Neurotransmitters in Anxiety

Hoehn‐Saric, Rudolf

doi:10.1001/archpsyc.1982.04290060075015

Cited by 140 publications

(33 citation statements)

References 99 publications

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“…While PK 9084 is poorly established as an anxioselective agent, buspirone has been shown to be efficaceous in several clinical trials (Goldberg & Finnerty, 1979;Goldberg & Finnerty, 1982;Rickels et al, 1982). These results are consistent with the conclusion that anxiety can be treated by modification of non-GABAergic neurotransmission, possibly including 5-hydroxytryptaminergic, noradrenergic and dopaminergic systems (for review, see: Hoehn-Saric, 1982;Braestrup, 1982).…”

Section: Drugsmentioning

confidence: 61%

Effects of non‐sedative anxiolytic drugs on responses to GABA and on diazepam‐induced enhancement of these responses on mouse neurones in cell culture

Deyn

Macdonald

1988

British J Pharmacology

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1 Intracellular microelectrode recording techniques were performed on mouse spinal cord and cerebral hemisphere neurones grown in primary dissociated cell culture. The effects of several anxiolytics applied by local pressure ejection on responses to y-aminobutyric acid (GABA) evoked by iontophoresis were investigated. Responses to GABA were depolarizing since intracellular chloride ion concentration was increased by injection from potassium chloride (3M)-filled recording micropipettes and neurones were held at large negative membrane potentials (-70 to -90mV). The agents studied were six 'non-sedative anxiolytics ', CL 218, 1,2,4-triazolo(4,3-b) pyridazine), PK 8165 (2-phenyl-442-(4-piperidinyl)5]decane-7,9-dione), and two sedative anxiolytics, diazepam and zopiclone ([6-5-2 Direct effects on responses to GABA were studied for all drugs applied in varying concentrations. For the drugs which significantly altered responses to GABA, the effects of the benzodiazepine receptor antagonists Ro 15-1788 (ethyl-8-fluoro-5,6-dihydro-5-methyl-6-oxo4H-imidazo(1,5a) (1,4)benzodiazepine-3-carboxylate) and CGS 8216 (2-phenylpyrazolo(4,3-c)-quinolin-3(5H-one) were evaluated. For

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Section: Drugsmentioning

confidence: 61%

Effects of non‐sedative anxiolytic drugs on responses to GABA and on diazepam‐induced enhancement of these responses on mouse neurones in cell culture

Deyn

Macdonald

1988

British J Pharmacology

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“…Brain GABAergic and noradrenergic (NA) neuronal systems have both been advocated roles in the pathophysiology of anxiety (e.g., Hoehn-Saric, 1982). The principal reason for implicating the former system in anxiety is the fact that the benzodiazepines (BDZs) appear to mediate their effects via specific BDZ receptors, which when activated enhance the binding of GABA to GABA-A receptors (Costa et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

?2-Adrenoceptor antagonists potentiate the anticonflict and the rotarod impairing effects of benzodiazepines

Söderpalm

Engel

1989

J. Neural Transmission

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Putative interactions between the specific alpha 2-adrenoceptor antagonist idazoxan and benzodiazepines (BDZs) were examined in two different rat conflict models; Vogel's drinking conflict test (VT) and Montgomery's conflict test (MT) (the elevated +-maze). In the MT, idazoxan (0.031 mg/kg) produced anxiogenic-like effects, which were counteracted both by the triazolo-BDZ alprazolam (APZ; 0.2 mg/kg) and the conventional BDZ diazepam (DIZ; 0.2 mg/kg). In fact, the anxiolytic-like effects of APZ were significantly potentiated when co-administering idazoxan. A tendency to such a phenomenon was seen also in rats treated with DIZ and idazoxan. In the VT, the anxiolytic-like effects both of APZ (1.0 mg/kg) and DIZ (4.0 mg/kg) were significantly enhanced when co-administering idazoxan (1.0 mg/kg) in a dose not affecting the behavior per se. Similar potentiating phenomena by behaviorally inert doses of alpha 2-adrenoceptor antagonists (idazoxan 1.0 mg/kg; yohimbine 2.0 mg/kg) were seen with regard to the ataxic/sedative effects of the BDZs (APZ 0.25 mg/kg; DIZ 1.5 mg/kg). The present results provide further support for the notion that the anxiolytic-like effects of BDZs are not related to attenuation of Locus Coeruleus activity. In addition, it is suggested that the potentiation caused by the alpha 2-adrenoceptor antagonist is mediated via a noradrenaline induced increase in signal-to-noise ratio in target neurons of the brain noradrenergic system.

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“…Investigations of the pathophysiology of panic have focused on the serotonergic (5-HT), noradrenergic (NE), and the GABA-benzodiazepine systems [83][84][85][86][87][88][89][90] among other neurotransmitters. Nevertheless, several lines of evidence suggest that DA may be involved in anxiety [68,91] and panic [31,68].…”

Section: Central Dopamine Turnover: Prelude To Anxiety and Emergence mentioning

confidence: 99%

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

Hebb¹,

Anger²,

Mendella³

et al. 2007

TOPJ

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Panic disorder is characterized by a progression of panic symptom severity with repeated attacks. Repeated panic episodes evoke heightened anticipatory anxiety, phobic avoidance and are typically associated with comorbid symptoms of depression. Due to the heterogeneity of the disorder, reliable neurochemical correlates attending panic have not been identified. However, variable neuropeptide interfacing with major and minor transmitter systems may modulate individual vulnerability to panic and account for variable panic profiles. The extensive colocalization of cholecystokinin (CCK) with other neurotransmitters, including dopamine (DA), enkephalin (ENK) and GABA, in specific central sites may influence various aspects of anxiety and panic. The behavioral correlates attending panic likely follow from variable neurochemical release and conditioning/sensitization. Clinicians maintain that recurrent panic attacks are spontaneous (unexpected, uncued) and fail to acknowledge the wealth of information implicating a prominent role for stressful life events in panic. Conditioning and sensitization of both behavior (e.g., fear-motivated) and neurochemical events (e.g., DA and CCK) in response to uncontrollable stressors parallel the diverse heterogeneity of panic amongst clinical samples. Cholecystokinin-4, pentagastrin, lactate acid, and CO 2 induce panic attacks that are dependent on subjective history, expectancy measures and panic profiles. Panic disorder is associated with chronic illness and familial sick-role modeling exacerbates the course of the illness. The current review outlines the evidence in support of a conditioning/sensitization model for panic, a model that may explain the variable efficacies of pharmacological interventions.

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Neurotransmitters in Anxiety

Cited by 140 publications

References 99 publications

Effects of non‐sedative anxiolytic drugs on responses to GABA and on diazepam‐induced enhancement of these responses on mouse neurones in cell culture

Effects of non‐sedative anxiolytic drugs on responses to GABA and on diazepam‐induced enhancement of these responses on mouse neurones in cell culture

?2-Adrenoceptor antagonists potentiate the anticonflict and the rotarod impairing effects of benzodiazepines

The Myth of Panic Spontaneity: Consideration of Behavioral and Neurochemical Sensitization

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