scholarly journals Inhibition of the Deep and Intermediate Layers of the Superior Colliculus Disrupts Sensorimotor Gating in Monkeys

2020 ◽  
Vol 14 ◽  
Author(s):  
Hannah F. Waguespack ◽  
Brittany L. Aguilar ◽  
Ludise Malkova ◽  
Patrick A. Forcelli

The deep and intermediate layers of the superior colliculus (DLSC) respond to visual, auditory, and tactile inputs and act as a multimodal sensory association area. In turn, activity in the DLSC can drive orienting and avoidance responses—such as saccades and head and body movements—across species, including in rats, cats, and non-human primates. As shown in rodents, DLSC also plays a role in regulating pre-pulse inhibition (PPI) of the acoustic startle response (ASR), a form of sensorimotor gating. DLSC lesions attenuate PPI and electrical stimulation of DLSC inhibits the startle response. While the circuitry mediating PPI is well-characterized in rodents, less is known about PPI regulation in primates. Two recent studies from our labs reported a species difference in the effects of pharmacological inhibition of the basolateral amygdala and substantia nigra pars reticulata (SNpr) on PPI between rats and macaques: in rats, inhibition of these structures decreased PPI, while in macaques, it increased PPI. Given that the SNpr sends direct inhibitory projections to DLSC, we next sought to determine if this species difference was similarly evident at the level of DLSC. Here, we transiently inactivated DLSC in four rhesus macaques by focal microinfusion of the GABAA receptor agonist muscimol. Similar to findings reported in rodents, we observed that bilateral inhibition of the DLSC in macaques significantly disrupted PPI. The impairment was specific to the PPI as the ASR itself was not affected. These results indicate that our previously reported species divergence at the level of the SNpr is not due to downstream differences at the level of the DLSC. Species differences at the level of the SNpr and basolateral amygdala emphasize the importance of studying the underlying circuitry in non-human primates, as impairment in PPI has been reported in several disorders in humans, including schizophrenia, autism, and PTSD.

2008 ◽  
Vol 23 ◽  
pp. S70 ◽  
Author(s):  
B.B. Quednow ◽  
I. Frommann ◽  
J. Berning ◽  
K.U. Kühn ◽  
W. Maier ◽  
...  

2020 ◽  
Vol 1727 ◽  
pp. 146570
Author(s):  
Alexandra Olimpio Siqueira Cunha ◽  
Marzieh Moradi ◽  
Junia Lara de Deus ◽  
Cesar Celis Ceballos ◽  
Nikollas Moreira Benites ◽  
...  

Neuroscience ◽  
2011 ◽  
Vol 195 ◽  
pp. 191-200 ◽  
Author(s):  
A. Edwards ◽  
C.D. Treiber ◽  
M. Breuss ◽  
R. Pidsley ◽  
G.-J. Huang ◽  
...  

2010 ◽  
Vol 25 (12) ◽  
pp. 1639-1648 ◽  
Author(s):  
C Salum ◽  
AC Issy ◽  
ML Brandão ◽  
FS Guimarães ◽  
EA Del Bel

Systemic injection of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (LNO) prevents the disruptive effect of amphetamine (Amph) on prepulse inhibition (PPI), a sensorimotor gating model in which the amplitude of the acoustic startle response (ASR) to a startling sound (pulse) is reduced when preceded immediately by a weaker stimulus (prepulse). Given that dopamine (DA) projections to the basolateral amygdala (BLA) are involved in the control of information processing, our aim was to investigate if intra-BLA administration of LNO would modify the disruption caused by the DA agonists, Amph, apomorphine (Apo) and quinpirole (QNP), on PPI. Male Wistar rats received bilateral intra-BLA microinjections (0.2 µL/min/side) of combined treatments (saline or LNO 11 µg followed by saline, QNP 3 µg, Apo 10 µg or Amph 30 µg). PPI was disrupted by intra-BLA Apo, QNP or Amph but not by LNO. Prior bilateral intra-BLA injection of LNO prevented the Apo- and QNP-induced disruption of PPI but did not affect that caused by Amph. APO- or QNP-induced increases in ASR to prepulse + pulse were also restored by LNO. Since local inhibition of NO formation affected the effects of direct, but not indirect, DA agonists, the results suggest that this modulation is not occurring at the level of DA release but may involve complex interactions with other neurotransmitter systems.


Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1572-1581 ◽  
Author(s):  
Damian G. Zuloaga ◽  
Cynthia L. Jordan ◽  
S. Marc Breedlove

Abstract Perinatal exposure to testosterone (T), which can act upon both the androgen receptor (AR) and, via aromatization of T into estrogens, upon estrogen receptors, organizes many adult behaviors in rodents. We compared behaviors in wild-type (WT) male rats and AR-deficient rats with the testicular feminization mutation (Tfm), which on the day of birth were either gonadectomized (Neo-Gdx) or sham operated. In adulthood, all rats were either gonadectomized or sham operated and implanted with T capsules to equilibrate circulating androgens. In each of four tests of behavior related to anxiety (open field, novel object exposure, light/dark box, and elevated plus maze), Neo-Gdx rats showed decreased indices of anxiety and increased activity compared with rats sham operated on the day of birth, with no differences between WT or Tfm males within treatment groups. These results indicate that testicular hormones act in development to increase adult indices of anxiety and decrease activity in males and that functional ARs are not required for this effect. Acoustic startle response was also reduced by Neo-Gdx, suggesting that postnatal testicular secretions potentiate this behavior as well. Adult corticosterone levels and sensorimotor gating, as measured by prepulse inhibition of the acoustic startle response, were increased by neonatal castration in both WT and Tfm rats. These findings indicate a role of T before adulthood in the organization of anxiety-related behaviors, activity, the hypothalamic-pituitary-adrenal axis, and sensorimotor gating in rats, all of which appears to be AR independent.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mingyu Yang ◽  
Nikos K. Logothetis ◽  
Oxana Eschenko

AbstractAn alerting sound elicits the Acoustic Startle Response (ASR) that is dependent on the sound volume and organisms’ state, which is regulated by neuromodulatory centers. The locus coeruleus (LC) neurons respond to salient stimuli and noradrenaline release affects sensory processing, including auditory. The LC hyperactivity is detrimental for sensorimotor gating. We report here that priming microstimulation of the LC (100-ms at 20, 50, and 100 Hz) attenuated the ASR in rats. The ASR reduction scaled with frequency and 100 Hz-stimulation mimicked pre-exposure to a non-startling tone (prepulse). A rapid (~ 40 ms) EEG desynchronization following the LC stimulation suggested that the ASR reduction was due to elevated cortical arousal. The effects of LC stimulation on the ASR and EEG were consistent with systematic relationships between the ASR, awake/sleep state, and the cortical arousal level; for that matter, a lower ASR amplitude corresponded to a higher arousal level. Thus, the LC appears to modulate the ASR circuit via its diffuse ascending projections to the forebrain saliency network. The LC modulation directly in the brainstem and/or spinal cord may also play a role. Our findings suggest the LC as a part of the brain circuitry regulating the ASR, while underlying neurophysiological mechanisms require further investigation.


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