A Primary Acoustic Startle Pathway: Obligatory Role of Cochlear Root Neurons and the Nucleus Reticularis Pontis Caudalis

Abstract

Davis et al. (1982) proposed a primary acoustic startle circuit in rats consisting of the auditory nerve, posteroventral cochlear nucleus, an area near the ventrolateral lemniscus (VLL), nucleus reticularis pontis caudalis (PnC), and spinal motoneurons. Using fiber-sparing lesions, the present study reevaluated these and other structures together with the role of neurons embedded in the auditory nerve [cochlear root neurons (CRNs)], recently hypothesized to be involved in acoustic startle. Small electrolytic lesions of the VLL of ventrolateral tegmental nucleus (VLTg) failed to eliminate startle. Large electrolytic lesions including the rostral ventral nucleus of the trapezoid body (rVNTB) and ventrolateral parts of PnC or lesions of the entire PnC blocked startle. However, small NMDA-induced lesions of the rVNTB failed to block startle, making it unlikely that the rVNTB itself is part of the startle pathway. In contrast, NMDA lesions of the full extension of the ventrolateral part of the PnC blocked startle completely, suggesting that the ventrolateral part of the PnC is critically involved. Bilateral kainic acid lesions of CRNs also blocked the startle reflex completely, providing the first direct evidence for an involvement of CRNs in startle. This blockade probably was not caused by damage to the auditory nerve, because the lesioned animals showed intact compound action potentials recorded from the ventral cochlear nucleus. Hence, a primary acoustic startle pathway may involve three synapses onto (1) CRNs, (2) neurons in PnC, and (3) spinal motoneurons.

Involvement of Pallidotegmental Neurons in Methamphetamine- and MK-801-Induced Impairment of Prepulse Inhibition of the Acoustic Startle Reflex in Mice: Reversal by GABAB Receptor Agonist Baclofen

“…The fast excitatory pathway of the acoustic startle system involves serial connections linking the auditory nerve, cochlear root neurons, PnC, and spinal motor neurons (Lee et al, 1996). We have previously demonstrated that pulse stimulus increased c-Fos expression in the PnC, which was attenuated by a weak prepulse before pulse stimulus in the PPI test (Takahashi et al, 2007).…”

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

“…Liang and colleagues (1992) reported that electrolytic lesions of the amygdala blocked CRH-enhanced startle, whereas CRH infused into the amygdala failed to mimic intracerebroventricular CRH effects on startle. Because the amygdala has direct projections to the nucleus reticularis pontis caudalis (Hitchcock and Davis, 1991), a part of the primary acoustic startle circuit (Davis et al, 1982;Lee et al, 1996), these data suggest that the amygdala may play an obligatory role in CRH-enhanced startle, even though it is not the primary receptor site for CRH given intracerebroventricularly. In other words, CRH given intracerebroventricularly may bind to receptors in structures afferent to the amygdala, such as the BNST or hippocampus, thereby exciting the amygdala indirectly.…”

GABA in the Deep Layers of the Superior Colliculus/Mesencephalic Reticular Formation Mediates the Enhancement of Startle by the Dopamine D1Receptor Agonist SKF 82958 in Rats

“…Taken together, these results add to a body of work showing that GABAergic transmission at the level of the deep SC/Me is an important component in the regulation and expression of motor behaviors. Because the deep SC/Me is not part of the primary acoustic startle pathway (Lingenhöhl and Friauf, 1994;Lee et al, 1996), the results of the present study suggest that the deep SC/Me exerts a modulatory influence on this reflex. A recent report from our laboratory has identified a heavy ipsilateral innervation from the deep SC/Me to the part of the PnC critical for startle (Meloni and Davis, 1999b).…”

“…Davis, 1984) and is mediated by a simple neural pathway in the brainstem consisting of cochlear root neurons (CRNs), neurons in the nucleus reticularis pontis caudalis (PnC), and motoneurons in the spinal cord (Lee et al, 1996). The amplitude of this short-latency response can be quantified easily and has been used extensively to study the neurocircuitry and neurochemistry involved in the modulation of reflex/motor behavior (cf.…”