Relevant bibliographies by topics / GABAergic / Books
To see the other types of publications on this topic, follow the link: GABAergic.

Books on the topic 'GABAergic'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 June 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 29 books for your research on the topic 'GABAergic.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

L, Erdő Sándor, and Bowery N. G, eds. GABAergic mechanisms in the mammalian periphery. New York: Raven Press, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Giovanni, Biggio, Concas Alessandra, and Costa Erminio, eds. GABAergic synaptic transmission: Molecular, pharmacological, and clinical aspects. New York: Raven Press, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke., eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

SanCartier, Nancy A. The role of the GABAergic system in the production of ultrasonic vocalization in rats. St. Catharines, Ont: Brock University, Dept. of Psychology, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Buzsáki, G. Abstracts of papers presented at the 2006 meeting on the GABAergic system: December 6-December 9, 2006. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Giovanni, Biggio, Costa Erminio, and Capo Boi Conference on Neuroscience (4th : 1985 : Villasimius, Italy), eds. GABAergic transmission and anxiety. New York: Raven Press, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Barberis, Andrea, and Alberto Bacci, eds. Plasticity of GABAergic Synapses. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-732-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

DeFelipe, Rockland, Javier, Kathleen S., ed. Cortical GABAergic neurons: stretching it. Frontiers Media SA, 2012. http://dx.doi.org/10.3389/978-2-88919-037-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Tyagarajan, Shiva K., Arianna Maffei, and Andrea Barberis, eds. Emerging Mechanisms in Dynamic GABAergic Inhibition. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-766-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Bowery, Norman G. Gabaergic Mechanisms in the Mammalian Periphery/Order 1646. Raven Pr, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
14

Biggio, Giovanni, and Alessandra Concas. Gabaergic Synaptic Transmission: Molecular, Pharmacological, and Clinical Aspects (Advances in Biochemical Psychopharmacology). Raven Pr, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
15

Jung, Bruce John. The Effects of repeated cocaine on striatal GABAergic neurotransmission in Sprague-Dawley rats. 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
16

Zhang, Xiao-Lei. Network synchrony of GABAergic interneurons in the intact hippocampus: Role of electrotonic coupling. 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
17

Luppi, Pierre-Hervé, Olivier Clément, Christelle Peyron, and Patrice Fort. Neurobiology of REM sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0003.

Full text
Abstract:
REM (paradoxical) sleep is a state characterized by rapid eye movements, EEG activation, and muscle atonia. REM sleep behavior disorder (RBD) is a parasomnia characterized by loss of muscle atonia during REM sleep. Cataplexy, a key symptom of narcolepsy, is a striking sudden episode of muscle weakness comparable to REM sleep atonia triggered by emotions during wakefulness. This chapter presents recent results on the neuronal network responsible for REM sleep and explores hypotheses explaining RBD and cataplexy. RBD could be due to a specific degeneration of glutamatergic neurons responsible for muscle atonia, localized in the pontine sublaterodorsal tegmental nucleus (SLD) or the glycinergic/GABAergic premotoneurons localized in the ventral medullary reticular nuclei. Cataplexy in narcoleptics could be due to activation during waking of SLD neurons. In normal conditions, activation of SLD neurons would be blocked by simultaneous excitation by hypocretins of REM sleep-off GABAergic neurons localized in the ventrolateral periaqueductal gray.
APA, Harvard, Vancouver, ISO, and other styles
18

Cavanna, Andrea E. Antiepileptic drugs and behaviour: mechanisms of action. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198791577.003.0002.

Full text
Abstract:
Antiepileptic drugs (AEDs) exert their pharmacological properties on both epileptic seizures and behaviour through different mechanisms of action. These include modulation of ion (mainly sodium and calcium) conductance through voltage-gated channels located within the neuronal membrane, as well as facilitation of inhibitory (GABAergic) neurotransmission and inhibition of excitatory (glutamatergic) neurotransmission, resulting in regulation of neuronal excitability.
APA, Harvard, Vancouver, ISO, and other styles
19

Kelmendi, Benjamin, Thomas G. Adams, Chadi Abdallah, Irina Esterlis, Ilan Harpaz-Rotem, Steve Southwick, and John H. Krystal. Investigational Agents in the Treatment of Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0040.

Full text
Abstract:
This chapter highlights the breadth of the range and shallowness of the depth with which novel therapeutics for PTSD have been evaluated. None of the new treatments reviewed in this chapter have sufficient data supporting their efficacy to be strongly recommended for the treatment of PTSD. Nonetheless, the interventional approaches reviewed here are guided by our current understanding of the neurobiology of stress in animals and PTSD in humans. The range of therapeutic targets considered in this chapter reflects our growing appreciation of the complex neurobiology of PTSD. Thus, it should not be surprising that drugs targeting glutamatergic, GABAergic, opiates, glucocorticoids, cannabinoids, and voltage-gated calcium channels are in various stages of evaluation.
APA, Harvard, Vancouver, ISO, and other styles
20

Graat, Ilse, Martijn Figee, and Damiaan Denys. Neurotransmitter Dysregulation in OCD. Edited by Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0025.

Full text
Abstract:
Obsessive-compulsive disorder (OCD) is associated with abnormalities in the cortico-striatal–thalamic–cortical (CSTC) circuitry, and may be associated with dysregulation of neurotransmitters within this network. The major neurotransmitters of the CSTC are serotonin, dopamine, glutamate and γ‎-aminobutyric acid (GABA. This chapter reviews evidence of the involvement of these neurotransmitters in OCD from pharmaocological, genetic, and imaging studies. yielding an integrated neurotransmitter model of OCD. It concludes that the neurotransmitter model of OCD involves dopaminergic and glutamatergic overactivity in frontostriatal pathways, along with diminished serotonergic and GABAergic neurotransmission in frontolimbic systems. These neurotransmitter imbalances may explain frontostriatal hyperactivity and impaired frontolimbic emotion regulation. Advancing our understanding of neurotransmitter abnormalities in OCD, and how abnormalities in different transmitter systems relate to one another, holds promise for the development of new pharmacotherapies.
APA, Harvard, Vancouver, ISO, and other styles
21

Rees, Gayla, Benjamin Shapiro, and Matthew Torrington. Integrative Approach to Sedative-Hypnotic Use Disorder. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0005.

Full text
Abstract:
Sedatives, hypnotics, and anxiolytics are CNS depressants with GABAergic activity that are potentially habit-forming due to their activity in brain reward pathways. They are central in the drug overdose epidemic with benzodiazepines (BZD) being involved in approximately 31% of all fatal overdoses. There are 4 withdrawal syndromes: High dose minor and major withdrawal, low dose withdrawal, and protracted withdrawal. Benzodiazepines are chemically related positive allosteric modulators of the GABA at the GABA-A receptor. In differential expression 5 different receptor subunits play a role in acute and prolonged withdrawal syndromes. Benzodiazepines have supplanted barbiturates for treatment of anxiety and insomnia due to their wider therapeutic index. Barbiturates can be helpful managing opiate and benazodiazapeine withdrawal. Traditional Chinese Medicine can improve hypnotics-dependent insomnia. Mindfulness-based relapse prevention and yoga may offer benefits but are poorly studied.
APA, Harvard, Vancouver, ISO, and other styles
22

Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.

Full text
Abstract:
This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
APA, Harvard, Vancouver, ISO, and other styles
23

van den Boogaard, Mark, and Paul Rood. Delirium in Critically Ill Patients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199398690.003.0002.

Full text
Abstract:
This chapter addresses delirium in critically ill patients in the intensive care unit (ICU), especially the mixed subtype (alternating hyperactivity and hypoactivity). The Confusion Assessment Method for the ICU and the Intensive Care Delirium Screening Checklist are discussed as useful delirium assessment tools in this setting. Several neurotransmitter pathways have been implicated in delirium, including cholinergic, GABAergic, and serotonergic pathways; cytokines and glucocorticoids also appear relevant. Risk factors for delirium in the ICU include older age, prior cognitive impairment, worse illness severity, recent delirium or coma, mechanical ventilation, admission category (especially trauma or neurological/neurosurgical admission), infection, metabolic acidosis, morphine and sedative administration, urea concentration, respiratory failure, and admission urgency. Prevention and treatment of delirium are discussed, including nonpharmacological interventions (frequent reorientation, providing eyeglasses and hearing aids if needed, promoting nighttime sleep, and early mobilization) and judicious use of opiate, sedative, and antipsychotic medications.
APA, Harvard, Vancouver, ISO, and other styles
24

Tononi, Giulio, and Chiara Cirelli. The Neurobiology of Sleep. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0011.

Full text
Abstract:
Sleep is required for health and well-being, and consumes roughly one-third of a human’s lifetime, yet its functions remain incompletely understood. This chapter provides an overview of so-called sleep architecture—the stages and cycles that characterize sleep, including rapid eye movement (REM) and non-REM periods. Also discussed are the numerous regions of brain and neurotransmitters that control the induction of sleep, the transitions between REM and non-REM sleep cycles, and wakefulness. Key brain systems include GABAergic neurons in the pre-optic area, the neuropeptide orexin in lateral hypothalamic neurons, histaminergic neurons in the hypothalamus, monoaminergic (norepinephrine and serotonin) and acetylcholinergic nuclei in the brainstem, and the brain’s adenosine system, all of which work in integrated circuits to control sleep and wakefulness. Overlaid on sleep-wake cycles are circadian rhythms, and the crucial role played by the suprachiasmatic nucleus in entraining such rhythms to environmental light.
APA, Harvard, Vancouver, ISO, and other styles
25

Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
26

Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2016.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
27

Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
28

Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

Full text
Abstract:
Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
APA, Harvard, Vancouver, ISO, and other styles
29

Modir, Shahla J., and Joel Morris. Traditional Chinese Medicine (TCM) and Acupuncture Approach to Addiction. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0016.

Full text
Abstract:
The first half of this chapter paints a broad overview of TCM (traditional Chinese medicine) with a focus on addiction. The second half details the Western studies, which address specific addictive substances. A glimpse of TCM’s history in the context of the medical models is discussed. The Western medical model is compared to and differentiated from TCM. Yin-yang and 5-element theory are detailed. The Zang Fu patterns are examined along with the principles of treatment and recognition of patterns. The 3 treasures (jing, qi, and shen) are discussed. Acupuncture was serendipitously found to be an addiction treatment with EA (electro acupuncture) and auricular points in 1972, which suggested a neuroendocrinological basis. Animal studies pointed toward involvement of different neurotransmitters in the basic mechanism of acupuncture, which are: the dopamine, GABAeric, and serotonergic systems. Most of the quality Western studies use the NADA (National Acupuncture Detoxification Association) protocols, which use 5 auricular points: shen men, kidney, liver, and lung. This protocol treats opiates, cocaine, nicotine, and AUDs. Regarding opiate detoxification, addicts assigned to the treatment groups were more consistent and more frequently attended treatment. Regarding alcohol, female participants (N = 185) who received acupuncture reported a decrease in cravings, depression, and anxiety with an increase in problem solving, when compared to controls (N = 101). There is less evidence that acupuncture is helpful for cocaine and nicotine. Acupuncture appears most helpful as an adjunct therapy, which keeps people more engaged in therapy longer, resulting in better outcomes.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'GABAergic' for other source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography