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Contributions of matrix metalloproteinases to neural plasticity, habituation, associative learning and drug addiction.

Wright JW, Harding JW - Neural Plast. (2010)

Bottom Line: It is presumed that while these ECM proteins are weakened, and/or detached, synaptic connections can form resulting in new neural pathways.We conclude with a consideration of the influence of these phenomena on drug addiction, given that these same processes may be instrumental in the formation of addiction and subsequent relapse.However, our knowledge concerning the precise spatial and temporal relationships among the mechanisms of neural plasticity, habituation, associative learning, and memory consolidation is far from complete and the possibility that these phenomena mediate drug addiction is a new direction of research.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA. wrightjw@wsu.edu

ABSTRACT
The premise of this paper is that increased expression of matrix metalloproteinases (MMPs) permits the reconfiguration of synaptic connections (i.e., neural plasticity) by degrading cell adhesion molecules (CAMs) designed to provide stability to those extracellular matrix (ECM) proteins that form scaffolding supporting neurons and glia. It is presumed that while these ECM proteins are weakened, and/or detached, synaptic connections can form resulting in new neural pathways. Tissue inhibitors of metalloproteinases (TIMPs) are designed to deactivate MMPs permitting the reestablishment of CAMs, thus returning the system to a reasonably fixed state. This review considers available findings concerning the roles of MMPs and TIMPs in reorganizing ECM proteins thus facilitating the neural plasticity underlying long-term potentiation (LTP), habituation, and associative learning. We conclude with a consideration of the influence of these phenomena on drug addiction, given that these same processes may be instrumental in the formation of addiction and subsequent relapse. However, our knowledge concerning the precise spatial and temporal relationships among the mechanisms of neural plasticity, habituation, associative learning, and memory consolidation is far from complete and the possibility that these phenomena mediate drug addiction is a new direction of research.

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Related in: MedlinePlus

Mean (± SEM) group changes in head-shake responses (HSR) per three-trial blocks during sessions I and II. These sessions were separated by 5 minutes, 2, 6, or 24 hours, respectively. There were no differences among these groups comparing the first trial blocks of Session I. Each group significantly differed from the others comparing the first trail blocks of Session II. Specifically, the 5 minute ISI group indicated very little spontaneous recovery suggesting excellent memory retention of the habituatory response. The 2 and 6 hours ISI groups showed increments in spontaneous recovery and thus some loss of memory retention, while the 24-hour ISI group revealed 95% spontaneous recovery suggesting nearly complete loss of memory retention for habituation of the HSR, *P < .05, modified from Wright et al. [115].
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fig2: Mean (± SEM) group changes in head-shake responses (HSR) per three-trial blocks during sessions I and II. These sessions were separated by 5 minutes, 2, 6, or 24 hours, respectively. There were no differences among these groups comparing the first trial blocks of Session I. Each group significantly differed from the others comparing the first trail blocks of Session II. Specifically, the 5 minute ISI group indicated very little spontaneous recovery suggesting excellent memory retention of the habituatory response. The 2 and 6 hours ISI groups showed increments in spontaneous recovery and thus some loss of memory retention, while the 24-hour ISI group revealed 95% spontaneous recovery suggesting nearly complete loss of memory retention for habituation of the HSR, *P < .05, modified from Wright et al. [115].

Mentions: Nonassociative learning includes the phenomena of habituation, dishabituation, and sensitization and is considered to be the simplest form of learning. Of these habituation is the most frequently studied and refers to a decrease in responding (as related to frequency, magnitude, or intensity) to a stimulus repeatedly presented, or presented for a prolonged period of time [99–101]. Habituation has been documented across many species and response systems ranging from the gill-withdrawal reflex in Aplysia [102] and tap withdrawal or chemotaxic response in the nematode Caenorhabditis elegans [103], to acoustic startle response in rats and mice [104], schedules of reinforcement in operant conditioning [105, 106] and feeding in humans [107]. Although the neural mechanism(s) underlying habituation has not been identified, the hippocampus has been implicated in the control of inhibitory processes, particularly habituation [108–110]. In support of this notion bilateral hippocampectomy in rats has been shown to interfere with habituation to familiar objects in an open field object recognition task [111, 112], severely impair the acquisition and recall of platform location in the Morris water maze task [113], but failed to alter the habituatory pattern or rate of head-shake response (HSR) [114]. The HSR consists of a rapid rotation of the head about the anterior to posterior axis in response to a mild air stimulus applied to the ear [115]. This response follows a remarkably predictable decreasing negatively accelerated function of stimulus frequency (Figure 2).


Contributions of matrix metalloproteinases to neural plasticity, habituation, associative learning and drug addiction.

Wright JW, Harding JW - Neural Plast. (2010)

Mean (± SEM) group changes in head-shake responses (HSR) per three-trial blocks during sessions I and II. These sessions were separated by 5 minutes, 2, 6, or 24 hours, respectively. There were no differences among these groups comparing the first trial blocks of Session I. Each group significantly differed from the others comparing the first trail blocks of Session II. Specifically, the 5 minute ISI group indicated very little spontaneous recovery suggesting excellent memory retention of the habituatory response. The 2 and 6 hours ISI groups showed increments in spontaneous recovery and thus some loss of memory retention, while the 24-hour ISI group revealed 95% spontaneous recovery suggesting nearly complete loss of memory retention for habituation of the HSR, *P < .05, modified from Wright et al. [115].
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2821634&req=5

fig2: Mean (± SEM) group changes in head-shake responses (HSR) per three-trial blocks during sessions I and II. These sessions were separated by 5 minutes, 2, 6, or 24 hours, respectively. There were no differences among these groups comparing the first trial blocks of Session I. Each group significantly differed from the others comparing the first trail blocks of Session II. Specifically, the 5 minute ISI group indicated very little spontaneous recovery suggesting excellent memory retention of the habituatory response. The 2 and 6 hours ISI groups showed increments in spontaneous recovery and thus some loss of memory retention, while the 24-hour ISI group revealed 95% spontaneous recovery suggesting nearly complete loss of memory retention for habituation of the HSR, *P < .05, modified from Wright et al. [115].
Mentions: Nonassociative learning includes the phenomena of habituation, dishabituation, and sensitization and is considered to be the simplest form of learning. Of these habituation is the most frequently studied and refers to a decrease in responding (as related to frequency, magnitude, or intensity) to a stimulus repeatedly presented, or presented for a prolonged period of time [99–101]. Habituation has been documented across many species and response systems ranging from the gill-withdrawal reflex in Aplysia [102] and tap withdrawal or chemotaxic response in the nematode Caenorhabditis elegans [103], to acoustic startle response in rats and mice [104], schedules of reinforcement in operant conditioning [105, 106] and feeding in humans [107]. Although the neural mechanism(s) underlying habituation has not been identified, the hippocampus has been implicated in the control of inhibitory processes, particularly habituation [108–110]. In support of this notion bilateral hippocampectomy in rats has been shown to interfere with habituation to familiar objects in an open field object recognition task [111, 112], severely impair the acquisition and recall of platform location in the Morris water maze task [113], but failed to alter the habituatory pattern or rate of head-shake response (HSR) [114]. The HSR consists of a rapid rotation of the head about the anterior to posterior axis in response to a mild air stimulus applied to the ear [115]. This response follows a remarkably predictable decreasing negatively accelerated function of stimulus frequency (Figure 2).

Bottom Line: It is presumed that while these ECM proteins are weakened, and/or detached, synaptic connections can form resulting in new neural pathways.We conclude with a consideration of the influence of these phenomena on drug addiction, given that these same processes may be instrumental in the formation of addiction and subsequent relapse.However, our knowledge concerning the precise spatial and temporal relationships among the mechanisms of neural plasticity, habituation, associative learning, and memory consolidation is far from complete and the possibility that these phenomena mediate drug addiction is a new direction of research.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA. wrightjw@wsu.edu

ABSTRACT
The premise of this paper is that increased expression of matrix metalloproteinases (MMPs) permits the reconfiguration of synaptic connections (i.e., neural plasticity) by degrading cell adhesion molecules (CAMs) designed to provide stability to those extracellular matrix (ECM) proteins that form scaffolding supporting neurons and glia. It is presumed that while these ECM proteins are weakened, and/or detached, synaptic connections can form resulting in new neural pathways. Tissue inhibitors of metalloproteinases (TIMPs) are designed to deactivate MMPs permitting the reestablishment of CAMs, thus returning the system to a reasonably fixed state. This review considers available findings concerning the roles of MMPs and TIMPs in reorganizing ECM proteins thus facilitating the neural plasticity underlying long-term potentiation (LTP), habituation, and associative learning. We conclude with a consideration of the influence of these phenomena on drug addiction, given that these same processes may be instrumental in the formation of addiction and subsequent relapse. However, our knowledge concerning the precise spatial and temporal relationships among the mechanisms of neural plasticity, habituation, associative learning, and memory consolidation is far from complete and the possibility that these phenomena mediate drug addiction is a new direction of research.

Show MeSH
Related in: MedlinePlus