimulation of Pitx2+ interneurons leads to activation of M2 receptors on motoneurons, regulation of Kv2.1 channels and greater motoneuron output due to an increase in the inter-spike afterhyperpolarization and a reduction in spike half-width. Our findings elucidate synaptic mechanisms by which cholinergic spinal interneurons modulate the final common pathway for motor output.

The role of neurotransmitters in mediating copulation-induced ovulation in the rat

1984 ◽  
Vol 100 (3) ◽  
pp. 361-365 ◽  
Author(s):  
R. E. Leipheimer ◽  
T. P. Condon ◽  
J. J. Curry
Keyword(s):  
Mating Behaviour ◽  
Cholinergic Receptors ◽  
Releasing Hormone ◽  
Induced Ovulation ◽  
Lh Releasing Hormone ◽  
Synaptic Mechanisms ◽  
Stimulation Of ◽  
Vaginal Stimulation

ABSTRACT Pentobarbitone-blocked pro-oestrous rats were subjected to either limited mating (maximum of 30 mounts), all-night cohabitation with males or stimulation of the vagina and cervix with a glass rod (2 or 5 min) to determine which type of stimulus was most effective in inducing ovulation. All-night cohabitation was the most successful procedure and resulted in 100% ovulation in those rats which mated. Treatment with either phenoxybenzamine, propranolol or pimozide did not interfere with this copulation-induced ovulation whereas methysergide treatment completely blocked copulation-induced ovulation. Administration of atropine resulted in a loss of mating behaviour and these animals therefore did not ovulate. Further experiments provided evidence that administration of atropine also blocked ovulation in response to vaginal stimulation with a glass rod. Pretreatment with methysergide or atropine had no effect upon the percentage of pentobarbitone-blocked, pro-oestrous rats ovulating in response to administration of LH releasing hormone (LHRH). However, those rats given atropine shed significantly fewer ova per rat following LHRH or LH infusion when compared with controls. These results suggest that the synaptic mechanisms responsible for mediating copulation-induced ovulation are different from those mediating steroid-induced ovulation, and that ovarian cholinergic receptors may play a role in ovulation. J. Endocr. (1984) 100, 361–365

Postsynaptic potentials and morphology of tectal cells responding to electrical stimulation of the bullfrog nucleus isthmi

1990 ◽  
Vol 5 (5) ◽  
pp. 479-488 ◽  
Author(s):  
S.R. Wang ◽  
N. Matsumoto
Keyword(s):  
Electrical Stimulation ◽  
Rana Catesbeiana ◽  
Lucifer Yellow ◽  
Optic Tract ◽  
Nucleus Isthmi ◽  
Postsynaptic Potentials ◽  
Tectal Neurons ◽  
Synaptic Mechanisms ◽  
Stimulation Of ◽  
In Cells

AbstractPostsynaptic responses of tectal cells in the bullfrog (Rana catesbeiana) were intracellularly recorded following electrical stimulation of the optic tract and the nucleus isthmi, and fluorescent dye, Lucifer yellow, was injected into some of the impaled cells to show their morphologies. Two main response types were found: The first type was an EPSP followed by an IPSP, and the second type was single IPSP. The first type predominates in cells responding to the optic tract stimulation and the second type prevails in cells responding to the isthmic stimulation. Fifteen cells stained with Lucifer yellow were localized in layer 6 (11 cells), layer 7 (1 cell), and layer 8 (3 cells). They were mainly identified as pear-shaped cells, large ganglionic cells, and stellate cells. Three injections demonstrated “dye-coupling,” which labeled up to six cells following one injection. Comparisons of postsynaptic potentials with cellular morphologies suggested that the nucleus isthmi could directly excite large ganglionic neurons in layer 6. Synaptic mechanisms for strong isthmic inhibition on the tectal neurons remain unknown.

scholarly journals µ-opioid receptor-mediated downregulation of midline thalamic pathways to basal and central amygdala

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
L. Goedecke ◽  
X. Bengoetxea ◽  
P. Blaesse ◽  
H.-C. Pape ◽  
K. Jüngling
Keyword(s):  
Social Rejection ◽  
Anxiety And Depression ◽  
Physical Pain ◽  
Central Amygdala ◽  
Dorsal Midline ◽  
Midline Thalamus ◽  
Excitatory Activity ◽  
Patch Clamp Electrophysiology ◽  
Synaptic Mechanisms ◽  
Stimulation Of

AbstractBrain µ-opioid receptors (MOR) mediate reward and help coping with pain, social rejection, anxiety and depression. The dorsal midline thalamus (dMT) integrates visceral/emotional signals and biases behavior towards aversive or defensive states through projections to the amygdala. While a dense MOR expression in the dMT has been described, the exact cellular and synaptic mechanisms of µ-opioidergic modulation in the dMT-amygdala circuitry remain unresolved. Here, we hypothesized that MORs are important negative modulators of dMT-amygdala excitatory networks. Using retrograde tracers and targeted channelrhodopsin expression in combination with patch-clamp electrophysiology, we found that projections of dMT neurons onto both basal amygdala principal neurons (BA PN) and central amygdala (CeL) neurons are attenuated by stimulation of somatic or synaptic MORs. Importantly, dMT efferents to the amygdala drive feedforward excitation of centromedial amygdala neurons (CeM), which is dampened by MOR activation. This downregulation of excitatory activity in dMT-amygdala networks puts the µ-opioid system in a position to ameliorate aversive or defensive behavioral states associated with stress, withdrawal, physical pain or social rejection.

Synaptic transmission in thoracic autonomic ganglia of the dog

1983 ◽  
Vol 61 (8) ◽  
pp. 793-801 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Neural Activity ◽  
Action Potentials ◽  
Compound Action Potentials ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Frequency Of Stimulation ◽  
Synaptic Mechanisms ◽  
Adrenergic And Cholinergic Receptors ◽  
Compound Action ◽  
Stimulation Of

Afferent stimulation of one canine thoracic cardiopulmonary nerve can generate compound action potentials in another ipsilateral cardiopulmonary nerve. These compound action potentials persist after acute decentralization of the middle cervical ganglion, indicating that they result from neural activity in the middle cervical ganglion and thoracic nerves. Changing the frequency of stimulation can alter the compound action potentials, suggesting that temporal facilitation or inhibition occurs in this middle cervical ganglion preparation. The compound action potentials can be modified by stimulation of sympathetic preganglionic fibers and by hexamethonium, atropine, phentolamine, propranolol, and (or) manganese. It thus appears that afferent cardiopulmonary nerves can activate efferent cardiopulmonary nerves via synaptic mechanisms in the stellate and middle cervical ganglia. It also appears that these mechanisms involve adrenergic and cholinergic receptors and are influenced by preganglionic sympathetic fibers arising from the cord.

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