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Noradrenergic locus coeruleus neurons: their distant connections and their relationship to neighboring (including cholinergic and GABAergic) neurons of the central gray and reticular formation.

Noradrenergic LC neurons appear to be relatively unique in the brain, being unsurpassed in the divergence and ubiquity of their projections through the central nervous system. In this regard, they share certain characteristics with peripheral noradrenaline neurons of the sympathetic nervous system. As such they would be assumed to play a very general role in modulating the activity of large populations of neurons in multiple, functionally diverse systems. Like other periventricular and reticular neurons, they have the potential to receive afferent information from multiple sources via long dendrites, upon which the majority of their inputs from brainstem and forebrain may arrive. They appear closely related to the cholinergic neurons of the laterodorsal tegmental nucleus, their neighbors that are located medial and rostral to them within the periventricular gray and that have similarly oriented and positioned long dendrites that would allow reception of similar afferent input as the LC neurons and also possibly interaction with the LC neurons. As evidenced by input to the noradrenergic cell bodies in the compact portion of the nucleus, a moderate GABAergic innervation, that may derive in part from local neurons, could have a potent influence on the activity of the cells. Periventricular GABAergic cells could also serve as intermediaries to other afferent input, from a distance, terminating in the periventricular region or from local neurons such as the cholinergic cells of the laterodorsal tegmental nucleus.

Acetylcholine↗

Evoked electrical responses of nucleus lateralis posterior of the rabbit thalamus and their dependence upon the functional state of the cortex and reticular formation.

The electrical responses of the thalamic pulvinar (of its analogue, the nucleus lateralis posterior (nLP)) to light stimuli of various intensity were recorded in awake rabbits, and their interrelationships with the responses of the retina, superior colliculi, and visual cortex were analyzed. It is postulated that a major role in the afferent supply of the rabbit nLP belongs to the optic track and the superior colliculi. The presence was demonstrated of a highly organized analyzer of the reticular control of nLP function that is of a facilitatory character. The most important role in reticular influence belongs to its adrenoresponsive mechanism. An inhibitory influence was demonstrated for the visual and sensorimotor regions of the cerebral cortex on the nLP neuronal apparatus producing responses to light stimuli. The influence of the visual cortex are the most pronounced and stable.

Animals↗

Somatostatin in the pontine reticular formation modulates fear potentiation of the acoustic startle response: an anatomical, electrophysiological, and behavioral study.

The amplitude of the acoustic startle response (ASP) in rats is increased in the presence of a cue that has previously been paired with an aversive stimulus such as a footshock. This phenomenon is called fear-potentiated startle and is a model to study the neuronal and neurochemical mechanisms of the acquisition and expression of fear. The present study investigated the role in fear-potentiated startle of somatostatin in the caudal pontine reticular nucleus (PnC) by a combination of anatomical, electrophysical, and behavioral methods. The PnC is an essential part of the primary startle circuit and is also the recipient of modulatory influences. First, we showed that the central gray (CG), which is involved in fear conditioning, is the main source of somatostatinergic input to the PnC. In the second experiment, we iontophoretically applied the somatostatin receptor agonist sandostatin on PnC neurons and extracellularly recorded the activity of PnC neurons. Sandostatin had no effect on tone-evoked or spontaneous activity, but markedly attenuated the increase of neuronal activity seen after the administration of glutamate. In our third experiment, we injected different doses of sandostatin into the PnC of awake rats. Sandostatin blocked fear potentiation of the ASR but had no effect on the baseline ASR amplitude. The present study indicates that the somatostatinergic projection from the CG to the PnC is important for the modulation of fear-potentiated startle. We present a possible neural circuitry for the expression of fear-potentiated startle based on these data and previous findings.

Acoustic Stimulation↗

Enhancement of the acoustic startle response by stimulation of an excitatory pathway from the central amygdala/basal nucleus of Meynert to the pontine reticular formation.

The acoustic startle response (ASR) is a simple motor reaction to intense and sudden acoustic stimuli. The neural pathway underlying the ASR in rats is already fairly well understood. As the ASR is subject to a variety of modulations, this reaction can serve as a model for vertebrate neuroethologists to investigate the neural mechanisms mediating sensorimotor transfer and their extrinsic modulation. We report here on experiments in rats which were undertaken in order to investigate the neural mechanisms underlying the enhancement of the ASR. An increased amplitude of the ASR can be observed during states of conditioned and unconditioned fear. By employing neuroanatomical tract-tracing methods, we describe a pathway from neurons of the medial division of the central amygdaloid nucleus (cA) and the basal nucleus of Meynert (B) to the caudal pontine reticular nucleus (PnC), an important relay station in the acoustic startle pathway. Extracellular recordings from acoustically responsive neurons in the PnC showed that electrical stimulation of the cA/B facilitates the tone-evoked response of these neurons. Behavioural tests following chemical stimulation of the cA/B with NMDA (N-methyl-d-aspartate) in awake rats indicated that activation of this pathway increases the ASR. The lack of sufficient spatial resolution of our stimulation techniques did not allow us to differentiate the relative contributions of the cA and the B to this effect. As the amygdaloid complex has been implicated in emotional behaviour, particularly in the mediation of fear, these findings substantiate the concept that the amygdaloid complex plays a key role for the enhancement of the ASR by conditioned and unconditioned fear.

Amygdala↗

[Influence of the brain stem reticular formation on seizure activity in the cerebral cortex].

Activation of the mesencephalic RF facilitates triggering of paroxysmal potentials and augments existing epileptic activity. Stimulation of nucleus reticularis pontis caudalis inhibits triggering of epileptic discharges. The microelectrode studies corroborated these data. The desynchronization elicited by the mesencephalic RF seems to be mostly activating, whereas desynchronization elicited by the nucleus reticularis pontis caudalis--mostly inhibitory.

Animals↗

[Role of the mesencephalon reticular formation in the effect of ethosuximide on a cortical epileptogenic focus].

Ethosuximide provoked in encéphale isolé cats a dose-dependent suppression or facilitation of strychnine focus spiking activity, and in combination with high frequency stimulation of formatio reticularis mesencephali a significant activation of the cortical focus. The results seem to show that the influence of ethosuximide on the formatio reticularis mesencephali is one--if not the main--component of the drug effect.

Action Potentials↗