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M2 receptors in LGF mediate hyperpolarization of interneurons when ACh present. Supresses inhibition at low levels of input, but at increased levels, hyperpolarization activates CA++ channels that cause increased firing, thus leading to inhibition similar to when ACh is absent (at these increased input levels only).
In 'bellum, fast inhibition delays inhibition, while slow inhibitory current decreases gain of inhibition.
Deciding when to decide. Integrative fxn that dictates when to act. What guides expectations in different environments? Neuromodulators? Couldn't be glut inputs, would have to be some kinda global signal.
In response to altered activity patterns, post synaptic neurons (in SCN) can alter their NT receptor expression from one type to another (e.g., glut to ACh). Novel form of plasticity. This was found in developing xenopus, but present in adulthoood too? "Reserver pool neurons."
Medial entorhinal cortex (MEC) is location of grid cells, which do not change firing pattern in same spatial location, even if space is populated with different objects or has varying physical shape (i.e., round vs square or black vs white). Place cells in CA3 will not change firing location to different objects, but firing rate is modulated. For example, as morph enclosure from square to circle, firing rate will gradually change (didn't I read something about all or nothing changes in place cells somewhere???). This firing rate modulation is dependent on the lateral EC. CA3 appears to integrate both 'where' and 'what' info from MEC and LEC, respectively, into a single memory trace.
Both amplitude and coherence of rhythmic firing affect the ability of population to activate targets. Amplitude of LFP is related to interval between cycles. Both excitatory and inhibitory signals in single cell are in phase with LFP signal. Hvr, IPSC is ~5x larger than EPSC and lags behind it by <1ms or so. Larger amplitude LFP signal = larger IPSP and hyperpolarization = longer time to begin next cycle of oscillation (larger pool of pyramidal cells firing will recruit more inhibitory neurons leading to increased inhibition).
Much larger excitatory input into L2/3 interneurons in olfactory cortex vs. pyramidal neurons (Caleb).
Learning-related fine-scale specificity imaged in motor cortex circuits of behaving mice
Task - odor discrimination in head-fixed mice. 2 odors: Odor A = lick for water reward. Odor B = no water/no lick. Incorrect response results in extended ITI. ~300+ trials/session. Show intra- and intersession learning. Pretty much 100% correct rejection by trial 250 of first session. Also, lick efficiency (overall number of licks, even to reward) decreases with learning.
Anatomy - Two lick-related areas in M1: alm and ppm (I think). alm elicits rudimentary tongue movements when stimulated. ppm may elicit some jaw movements. Deactivation of either (muscimol) inhibits licking movement in awake animals. Retrograde tracers (rabies) injected into tongue show labeling in both areas (or just ppm?) via motor pathway (motor nuclei in brainstem, reticular formation, M1). Anterograde tracing (AAV) shows labeling in reticular.
Cell activation - Ca dye in-vivo imaging of L2/3 neurons in alm and ppm. Classified cells based on level of response (dye activation via firing) during 'hit' trials and 'correct rejection' trials. Found cells showing increased activation to hit trials, CR trials, both, or neither. All types found in both areas (alm and ppm), in (somewhat) similar proportions. more hit than CR. More neither than any other classification (roughly half of all cells visualized). Population of hit and CR cells decreased a bit with learning (more efficient? Stereotyped behavior adopted?). Level of activation during response (and even cell classification) could change with learning. CR cells are associated with withholding of licking - are these inhibitory???
Population analysis - both hit and CR cells are intermingled spatially. Did correlation analysis for activity. Cells with same response classification showed more coincident activity, and also I believe were more likely to be spatially close vs other cells? (hit vs CR). Best part - coincident activation within a population increased with "learning" (both within and between sessions). Seen for both cell classification types. So, circuit of functionally related cell types exists and is strengthened (perhaps) with learning (I think training). Over learning, rate of firing stays the same, just that correlation between functionally related neurons increases (and more neurons included in network).
Two scenarios jump out which may be responsible for increased correlation of 'functionally related' cells: 1) increased connectivity between these cells (likely due to repetitive, coincident firing during motor training (or, as he sees it, learning)). 2) selective increased input from outside the network, which controls or coordinates this movement (or maybe even is responsible for discrimination of trials and selection of motor output - although withholding of response is not a motor output).