Habituation and Sensitization of Startle Reflexes Elicited Electrically from the Brainstem

Davis, Michael T.; Parisi, Thomas; Gendelman, David S.; Tischler, Mark B.; Kehne, John H.

doi:10.1126/science.7134967

Cited by 119 publications

(53 citation statements)

References 13 publications

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“…The emphasis on interneurons as potential loci for habituation brings our results examining habituation of tail-elicited reflexes in Aplysia into register with several other model systems used to study habituation, such as crayfish escape (Krasne and Teshiba, 1995), frog spinal cord (Farel, 1974), rat audition (Davis et al, 1982), spinal cat Wickelgren, 1967;Thompson and Glanzman, 1976), and human eyeblink (Sanes and Ison, 1983). In all of these systems it seems that habituation is mediated at interneuronal sites, perhaps suggesting a general design feature in these diverse systems for the expression of this fundamental form of learning.…”

Section: Functional Implications Of Distributed Facilitation and Decrmentioning

confidence: 99%

Heterosynaptic Facilitation of Tail Sensory Neuron Synaptic Transmission during Habituation in Tail-Induced Tail and Siphon Withdrawal Reflexes ofAplysia

Stopfer¹,

Carew

1996

J. Neurosci.

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In cellular studies of habituation, such as in the gill and siphon withdrawal reflex to tactile stimulation of the siphon of Aplysia, a mechanism that has emerged as an explanation for response decrement during habituation is homosynaptic depression at sensory neurons mediating the behavioral response. We have examined the contribution of homosynaptic depression to habituation in sensory neurons that contribute to two reflex behaviors in Aplysia, tail withdrawal and siphon withdrawal, both elicited by threshold-level tail stimulation. In a companion paper (this issue), we reported that repeated tail stimulation, identical to that producing habituation in siphon withdrawal in freely moving animals, also produces habituation in reduced preparations. In this paper, we extend these behavioral findings by showing that in reduced preparations, identical tail stimulation also produces habituation of the tail withdrawal reflex. In addition, our cellular experiments show that (1) identified sensory and motor neurons in both reflex systems respond to identical repeated tail stimulation; in sensory neurons it produces a progressive decrease in spike number and increase in spike latency, and in motor neurons it produces progressive decrement in complex EPSPs and spike output. (2) Homosynaptic depression of the tail sensory neuron to tail motor neuron synapse does occur when the sensory neurons are activated repetitively by intracellular current. (3) Homosynaptic depression at this synapse does not occur when the sensory neurons are activated repetitively by threshold-level tail stimuli that elicit the behavioral reflex and cause habituation; rather, the sensory neurons exhibit significant heterosynaptic facilitation. Thus, in these reflexes, habituation is not accompanied by homosynaptic depression at the sensory neurons, suggesting that the plasticity underlying habituation occurs primarily at interneuronal sites.

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Section: Functional Implications Of Distributed Facilitation and Decrmentioning

confidence: 99%

Heterosynaptic Facilitation of Tail Sensory Neuron Synaptic Transmission during Habituation in Tail-Induced Tail and Siphon Withdrawal Reflexes ofAplysia

Stopfer¹,

Carew

1996

J. Neurosci.

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“…The acoustic startle response (ASR) of mammals is mediated by a simple threesynapse neuronal circuit located in the lower brainstem. Neurons of the caudal pontine reticular nucleus are key elements of this primary ASR pathway (Davis et al, 1982;Koch, 1999). In humans, the eye-blink component of the ASR is quantified by using electromyographic (EMG) measurements of the orbicularis oculi facial muscle (Hoffman and Searle, 1968).…”

Section: Introductionmentioning

confidence: 99%

Prepulse Inhibition and Habituation of Acoustic Startle Response in Male MDMA (‘Ecstasy’) Users, Cannabis Users, and Healthy Controls

Quednow

Kühn

Hoenig

et al. 2004

Neuropsychopharmacol

109

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Chronic administration of 3,4-methylenedioxymethamphetamine (MDMA) is associated with long-term depletion of serotonin (5-HT) and loss of 5-HT axons in the brains of rodents and nonhuman primates. Despite the broad database concerning the selective serotonergic neurotoxicity of recreational MDMA consumption by humans, controversy still exists with respect to the question of whether the well-known functional consequences of these neurotoxic effects, such as memory impairment, were caused by chronic 5-HT deficiency. Habituation and prepulse inhibition (PPI) of the acoustic startle response (ASR) can be used as a marker of central serotonergic functioning in rodents and humans. Thus, we investigated the functional status of the central serotonergic system in chronic but abstinent MDMA users by measuring PPI and habituation of ASR. PPI and habituation of ASR were measured in three groups. The first group (MDMA group) included 20 male drug-free chronic users of MDMA; the second group (cannabis group) consisted of 20 male drug-free chronic users of cannabis; and the third group (healthy controls) comprised 20 male participants with no history of illicit drug use. Analysis revealed significantly increased PPI of MDMA users compared to those of cannabis users and healthy controls. Cannabis users and healthy controls showed comparable patterns of PPI. There were no differences in habituation among the three groups. These results suggest that the functional consequences of chronic MDMA use may be explained by 5-HT receptor changes rather than by a chronic 5-HT deficiency condition. Use of cannabis does not lead to alterations of amplitude, habituation, or PPI of ASR.

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“…Startle responses are modulated by emotions, learning, and sensorimotor gating, and presumably mediated by projections from different brain areas to the PnC (for review, see Koch and Schnitzler, 1997). In contrast, short-term habituation is considered to be caused by synaptic changes within the primary startle pathway itself, specifically by depression of synaptic input from sensory afferents to PnC giant neurons (Davis et al, 1982;Lingenhöhl and Friauf, 1992;Weber et al, 2002;SimonsWeidenmaier et al, 2006). There is preliminary evidence for a possible role of mGluRIIIs in depression of this synaptic input (Davis and Gendelman, 1977;Weber et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Group III Metabotropic Glutamate Receptors Inhibit Startle-Mediating Giant Neurons in the Caudal Pontine Reticular Nucleus But Do Not Mediate Synaptic Depression/Short-Term Habituation of Startle

Schmid¹,

Brown²,

Simons-Weidenmaier³

et al. 2010

J. Neurosci.

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Short-term habituation is a basic form of learning that is analyzed in different species and using different behavioral models. Previous studies on mechanisms of short-term habituation yielded evidence for a potential role of group III metabotropic glutamate receptors (mGluRIIIs). Here we tested the hypothesis that mGluRIII mediate short-term habituation of startle in rats, combining electrophysiological experiments in vitro with behavioral studies in vivo. We applied different mGluRIII agonists and antagonists on rat brainstem slices while recording from startle-mediating neurons in the caudal pontine reticular nucleus (PnC) and monitoring synaptic depression presumably underlying habituation. Furthermore, we injected the mGluRIII antagonist (RS)-␣-phosphonophenylglycine (MPPG) and the agonist L-(ϩ)-2-amino-4-phosphonobutyric acid (L-AP4) into the PnC of rats in vivo and measured its effect on startle habituation. Our results show that activation of mGluRIIIs in the PnC strongly inhibits startle-mediating giant neurons in vitro. Accordingly, L-AP4 reduced startle responses in vivo. However, synaptic depression in the slice was not disrupted by mGluRIII antagonists or agonists. Correspondingly, the in vivo application of the mGluRIII antagonist MPPG failed to show any effect on short-term habituation of startle responses. We therefore conclude that mGluRs are expressed within the primary startle pathway and that they inhibit startle responses upon activation; however, this inhibition does not play any role in synaptic depression and short-term habituation of startle. This is in contrast to the role of mGluRIIIs in other forms of habituation and supports the notion that there are different mechanisms involved in habituation of sensory-evoked behaviors.

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Habituation and Sensitization of Startle Reflexes Elicited Electrically from the Brainstem

Cited by 119 publications

References 13 publications

Heterosynaptic Facilitation of Tail Sensory Neuron Synaptic Transmission during Habituation in Tail-Induced Tail and Siphon Withdrawal Reflexes ofAplysia

Heterosynaptic Facilitation of Tail Sensory Neuron Synaptic Transmission during Habituation in Tail-Induced Tail and Siphon Withdrawal Reflexes ofAplysia

Prepulse Inhibition and Habituation of Acoustic Startle Response in Male MDMA (‘Ecstasy’) Users, Cannabis Users, and Healthy Controls

Group III Metabotropic Glutamate Receptors Inhibit Startle-Mediating Giant Neurons in the Caudal Pontine Reticular Nucleus But Do Not Mediate Synaptic Depression/Short-Term Habituation of Startle

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