scholarly journals Plasticity of Horizontal Connections at a Functional Border in Adult Rat Somatosensory Cortex

2009 ◽  
Vol 2009 ◽  
pp. 1-15 ◽  
Author(s):  
Sally A. Marik ◽  
Peter W. Hickmott
Keyword(s):  
Synaptic Plasticity ◽  
Low Frequency ◽  
Cortical Reorganization ◽  
Adult Rat ◽  
Horizontal Connections ◽  
Frequency Stimulation ◽  
Rat Somatosensory Cortex ◽  
Cortical Regions

Horizontal connections in superficial cortical layers integrate information across sensory maps by connecting related functional columns. It has been hypothesized that these connections mediate cortical reorganization via synaptic plasticity. However, it is not known if the horizontal connections from discontinuous cortical regions can undergo plasticity in the adult. Here we located the border between two discontinuous cortical representations in vivo and used either pairing or low-frequency stimulation to induce synaptic plasticity in the horizontal connections surrounding this border in vitro. Individual neurons revealed significant and diverse forms of synaptic plasticity for horizontal connections within a continuous representation and discontinuous representations. Interestingly, both enhancement and depression were observed following both plasticity paradigms. Furthermore, plasticity was not restricted by the border's presence. Depolarization in the absence of synaptic stimulation also produced synaptic plasticity, but with different characteristics. These experiments suggest that plasticity of horizontal connections may mediate functional reorganization.

scholarly journals In vivo potentiation of post-tetanic twitch across age and sex

2021 ◽  
Vol 154 (9) ◽  
Author(s):  
Mina P. Peyton ◽  
Dawn A. Lowe
Keyword(s):  
Skeletal Muscle ◽  
Low Frequency ◽  
Twitch Force ◽  
Main Effect ◽  
Frequency Stimulation ◽  
Post Tetanic Potentiation ◽  
Main Effects ◽  
Age And Sex

Twitch force potentiation of fast-twitch skeletal muscle is produced by repetitive stimulation that can be achieved from either (1) the staircase effect (continual low frequency stimulation) or (2) post-tetanic potentiation (a 1–2 s high-frequency tetanic stimulation). Previous studies examining twitch force potentiation have been conducted in vitro and shown that it is related to phosphorylation of myosin regulatory light chain (pRLC). We previously found, in vitro, reduced potentiation of twitch force and decreased pRLC in ovariectomized (Ovx, estrogen-deficient) compared with sham-operated (estrogen-replete) mice. Thus, we questioned whether this phenomenon occurred in vivo and whether age and sex would affect the potentiation of twitch force. Using an in vivo post-tetanic potentiation method (one twitch contraction followed by a tetanic contraction—100 Hz for 1,000 ms with 0.01 ms pulses, and two post-tetanic twitch contractions), we investigated twitch torque potentiation in C57BL/6 young and old, male and female mice. There were significant main effects of sex (P < 0.001) and age (P < 0.001) on body mass and significant main effects of sex (P < 0.001) on tibialis anterior and extensor digitorum longus muscle masses, with males and aged being relatively greater. Analysis of twitch torque using a three-way ANOVA across time, age, and sex showed a significant main effect of time (pre < post; P < 0.001), time × age (P = 0.038), and time × sex (P = 0.028), indicating potentiation occurred in young and old, males and females. Analysis of twitch torque potentiation (percent increase) using a two-way ANOVA revealed a significant main effect of age (young = 45.16 ± 2.04 versus old = 27.88 ± 9.96; P < 0.001) with no effect of sex (P = 0.215). In summary, enhanced generation of twitch force of skeletal muscle using a post-tetanic potentiation method does occur in vivo and is affected by age but not sex, as there is greater twitch torque potentiation in young than old mice.

Local Circuit Properties Underlying Cortical Reorganization

2002 ◽  
Vol 88 (3) ◽  
pp. 1288-1301 ◽  
Author(s):  
Peter W. Hickmott ◽  
Michael M. Merzenich
Keyword(s):  
Cortical Reorganization ◽  
The Novel ◽  
Adult Rats ◽  
Postsynaptic Potentials ◽  
Local Circuit ◽  
Adult Rat ◽  
The Times ◽  
Stimulation Of

Peripheral denervation has been shown to cause reorganization of the deafferented somatotopic region in primary somatosensory cortex (S1). However, the basic mechanisms that underlie reorganization are not well understood. In the experiments described in this paper, a novel in vivo/in vitro preparation of adult rat S1 was used to determine changes in local circuit properties associated with the denervation-induced plasticity of the cortical representation in rat S1. In the present studies, deafferentation of rat S1 was induced by cutting the radial and median nerves in the forelimb of adult rats, resulting in a rapid shift of the location of the forepaw/lower jaw border; the amount of the shift increased over the times assayed, through 28 days after denervation. The locations of both borders (i.e., original and reorganized) were marked with vital dyes, and slices from the marked region were used for whole-cell recording. Responses were evoked using electrical stimulation of supragranular S1 and recorded in supragranular neurons close to either the original or reorganized border. For each neuron, postsynaptic potentials (PSPs) were evoked by stimulation of fibers that crossed the border site (CB stim) and by equivalent stimulation that did not cross (NCB stim). Monosynaptic inhibitory postsynaptic potentials (IPSPs) were also examined after blocking excitatory transmission with 15 μM CNQX plus 100 μMdl-APV. The amplitudes of PSPs and IPSPs were compared between CB and NCB stimulation to quantify effects of the border sites on excitation and inhibition. Previous results using this preparation in the normal (i.e., without induced plasticity) rat S1 demonstrated that at a normal border both PSPs and IPSPs were smaller when evoked with CB stimulation than with NCB stimulation. For most durations of denervation, a similar bias (i.e., smaller responses with CB stimulation) for PSPs and IPSPs was observed at the site of the novel reorganized border, while no such bias was observed at the suppressed original border site. Thus changes in local circuit properties (excitation and inhibition) can reflect larger-scale changes in cortical organization. However, specific dissociations between these local circuit properties and the presence of the novel border at certain durations of denervation were also observed, suggesting that there are several intracortical processes contributing to cortical reorganization over time and that excitation and inhibition may contribute differentially to them.

Long-Term Synaptic Plasticity in the Honeybee

1997 ◽  
Vol 78 (1) ◽  
pp. 528-532 ◽  
Author(s):  
S. Oleskevich ◽  
J. D. Clements ◽  
M. V. Srinivasan
Keyword(s):  
Synaptic Plasticity ◽  
Field Potential ◽  
Low Frequency ◽  
Fold Increase ◽  
Afferent Input ◽  
Insect Brain ◽  
Paired Pulse ◽  
Frequency Stimulation

Oleskevich, S., J. D. Clements, and M. V. Srinivasan. Long-term synaptic plasticity in the honeybee. J. Neurophysiol. 78: 528–532, 1997. A monosynaptic response was recorded in vivo in the mushroom body of the bee brain, an important site for memory consolidation. Focal electrical stimulation of a major afferent input evoked an extracellular field potential that consisted of a presynaptic fiber volley and a postsynaptic response. We report a long-lasting potentiation of the synaptic response (2.6-fold increase; ≤3.5 h). Potentiation of the response was induced by low-frequency stimulation (0.02–1.0 Hz), was input specific, and was maintained in the absence of stimulation. Paired-pulse facilitation of the response was converted to paired-pulse depression after potentiation, suggesting a presynaptic mechanism. This is the first demonstration of long-term synaptic plasticity in the insect brain.

scholarly journals Potential Role of Synaptic Activity to Inhibit LTD Induction in Rat Visual Cortex

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Matthew R. Stewart ◽  
Hans C. Dringenberg
Keyword(s):  
Visual Cortex ◽  
Low Frequency ◽  
Synaptic Activity ◽  
Brain State ◽  
Complex Activity ◽  
Intact Brain ◽  
Frequency Stimulation ◽  
Cortical Synapses

Long-term depression (LTD), a widely studied form of activity-dependent synaptic plasticity, is typically induced by prolonged low-frequency stimulation (LFS). Interestingly, LFS is highly effective in eliciting LTDin vitro, but much less so underin vivoconditions; the reasons for the resistance of the intact brain to express LTD are not well understood. We examined if levels of background electrocorticographic (ECoG) activity influence LTD induction in the thalamocortical visual system of rats under very deep urethane anesthesia, inducing a brain state of reduced spontaneous cortical activity. Under these conditions, LFS applied to the lateral geniculate nucleus resulted in LTD of field postsynaptic potentials (fPSPs) recorded in the primary visual cortex (V1). Pairing LFS with stimulation of the brainstem (pedunculopontine) reticular formation resulted in the appearance of faster, more complex activity in V1 and prevented LTD induction, an effect that did not require muscarinic or nicotinic receptors. Reticular stimulation alone (without LFS) had no effect on cortical fPSPs. These results show that excitation of the brainstem activating system blocks the induction of LTD in V1. Thus, higher levels of neural activity may inhibit depression at cortical synapses, a hypothesis that could explain discrepancies regarding LTD induction in previousin vivoandin vitrowork.

Implications of Kindling And Quenching For the Possible Frequency Dependence Of rTMS

CNS Spectrums ◽  
1997 ◽  
Vol 2 (1) ◽  
pp. 54-60 ◽  
Author(s):  
R. M. Post ◽  
T. Kimbrell ◽  
M. Frye ◽  
M. George ◽  
U. McCann ◽  
...  
Keyword(s):  
Low Frequency ◽  
Repeated Administration ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Seizure Threshold ◽  
Frequency Stimulation ◽  
Stimulation Of

AbstractKindling involves repeated administration of brief high-frequency electrophysiological stimulation of the brain at initially subthreshold intensities that eventually evoke full-blown seizures. It has thus been used not only as a model of epileptogenesis, but of long-term neuronal memory. Quenching is a phenomenon that utilizes low-frequency stimulation for much longer periods of time (eg, 1 Hz for 15 minutes), and appears to exert preventive effects on the development of kindling and inhibit the manifestation of full-blown kindled seizures by markedly increasing the amygdala afterdischarge and seizure threshold. (See also “Kindling and Quenching: Conceptual Implications for rTMS,” by Weiss and Post, page 32). The parameters of kindling and quenching with intracerebral stimulation of the amygdala in vivo are highly similar to those achieved in vitro in hippocampai slice preparations for inducing long-term potentiation (LTP) and longterm depression (LTD), respectively. These neuroplastic changes are relatively long lasting and appear reversible at the level of synaptic function with either LTD or LTP capable of countering the effects of the other.

A Detailed Examination of the in vivo and in vitro Effects of ACTH on Gonadotropin Secretion in the Adult Rat

1985 ◽  
Vol 40 (4) ◽  
pp. 297-302 ◽  
Author(s):  
David R. Mann ◽  
Diane Evans ◽  
Festus Edoimioya ◽  
Freja Kamel ◽  
George M. Butterstein
Keyword(s):  
Detailed Examination ◽  
Gonadotropin Secretion ◽  
Adult Rat ◽  
In Vitro Effects

scholarly journals Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation

2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Protein Kinase ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Protein Kinase D

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

scholarly journals Regulation of GABAergic synapse formation and plasticity by GSK3β-dependent phosphorylation of gephyrin

2010 ◽  
Vol 108 (1) ◽  
pp. 379-384 ◽  
Author(s):  
Shiva K. Tyagarajan ◽  
Himanish Ghosh ◽  
Gonzalo E. Yévenes ◽  
Irina Nikonenko ◽  
Claire Ebeling ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Hippocampal Neurons ◽  
Glycogen Synthase ◽  
Phosphorylation Site ◽  
Scaffolding Protein ◽  
Scaffolding Proteins ◽  
Gabaergic Synapse ◽  
Gabaergic Synapses

Postsynaptic scaffolding proteins ensure efficient neurotransmission by anchoring receptors and signaling molecules in synapse-specific subcellular domains. In turn, posttranslational modifications of scaffolding proteins contribute to synaptic plasticity by remodeling the postsynaptic apparatus. Though these mechanisms are operant in glutamatergic synapses, little is known about regulation of GABAergic synapses, which mediate inhibitory transmission in the CNS. Here, we focused on gephyrin, the main scaffolding protein of GABAergic synapses. We identify a unique phosphorylation site in gephyrin, Ser270, targeted by glycogen synthase kinase 3β (GSK3β) to modulate GABAergic transmission. Abolishing Ser270 phosphorylation increased the density of gephyrin clusters and the frequency of miniature GABAergic postsynaptic currents in cultured hippocampal neurons. Enhanced, phosphorylation-dependent gephyrin clustering was also induced in vitro and in vivo with lithium chloride. Lithium is a GSK3β inhibitor used therapeutically as mood-stabilizing drug, which underscores the relevance of this posttranslational modification for synaptic plasticity. Conversely, we show that gephyrin availability for postsynaptic clustering is limited by Ca2+-dependent gephyrin cleavage by the cysteine protease calpain-1. Together, these findings identify gephyrin as synaptogenic molecule regulating GABAergic synaptic plasticity, likely contributing to the therapeutic action of lithium.

Effects of hypophysectomy and subsequent FSH and testosterone treatment on inhibin production by adult rat testes

1985 ◽  
Vol 105 (1) ◽  
pp. 1-6 ◽  
Author(s):  
C. L. Au ◽  
D. M. Robertson ◽  
D. M. de Kretser
Keyword(s):  
Seminiferous Tubule ◽  
Hormonal Control ◽  
Human Chorionic Gonadotrophin ◽  
Experimental Conditions ◽  
Adult Rats ◽  
Adult Rat ◽  
Fluid Production ◽  
Tubule Fluid

ABSTRACT The hormonal control of inhibin production by adult rat testes was investigated using an in-vitro inhibin bioassay validated for the measurement of inhibin activity in charcoal-treated rat testicular extracts. The effect of hypophysectomy examined at 16 h, 3, 7 and 42 days after surgery showed a decrease in testicular inhibin content and seminiferous tubule fluid production by 7 days and a decrease in inhibin production by 42 days. Serum FSH and LH were suppressed 3 days after surgery. In 30-day chronically hypophysectomized adult rats treated for 3 days with twice daily s.c. injections of (a) human FSH (hFSH, 22 i.u./rat per day), (b) testosterone (5 mg/rat per day), (c) hFSH + testosterone (same doses as a and b), or (d) human chorionic gonadotrophin (hCG, 12 i.u./rat per day), hFSH or hFSH and testosterone stimulated an increase in testicular inhibin content but not in inhibin production or tubule fluid production. Testosterone and hCG had no effect on these parameters. It is concluded that in vivo, FSH alone stimulates an increase in testicular inhibin content. The failure to observe an increase in inhibin production in vivo is attributed to the suppression of seminiferous tubule fluid production under the same experimental conditions. J. Endocr. (1985) 105, 1–6

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