Regular-spiking neurons responded with single spikes early in the train and bursts later, whereas bursting neurons fired bursts early in the train and single spikes later (Figures 4A and 4B). As both types of neurons can

and do elicit bursts, the present nomenclature for the observed physiological heterogeneity is misleading. Therefore, we introduce a new nomenclature: late-bursting (previously “regular-spiking”) and early-bursting (previously “bursting”) pyramidal neurons. Although we chose names based on their bursting patterns in response to trains of inputs, there are many additional differences between the two cell types (summarized in Table 2). We studied the long-lasting modulation of pyramidal cell firing patterns using synaptic theta-burst stimulation (TBS)—a commonly used plasticity-induction

protocol that mimics hippocampal activity in vivo during spatial exploration and other learning tasks. To establish a normative baseline prior to plasticity Dolutegravir in vivo induction, we adjusted the somatic current injection amplitude to elicit on average four bursts out of ten inputs per train during the baseline period and held this amplitude constant for the duration of the experiment. After measuring neuronal output by counting the number of bursts elicited by each train during a 10 min baseline period, we delivered TBS (see Experimental Procedures) and measured the ensuing changes in bursting. Because neuronal output in response to somatic current injection is controlled by activation of intrinsic voltage-gated or Ca2+-activated ion channels, changes in the those number of burst responses were a measure of altered intrinsic click here postsynaptic excitability.

Expanding on previous work focusing on early-bursting cells (Moore et al., 2009), we found that both types of neurons throughout CA1 and the subiculum displayed a long-lasting increase in bursting after synaptic TBS in normal artificial cerebrospinal fluid (ACSF) (Figures 4C–4E and Figure S3). As shown for a representative late-bursting neuron in CA1 and an early-bursting neuron in the subiculum, four bursts were elicited during the baseline period (Figure 4A) and nine bursts were elicited by the same stimulus after TBS (Figure 4C). This plasticity of bursting (“burst plasticity”) was activity dependent—in the absence of synaptic TBS, the level of bursting did not change over the course of 50 min (Figure S3A). We investigated the pharmacology of burst plasticity induction in the two cell types throughout CA1 and the subiculum. We found that the induction of burst plasticity in both cell types did not require activation of ionotropic glutamate receptors or GABAA and GABAB receptors (Figures S3B and S3C). Rather, plasticity induction depended on selective activation of metabotropic glutamate receptors (mGluRs) and muscarinic acetylcholine receptors (mAChRs). Interestingly, the two types of neurons differed strikingly in their response to the activation of specific subtypes of receptors (Figure 4F and Figures S3D–S3K).