The stability of 6-hydroxydopamine under minipump conditions

Haycock, Dean A.; Bear, Mark F.

doi:10.1007/bf00237455

Cited by 5 publications

(2 citation statements)

References 6 publications

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“…It appears that, aside from the series of data we presented, the crucial aspects in methodology ( e.g., Kasamatsu & Schmidt, 1997. See also Haycock & Bear, 1984) were apparently not taken seriously in the similar studies by other investigators in the field. Without having established the chemical stability and specificity as applied to the visual cortex in vivo, 6‐OHDA, NA and related molecules were tested to either reject the NAergic regulation of ODP or claim the involvement of various other molecules (e.g., Rauschecker, Egert, & Kossel, 1990).…”

Section: A Strategic Development In Search Of Molecular Bases Of Cortmentioning

confidence: 90%

Ocular dominance plasticity: Molecular mechanisms revisited

Kasamatsu

Imamura

2020

J of Comparative Neurology

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Ocular dominance plasticity (ODP) is a type of cortical plasticity operating in visual cortex of mammals that are endowed with binocular vision based on the competition-driven disparity. Earlier, a molecular mechanism was proposed that catecholamines play an important role in the maintenance of ODP in kittens. Having survived the initial test, the hypothesis was further advanced to identify noradrenaline (NA) as a key factor that regulates ODP in the immature cortex. Later, the ODPpromoting effect of NA is extended to the adult with age-related limitations. Following the enhanced NA availability, the chain events downstream lead to the β-adrenoreceptor-induced cAMP accumulation, which in turn activates the protein kinase A. Eventually, the protein kinase translocates to the cell nucleus to activate cAMP responsive element binding protein (CREB). CREB is a cellular transcription factor that controls the transcription of various genes, underpinning neuronal plasticity and long-term memory. In the advent of molecular genetics in that various types of new tools have become available with relative ease, ODP research has lightly adopted in the rodent model the original concepts and methodologies. Here, after briefly tracing the strategic maturation of our quest, the review moves to the later development of the field, with the emphasis placed around the following issues: (a) Are we testing ODP per se? (b) What does monocular deprivation deprive of the immature cortex? (c) The critical importance of binocular competition, (d) What is the adult plasticity? (e) Excitation-Inhibition balance in local circuits, and (f) Species differences in the animal models.

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Section: A Strategic Development In Search Of Molecular Bases Of Cortmentioning

confidence: 90%

Ocular dominance plasticity: Molecular mechanisms revisited

Kasamatsu

Imamura

2020

J of Comparative Neurology

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“…An additional potentially confounding variable with minipump experiments is that drugs may not be stable in solution at 38°C for extended periods of time (see Haycock and Bear, 1984). We addressed this question by studying the effectiveness of APV which had been maintained at 38°C for 7 d in blocking responses in vitro that are dependent on NMDA receptors (Artola and Singer, 1987).…”

Section: Methodsmentioning

confidence: 99%

Disruption of experience-dependent synaptic modifications in striate cortex by infusion of an NMDA receptor antagonist

et al. 1990

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To assess the possibility that NMDA receptors play a special role in visual cortical plasticity, the selective antagonist 2-amino-5- phosphonovaleric acid (APV) was continuously infused into the striate cortex of kittens as the visual environment was manipulated during the critical period. The cortex was studied using single-unit recording from sites between 3 and 6 mm from the infusion cannulae. One week of D,L-APV infusion coincident with monocular deprivation or “reverse suture” produced a concentration-dependent increase in the percentage of neurons that (1) lacked normal orientation selectivity and (2) were responsive to stimulation of the deprived eye. These effects outlasted the presence of the drug in the tissue. APV treatment also prevented the acquisition of selectivity and visual responsiveness that normally results from monocular visual experience after dark-rearing. Lasting effects of chronic APV infusion were not observed in adult striate cortex. The effects of APV on kitten striate cortex depended on the presence of the D stereoisomer as infusion of L-APV was without effect. Estimates of extracellular concentration using 3H-APV indicated that significant effects could be obtained with concentrations as low as 20 microM D,L-APV. Recordings from units during infusion indicated that visual responses were reduced by APV. Nonetheless, a normal percentage of visually responsive neurons was found at sites greater than or equal to 3 mm from the infusion cannula. There was no evidence that chronic APV infusion affected the sampling frequency of recorded neurons or disrupted cytoarchitecture at the sites further than 3 mm from the infusion cannula. Taken together, the data indicate that the effects of APV on kitten striate cortex are likely due specifically to the blockade of NMDA receptors. These data are considered in relation to several hypotheses concerning the role of NMDA receptors in the experience-dependent development of striate cortex.

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