Joel P. Gallagher mostly deals with Neuroscience, Internal medicine, Endocrinology, Septal nuclei and Electrophysiology. His work deals with themes such as Receptor, Acetylcholine and Metabotropic glutamate receptor, which intersect with Neuroscience. As a member of one scientific family, Joel P. Gallagher mostly works in the field of Acetylcholine, focusing on Depolarization and, on occasion, Stereochemistry and Membrane.
His research in Septal nuclei focuses on subjects like Slice preparation, which are connected to Rhinencephalon, Antidromic, Neuron, Stimulation and Tetrodotoxin. His biological study spans a wide range of topics, including Baclofen and GABAA receptor. His research investigates the connection between Excitatory postsynaptic potential and topics such as Postsynaptic potential that intersect with problems in Corticotropin-releasing hormone receptor 1.
Joel P. Gallagher mainly focuses on Neuroscience, Endocrinology, Internal medicine, Depolarization and Biophysics. His research combines Neurotransmission and Neuroscience. His Endocrinology research integrates issues from Agonist, Long-term potentiation, NMDA receptor and Calcium.
His work on Serotonin, 5-HT receptor, Aminophylline and Propranolol as part of general Internal medicine research is often related to Soleus muscle, thus linking different fields of science. His Depolarization research includes themes of Acetylcholine, Membrane potential and Intracellular. His study focuses on the intersection of Biophysics and fields such as Bicuculline with connections in the field of Picrotoxin.
The scientist’s investigation covers issues in Neuroscience, Amygdala, Internal medicine, Endocrinology and Neurotransmission. His Neuroscience research incorporates themes from Glutamate receptor, Receptor and Anatomy. His studies deal with areas such as Long-term potentiation and Kindling as well as Amygdala.
The study of Internal medicine is intertwined with the study of Cognition in a number of ways. His research in Endocrinology is mostly focused on Emotional memory. Joel P. Gallagher has researched Neurotransmission in several fields, including Postsynaptic potential and Excitatory postsynaptic potential.
Joel P. Gallagher mainly investigates Neuroscience, Amygdala, Long-term potentiation, Receptor and Corticotropin-releasing hormone receptor 1. Many of his studies on Neuroscience apply to Neurotransmission as well. Joel P. Gallagher is investigating Internal medicine and Endocrinology as part of his examination of Amygdala.
His work on Excitatory postsynaptic potential as part of general Receptor study is frequently linked to Abstinence, Cocaine craving and Brain stimulation reward, therefore connecting diverse disciplines of science. Joel P. Gallagher has included themes like Central nucleus of the amygdala and Glutamatergic in his Excitatory postsynaptic potential study. His Corticotropin-releasing hormone receptor 1 study combines topics from a wide range of disciplines, such as Postsynaptic potential and Postsynaptic density.
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Characterization and ionic basis of GABA-induced depolarizations recorded in vitro from cat primary afferent neurones.
J P Gallagher;H Higashi;S Nishi.
The Journal of Physiology (1978)
Metabotropic glutamate receptors are required for the induction of long-term potentiation.
Fang Zheng;Joel P. Gallagher.
Neuron (1992)
Biochemical and Electrophysiological Characteristics of Mammalian Gaba Receptors
Salvatore J. Enna;Joel P. Gallagher.
International Review of Neurobiology (1983)
Corticotropin-Releasing Factor and Urocortin I Modulate Excitatory Glutamatergic Synaptic Transmission
Jie Liu;Baojian Yu;Volker Neugebauer;Dimitri E. Grigoriadis.
The Journal of Neuroscience (2004)
Synaptic physiology of central CRH system.
Joel P. Gallagher;Luis F. Orozco-Cabal;Jie Liu;Patricia Shinnick-Gallagher.
European Journal of Pharmacology (2008)
Primary afferent excitatory transmission recorded intracellularly in vitro from rat medial vestibular neurons.
Michael R. Lewis;Kevin D. Phelan;Patricia Shinnick‐Gallagher;Joel P. Gallagher.
Synapse (1989)
Adenosine mediates a slow hyperpolarizing synaptic potential in autonomic neurones.
T. Akasu;P. Shinnick-Gallagher;J. P. Gallagher.
Nature (1984)
Cocaine withdrawal enhances long‐term potentiation induced by corticotropin‐releasing factor at central amygdala glutamatergic synapses via CRF1, NMDA receptors and PKA
Sebastian Pollandt;Jie Liu;Luis Orozco-Cabal;Dimitri E. Grigoriadis.
European Journal of Neuroscience (2006)
Cocaine and Kindling Alter the Sensitivity of Group II and III Metabotropic Glutamate Receptors in the Central Amygdala
Volker Neugebauer;Fatiha Zinebi;Rex Russell;Joel P. Gallagher.
Journal of Neurophysiology (2000)
Chemoreceptors for serotonin (5-HT), acetylcholine (ACh), bradykinin (BK), histamine (H) and γ-aminobutyric acid (GABA) on rabbit visceral afferent neurons
H. Higashi;N. Ueda;S. Nishi;J.P. Gallagher.
Brain Research Bulletin (1982)
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