Nitric oxide synthesis in the basolateral complex of the amygdala is required for the consolidation and expression of fear potentiated startle but not shock sensitization of the acoustic startle.

Nitric oxide (NO) is synthesized as a result of N-methyl-d-asparate (NMDA) receptor activation, it acts as an retrograde neurotransmitter freely diffusing across cell membranes interacting with its targets in a non-synaptic manner. Consequently, NO has been described as an extension of NMDA receptor activation. The targets of NO include cellular components within the basolateral complex of the amygdala (BLA) that are necessary for the consolidation of conditioned fear as well as targets that can significantly modulate neurotransmission associated with its expression.

Amygdaloid GABA, not glutamate neurotransmission or mRNA transcription controls footshock-associated fear arousal in the acoustic startle paradigm.

In Pavlovian conditioning the fear-evoking properties of the aversive unconditioned stimulus are represented by the conditioned stimulus. A major challenge for theories of classical fear conditioning has been to understand how associations are formed between a conditioned stimulus and unconditioned stimulus. Although the cellular mechanisms in the amygdala that underlie fear learning have received considerable attention relatively little is known about the neural substrates underlying unconditioned stimulus-associated fear.

Extinction deficit and fear reinstatement after electrical stimulation of the amygdala: implications for kindling-associated fear and anxiety.

Generalized seizures produced by electrical kindling of the amygdala in laboratory rats are a widely used animal model of temporal lobe epilepsy. In addition to seizure evolution amygdala kindling enhances emotionality. The relative roles of electrical stimulation and seizure induction in fear responding are unclear.

Further evidence for the depressive effects of cytokines: anhedonia and neurochemical changes.

Although human studies have emphasized a role for IL-2 in depressive illness, limited attention has been devoted to the behavioral and neurochemical effects of this cytokine in animal studies. The present review assesses the behavioral effects of IL-2 in rodents, in counterpoint to the effects of interleukin-1beta (IL-1beta), necrosis factor-alpha (TNF-alpha) and endotoxin challenge. Unlike IL-1beta, systemic IL-2 provokes modest effects on hypothalamic-pituitary-adrenal (HPA) functioning, and does not provoke marked signs of illness or anxiety.

Ventral tegmental area dopamine neurons mediate the shock sensitization of acoustic startle: a potential site of action for benzodiazepine anxiolytics.

Dopamine (DA)-containing neurons in the ventral tegmental area (VTA) are thought to play an important role in fear motivation. The primary objective of the present study was to determine the connection between DA D2, gamma aminobutyric acid (GABA)A, and benzodiazepine receptors in the VTA and footshock-associated emotionality. Microinfusion of the DA D2 receptor agonist quinpirole.